Antioxidants E-Book
216,99 €
Mehr erfahren.
- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Sprache: Englisch
This book provides a comprehensive exploration of the role antioxidants play in preventing and managing a variety of diseases and critically examines current research on the effects of nutritional antioxidants on specific disease states.
Antioxidants: Nature’s Defense Against Disease investigates the complex relationship between oxidative stress and many health disorders, providing essential insights into the role of antioxidants in disease prevention. It investigates how oxidative stress, induced by an imbalance of free radicals and antioxidants in the body, leads to the development and progression of maladies ranging from cardiovascular disorders to neurological diseases. The book includes evidence-based ways for harnessing antioxidants from natural sources such as fruits, vegetables, and herbs to reduce the impact of oxidative damage and improve general health.
The book presents the most recent scientific advances and clinical findings in antioxidant therapy. It is a comprehensive resource for healthcare professionals and researchers and covers everything from the molecular mechanisms that underpin oxidative stress to the protective benefits of antioxidants against chronic diseases. Through its interdisciplinary approach and practical insights, Antioxidants: Nature’s Defense Against Disease provides readers with the knowledge and tools they need to optimize antioxidant consumption, empowering them to control their health and lower their risk of severe diseases.
Audience
The core audiences for this book are nutritionists, dieticians, researchers, and graduate students in health sciences, and those interested in preventive healthcare, such as health, nutrition, fitness, and wellness enthusiasts, looking to deepen their understanding of implementing antioxidant strategies and improving lifestyle choices.
Sie lesen das E-Book in den Legimi-Apps auf:
Seitenzahl: 1481
Veröffentlichungsjahr: 2024
Ähnliche
Table of Contents
Cover
Table of Contents
Series Page
Title Page
Copyright Page
Preface
1 Basics of Antioxidants and Their Importance
Abbreviations
1.1 Introduction
1.2 Generalization of Antioxidant
1.3 Reactive Oxygen Species (ROS) and Free Radicals
1.4 Importance of Antioxidant in Medicine
1.5 Conclusion
References
2 Antioxidants in Cancer Prevention
2.1 Introduction
2.2 Free Radicals
2.3 Antioxidants
2.4 Roles of Antioxidants in Cancer Prevention
2.5 Can Antioxidant Supplements Help to Prevent Cancer?
2.6 Pharmacokinetics of Antioxidants
2.7 Safety Assessment
2.8 Antioxidants can be Pro-Oxidants
2.9 Quality Control of Antioxidant Supplements
2.10 Conclusions
References
3 Antioxidants in Inflammatory Diseases
3.1 Introduction
3.2 Inflammatory Disease: An Overview, Definition and Classification of Inflammatory Diseases
3.3 Pathogenesis of Inflammation, Role of Oxidative Assault in Inflammatory Disease Development
3.4 Introduction to Antioxidants, Definition and Classification of Antioxidants, Mechanisms of Antioxidant Action, Sources of Dietary Antioxidants
3.5 Enzymatic Activity
3.6 Sources of Dietary Antioxidants
3.7 Mechanisms of Oxidative Assault in Inflammatory Disease
3.8 Antioxidants and Inflammatory Disease
3.9 Antioxidants in Specific Inflammatory Diseases
3.10 Therapeutic Strategies Targeting Oxidative Assault
3.11 Challenges and Future Directions
3.12 Conclusion
References
4 Antioxidants in Cardiovascular Disease: Molecular Interaction and Therapeutic Implications
4.1 Introduction
4.2 Oxidative Assault and Cardiovascular Health
4.3 Oxidative Assault and Association with CVDs
4.4 Antioxidants and Their Sources
4.5 Potential Antioxidant-Based Experimental Interventions
4.6 Conclusion
References
5 Antioxidant Therapy: A Promising Avenue for Regulating Inflammation in Psoriasis
5.1 Introduction
5.2 Pathogenesis of Psoriasis
5.3 Understanding Antioxidants
5.4 The Potential of Antioxidant Therapy in Psoriasis
5.5 Clinical Trials and Evidence-Based Findings
5.6 Future Perspectives and Challenges
5.7 Conclusion
References
6 Antioxidants in Infectious Disease Management
6.1 Introduction
6.2 Phytochemicals
6.3 Antioxidants
6.4 Disease and Causes of Death
6.5 Bases of Use of Antioxidants in the Management of Infectious Diseases
6.6 Sources of Antioxidant Beneficial in the Management of Infectious Diseases
6.7 Conclusion
Acknowledgement
References
7 Role of Antioxidant Therapy in Respiratory Disease Management
7.1 Introduction
7.2 Respiratory Diseases
7.3 Antioxidants and Their Therapies for Respiratory Diseases
7.4 Barriers to Pulmonary Delivery
7.5 Novel Approaches for Antioxidant Drug Delivery
7.6 Future Perspectives and Conclusion
References
8 Antioxidants in Aging
8.1 Introduction
8.2 Mechanisms of Action of Various Antioxidant
8.3 Antioxidants in the Diet
8.4 The Role of Antioxidants in Cellular Senescence
8.5 Antioxidants and Age-Related Neurodegenerative Diseases
8.6 Antioxidants and Skin Aging
8.7 Lifestyle Factors and Antioxidant Defense
8.8 Recent Advancements in Antioxidants Research in Aging and Age-Related Diseases
8.9 Conclusion
References
9 Antioxidants Against Neurological Disorders
9.1 Introduction
9.2 Sources of Antioxidants
9.3 Relationship Between Oxidative Stress and Neurological Illnesses
9.4 Role of Antioxidants in Neurological Diseases
9.5 Therapeutic Strategies Using Antioxidants for Treatment of Neurological Disorder
9.6 Clinical Trials of Nanoformulations Containing Antioxidants Against Neurological Disorders
9.7 Conclusion
References
10 Role of Antioxidants for the Treatment of Metabolic Disorders
10.1 Introduction
10.2 Correlation of Metabolic Disorders and Oxidative Stress and ROS
10.3 Role of Oxidative Stress in Metabolic Disorders
10.4 Role of Antioxidants in Metabolic Disorders
10.5 Conclusion
References
11 Hepatoprotective Potential of Antioxidants in Medicinal Plants
11.1 Introduction
11.2 Understanding Antioxidants
11.3 Role of Nano-Antioxidants in Liver Function
11.4 Medicinal Plants with Hepatoprotective Properties
11.5 Clinical Studies on Medicinal Plants and Liver Diseases
11.6 Challenges and Limitations in Utilizing Medicinal Plants as Hepatoprotective Agents
11.7 Future Perspectives and Research Directions
11.8 Conclusion
References
12 Antioxidant Effects of Medicinal Plants for the Treatment of Epilepsy
12.1 Introduction
12.2 Epilepsy: An Overview
12.3 Oxidative Stress in Epilepsy
12.4 Mechanisms of Antioxidant Effects in Medicinal Plants
12.5 Medicinal Plant with Antioxidant Effect on Epilepsy Treatment
12.6 The Synergy Between Antioxidants and Conventional Antiepileptic Drugs (AEDs)
12.7 Challenges and Future Direction
12.8 Conclusion
References
13 Antioxidants and Obesity
13.1 Introduction
13.2 Pathological Role of Oxidative Stress in Obesity
13.3 Obesity Regulating Diverse Chemical Groups as Natural Antioxidants from Plant Sources
13.4 Nano Herbal Formulations with Anti-Obese Effects
13.5 Clinical Trials
13.6 Conclusion and Future Perspectives
References
14 Antioxidants in Hypertension
14.1 Introduction
14.2 Pathophysiology of Hypertension
14.3 Contribution of Antioxidants in Managing Hypertension
14.4 Antioxidant Therapy in Hypertension
14.5 Antioxidants to Treat Neurohumoral System-Induced Hypertension
14.6 Translating Antioxidant Research into Hypertension Management: Preclinical to Clinical
14.7 Future Scope and Conclusion
14.8 Acknowledgement
References
15 Antioxidants and Rheumatoid Arthritis
15.1 Introduction
15.2 Oxidative Stress and Rheumatoid Arthritis
15.3 Antioxidants in the Management of Rheumatoid Arthritis
15.4 Mechanisms of Antioxidants in the Prevention of Rheumatoid Arthritis
15.5 Conclusion and Future Perspectives
References
16 Antioxidants in Skin Disorders
16.1 Introduction
16.2 Importance of Antioxidants in Combating Free Radicals
16.3 Types of Antioxidants
16.4 Antioxidants Relevance to Skin Health
16.5 Clinical Studies and Evidences
16.6 Incorporating Antioxidants in Skincare
16.7 Challenges and Future Directions
16.8 Targeted Solutions for Specific Conditions
16.9 Conclusion
References
17 Antioxidants and Toxicity
17.1 Introduction
References
18 Exploring the Therapeutic and Pharmaceutical Potential of Antioxidants
18.1 Introduction
18.2 Roles of Antioxidants in Medical Science
18.3 Technological Requirements in Improving the Therapeutic Potential of Antioxidants
18.4 Economic Implication of the Therapeutic Potential of Antioxidants
18.5 Environmental Implication of the Therapeutic Potential of Antioxidants
18.6 Industrial Consideration of the Therapeutic Potential of Antioxidants
18.7 Quality Control in the Application of Antioxidants
18.8 Legal Considerations of the Application of Antioxidants
18.9 Roles of Antioxidants in the Implication of Policies and Governance in Healthcare Sector
18.10 Roles of Stakeholder’s Interest in Analyzing the Therapeutic Potential of Antioxidants
18.11 Health and Safety Consideration of the Application of Antioxidants
18.12 Challenges of the Application of Antioxidants
18.13 Future Perspective
18.14 Conclusion
References
19 Regulatory Aspects of Antioxidants
19.1 Introduction
19.2 Antioxidants Classification
19.3 Importance of Regulations in the Approval of Antioxidants
19.4 Regulatory Aspects of Antioxidants in Food
19.5 Toxicological Aspects
19.6 Antioxidant Labeling
19.7 Antioxidants Used as Excipients in Formulations
19.8 Excipient Data Required to be Submitted in Regulatory Dossier
19.9 Antioxidants Used to Treat Diseases
19.10 Clinical Trial Status of Antioxidants
19.11 Antioxidant-Based Clinical Trials for Alzheimer’s and Moderate Cognitive Impairment
19.12 Conclusion
References
Index
End User License Agreement
List of Tables
Chapter 2
Table 2.1 List of free radicals.
Table 2.2 Total phenolic, flavonoid, and carotenoid content in fruits.
Table 2.3 Antioxidants and polyphenols from fruits.
Table 2.4 Total phenolic, flavonoid, and carotenoid content in vegetables.
Table 2.5 Vitamin and mineral content in fruits.
Table 2.6 Vitamin and mineral content in selected vegetables.
Chapter 7
Table 7.1 Classification of antioxidants
Table 7.2 Various drug delivery systems employed for antioxidant delivery.
Table 7.3 Pulmonary diseases and their therapies followed by their mode of dru...
Chapter 8
Table 8.1 Summarized various endogenous and exogenous antioxidants derived fro...
Table 8.2 Summarization of key effects of nutrients and diet in skin aging [46...
Table 8.3 Some of the plants commonly used as the potential source of antioxid...
Chapter 9
Table 9.1 Mechanisms of different antioxidants against various neurological di...
Table 9.2 Various nanoformulations of antioxidants against neurodegenerative a...
Chapter 10
Table 10.1 Antioxidants in metabolic disorders.
Chapter 11
Table 11.1 Anti-hepatotoxic drugs based on herbal plants with their mechanism ...
Chapter 12
Table 12.1 Flavonoids with their target area.
Chapter 14
Table 14.1 Important antioxidants involved in the scavenging of oxidative stre...
Table 14.2 Molecular mechanism of several antioxidant therapies to treat hyper...
Chapter 17
Table 17.1 Biomarkers and their advantages and disadvantages.
Chapter 18
Table 18.1 Effects of different antioxidants on human health.
Chapter 19
Table 19.1 ADIs (Acceptable Daily Intake) of some antioxidants permitted in fo...
Table 19.2 Food use, maximum usage level approved, regulatory approval status ...
Table 19.3 List of USP general chapters used to assess the antioxidant propert...
Table 19.4 Antioxidants used as excipients in formulations.
Table 19.5 List of antioxidants used to treat diseases.
List of Illustrations
Chapter 1
Figure 1.1 Autoxidation process [20].
Figure 1.2 Sources of antioxidants.
Figure 1.3 Mechanism of action of antioxidants.
Figure 1.4 Mechanism of action of different natural antioxidants [89, 90].
Chapter 2
Figure 2.1 Chemical structures of antioxidant and anticancer compounds from fr...
Figure 2.2 Anticancer mechanism of flavonoids. Reproduced from Anna Rudzinska,...
Figure 2.3 Anticancer mechanism of phenolic acids. Reproduced from Anna Rudzin...
Figure 2.4 Anticancer mechanism of carotenoids. Reproduced from Anna Rudzinska...
Chapter 3
Figure 3.1 Oxidative assault-induced inflammation in RA.
Figure 3.2 ROS-induced IEC impairment in IBD.
Figure 3.3 ROS-induced atherosclerotic plaque formation and antioxidants.
Chapter 4
Figure 4.1 NOX-mediated ROS production.
Figure 4.2 ROS-mediated ox-LDL production and formation of fibrous plaque.
Figure 4.3 Antioxidant mechanisms of nuts,
Morus alba
and
Zizanialatifolia
.
Chapter 7
Figure 7.1 Pathophysiology of asthma.
Figure 7.2 Pathophysiology of COPD.
Figure 7.3 Pathophysiology of idiopathic pulmonary fibrosis.
Figure 7.4 Pathophysiology of lung cancer.
Figure 7.5 Pathophysiology of pulmonary arterial hypertension.
Figure 7.6 Barriers to pulmonary drug delivery.
Chapter 8
Figure 8.1 Sources of ROS generation. (
Created with Biorender
).
Figure 8.2 Mechanism of SOD and catalase as antioxidants. (
Created with Bioren
...
Figure 8.3 Age dependent neurodegeneration due to protein aggregation & mitoch...
Figure 8.4 Balancing of oxidative stress. (
Created with Biorender
).
Chapter 9
Figure 9.1 Role of various antioxidants used to treat neurological disorders [...
Chapter 10
Figure 10.1 Types of metabolic disorders.
Figure 10.2 Contributing factors for ROS generation.
Chapter 11
Figure 11.1 The impact of ROS from CCl4 on antioxidant enzymes and phytochemic...
Figure 11.2 Antioxidant enzyme system.
Figure 11.3 Classification of antioxidants.
Figure 11.4 The lipid mechanistic understanding of herbal medicine’s anti-NAFL...
Figure 11.5 The inflammatory mechanistic understanding of herbal medicine’s an...
Figure 11.6 Biological targets leading to ALD and targets for herbal remedies.
Figure 11.7 Liver damage and herbal plants’ preventive effects.
Chapter 12
Figure 12.1 ILAE classification of epilepsies.
Figure 12.2 Summary of the mechanisms involved in oxidative stress.
Figure 12.3 The role of oxidative stress and neuroinflammation in the etiology...
Chapter 13
Figure 13.1 Pathophysiological role in obesity.
Chapter 14
Figure 14.1 Antioxidant’s role and pathophysiology of hypertension through oxi...
Figure 14.2 Antioxidant therapy in the prevention of hypertension. By activati...
Chapter 15
Figure 15.1 Normal knee Joint vs. rheumatoid arthritis knee joint.
Figure 15.2 Types of antioxidants used for the management of RA.
Chapter 16
Figure 16.1 Effect of free radicals and oxidative stress on the normal cells o...
Figure 16.2 Effect of oxidation on collagen fibers in skin.
Chapter 18
Figure 18.1 Redox equilibrium in cells.
Figure 18.2 Causes of oxidative stress and its effects on health.
Figure 18.3 Technological requirements in improving the therapeutic potential ...
Figure 18.4 Economic implication of the therapeutic potential of antioxidants.
Figure 18.5 Environmental implication of the therapeutic potential of antioxid...
Figure 18.6 Industrial consideration of the therapeutic potential of antioxida...
Figure 18.7 Quality control in the application of antioxidants.
Figure 18.8 Legal considerations of the application of antioxidants.
Figure 18.9 Roles of antioxidants in the implication of policies and governanc...
Figure 18.10 Stakeholder’s involved in the analysis and use of antioxidants.
Figure 18.11 Health and safety consideration of the application of antioxidant...
Figure 18.12 Challenges of the application of antioxidants.
Figure 18.13 Future perspectives.
Guide
Cover Page
Table of Contents
Series Page
Title Page
Copyright Page
Preface
Begin Reading
Index
WILEY END USER LICENSE AGREEMENT
Pages
ii
iii
iv
xxiii
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
61
62
63
64
65
66
67
68
69
70
71
72
73
74
75
76
77
78
79
80
81
83
84
85
86
87
88
89
90
91
92
93
94
95
96
97
98
99
100
101
102
103
104
105
106
107
108
109
110
111
112
113
114
115
116
117
118
119
120
121
122
123
124
125
126
127
128
129
130
131
132
133
134
135
136
137
138
139
140
141
142
143
144
145
146
147
148
149
150
151
153
154
155
156
157
158
159
160
161
162
163
164
165
166
167
169
170
171
172
173
174
175
176
177
178
179
180
181
182
183
184
185
186
187
188
189
190
191
192
193
194
195
196
197
198
199
200
201
202
203
204
205
206
207
208
209
210
211
212
213
214
215
216
217
218
219
220
221
222
223
224
225
226
227
228
229
230
231
232
233
234
235
236
237
238
239
240
241
242
243
244
245
246
247
248
249
250
251
252
253
254
255
257
258
259
260
261
262
263
264
265
266
267
268
269
270
271
272
273
274
275
276
277
278
279
280
281
282
283
285
286
287
288
289
290
291
292
293
294
295
296
297
298
299
300
301
302
303
304
305
306
307
308
309
310
311
312
313
314
315
316
317
318
319
320
321
322
323
324
325
326
327
328
329
330
331
332
333
334
335
336
337
338
339
340
341
342
343
344
345
346
347
348
349
350
351
352
353
354
355
356
357
358
359
360
361
362
363
364
365
366
367
369
370
371
372
373
374
375
376
377
378
379
380
381
382
383
384
385
386
387
388
389
390
391
392
393
394
395
396
397
398
399
400
401
402
403
404
405
406
407
408
409
410
411
412
413
414
415
416
417
418
419
420
421
422
423
424
425
426
427
428
429
430
431
432
433
434
435
436
437
438
439
440
441
442
443
444
445
446
447
448
449
450
451
452
453
454
455
456
457
458
459
460
461
462
463
464
465
466
467
468
469
470
471
472
473
474
475
476
477
478
479
480
481
482
483
484
485
486
487
488
489
491
492
493
494
495
496
497
498
499
500
501
502
503
504
505
506
507
508
509
510
511
512
513
514
515
516
517
518
519
520
521
522
523
524
525
526
527
528
529
530
531
532
533
534
535
536
537
538
539
540
541
542
543
544
545
546
547
548
549
551
552
553
554
555
556
557
558
559
560
561
562
563
564
565
566
567
568
569
570
571
572
573
574
575
576
577
578
579
580
581
582
583
584
585
586
587
588
589
590
591
592
593
594
595
596
597
598
599
600
601
602
603
604
605
606
607
608
609
610
611
612
613
614
615
616
617
618
619
620
621
622
623
624
625
626
627
628
629
630
631
632
633
634
635
636
637
638
639
640
641
Scrivener Publishing100 Cummings Center, Suite 541JBeverly, MA 01915-6106
Publishers at ScrivenerMartin Scrivener ([email protected])Phillip Carmical ([email protected])
Antioxidants
Nature’s Defense Against Disease
Edited by
Rakesh K. Sindhu
School of Pharmacy, Sharda University, Greater Noida, Uttar Pradesh, India
Inderbir Singh
Chitkara College of Pharmacy, Chitkara University, Patiala, Punjab, India
and
M. Arockia Babu
Institute of Pharmaceutical Research, GLA University, Mathura, Uttar Pradesh, India
This edition first published 2025 by John Wiley & Sons, Inc., 111 River Street, Hoboken, NJ 07030, USA and Scrivener Publishing LLC, 100 Cummings Center, Suite 541J, Beverly, MA 01915, USA© 2025 Scrivener Publishing LLCFor more information about Scrivener publications please visit www.scrivenerpublishing.com.
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, except as permitted by law. Advice on how to obtain permission to reuse material from this title is available at http://www.wiley.com/go/permissions.
Wiley Global Headquarters111 River Street, Hoboken, NJ 07030, USA
For details of our global editorial offices, customer services, and more information about Wiley products visit us at www.wiley.com.
Limit of Liability/Disclaimer of WarrantyWhile the publisher and authors have used their best efforts in preparing this work, they make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of merchant-ability or fitness for a particular purpose. No warranty may be created or extended by sales representatives, written sales materials, or promotional statements for this work. The fact that an organization, website, or product is referred to in this work as a citation and/or potential source of further information does not mean that the publisher and authors endorse the information or services the organization, website, or product may provide or recommendations it may make. This work is sold with the understanding that the publisher is not engaged in rendering professional services. The advice and strategies contained herein may not be suitable for your situation. You should consult with a specialist where appropriate. Neither the publisher nor authors shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages. Further, readers should be aware that websites listed in this work may have changed or disappeared between when this work was written and when it is read.
Library of Congress Cataloging-in-Publication Data
ISBN 978-1-394-27054-5
Front cover images courtesy of Pixabay.comCover design by Russell Richardson
Preface
Free radicals, also known as reactive oxygen species (ROS), are formed in the human body as by-products of normal cellular processes. These reactive molecules, particularly capable of damaging cellular components such as DNA, lipids, and proteins, can initiate a process called oxidative stress. Leading experts from various disciplines have contributed chapters to this book, exploring a wide range of topics, including the role of antioxidants in the management of cancer, gastrointestinal disorders, skin conditions, cardiovascular diseases, and rheumatoid arthritis.
Antioxidants serve as a crucial defense mechanism against oxidative stress, acting as free radical scavengers that neutralize these harmful molecules before they can cause cellular damage. These chemicals may be synthesized endogenously within the body or derived exogenously from natural sources such as fruits, vegetables, whole grains, and nuts. This book delves into the role of antioxidants in preventing and managing a variety of diseases and critically examines current research on the effects of nutritional antioxidants on specific disease states.
This book is intended for a broad audience, including healthcare professionals seeking a deeper understanding of the relationship between antioxidants and disease prevention, nutritionists and dietitians looking to incorporate this knowledge into clinical dietary plans, and individuals interested in making informed dietary choices for better health. By providing a thorough and evidence-based exploration of this field, we aim to empower readers to adopt proactive strategies for long-term health and well-being.
As editors, we believe this book will serve as a milestone for future research and development in the study of antioxidants and their health benefits. We extend our gratitude to all the contributors, whose dedication and expertise have enriched this volume, and to Martin Scrivener and Scrivener Publishing for their support and publication.
Prof. (Dr.) Rakesh K. Sindhu
Prof. (Dr.) Inderbir Singh
Prof. (Dr.) M. Arockia Babu
1Basics of Antioxidants and Their Importance
Shuchi Goyal1, Divya Thirumal2, Sumitra Singh3, Dinesh Kumar4, Inderbir Singh1, Gautam Kumar5 and Rakesh K. Sindhu5*
1Chitkara College of Pharmacy, Chitkara University, Punjab, India
2Manipal College of Pharmaceutical Sciences, Manipal University, Manipal, Karnatka, India
3Department of Pharmaceutical Sciences, Guru Jambheshwar University of Science and Technology, Hisar, Haryana, India
4Department of Pharmaceutical Sciences, Central University of Haryana, Jant-Pali, Mahendergarh, India
5School of Pharmacy, Sharda University, Greater Noida, Uttar Pradesh, India
Abstract
Fast living leads to an overabundance of free radicals in the body, which ultimately leads to mortality and a reduction in life expectancy by damaging cells, tissues, and organs. Consuming antioxidants aids in scavenging free radicals to ward off both acute and persistent illnesses. Antioxidants are essential that reducing the reactive mechanisms and the negative consequences of reactive oxygen species (ROS) throughout the chain supply and individual physiology. ROS are crucial for neuronal signaling, differentiation, tissue homeostasis, and longevity. In this overview, we go over the many forms of ROS, how they affect the function of cells, and whether they promote or inhibit cancer development. ROSs’ detrimental impacts and their significance in the initiation of pathology are explored. A crucial part of these defense strategies is played by antioxidants. It is generally recognized that the inclusion of phenolic chemicals, particularly phenolic acids and flavonoids, is associated with antioxidative and pharmacologic effects. Antioxidants are now a crucial component of sophisticated health care. Antioxidants, whether they be organic or artificial, can help combat many diseases early on and works best when they are present in high concentrations. They affect how adequately the therapy responds. In addition to its usage in nutritious dietary supplements, emphasis is being placed on utilizing them as natural substitutes for synthetic versions to improve food durability and prevent degradation by oxidation throughout manufacturing and preservation. In purpose to support technological improvement in this domain, this overview summarizes relevant and widely recognized findings on the efficient significance of organic and synthesized antioxidants with associated therapeutic value.
Keywords: Antioxidants, ROS, free radicals, pathology, importance, applications
Abbreviations
RON
reactive oxygen and nitrogen species
ET
electron transfer
HTD
hydrogen atom donation
EDTA
ethylenediaminetetraacetic acid
CA
citric acid
Vit C
Vitamin C
Vit B
Vitamin B
Vit A
Vitamin A
MDA
malondialdehyde
8-OHdG
8-hydroxy-2′-deoxyguanosine levels
1.1 Introduction
Imagine your body as a bustling city, with millions of residents busily going about their daily activities. In this city, just like in any vibrant community, there is a natural process of wear and tear. As time passes, structures deteriorate, and waste accumulates. However, to maintain the city’s vitality and ensure its residents’ well-being, there are diligent workers known as “antioxidants.” Antioxidants, pivotal in cellular protection, counteract the harm induced by unstable molecules termed free radicals. These radicals, through oxidative reactions, instigate cellular damage, potentially culminating in conditions like cancer. Antioxidants engage with free radicals, stabilizing them and thwarting potential harm. Key antioxidants encompass bella carotin, carotenoid, vit A, B, C, as well as various polyphenols [1]. An antioxidant has the ability to slow down or prevent different compounds from oxidizing, which is the chemical process by which ions move from one material to an oxidation agent. This decay procedure births liberated, setting off detrimental chain reaction within cells [2, 3]. Antioxidants step in, oxidizing themselves and removing the free radical intermediates that cause these chain reactions to stop. Interestingly, several antioxidants—such as polyphenols, thiols, and ascorbic acid—also function as reducing agents [4]. While oxidation reactions are vital for life, their immoderation can prove deleterious. Consequently, organisms, both flora and fauna, maintain intricate antioxidant defense systems. These include a range of enzymes, including catalase, superoxide dismutase, and several oxidoreductases, as well as antioxidants, including glutathione, vitamin C, and vitamin E [5]. Free radical damage can be brought on by low antioxidant levels or malfunctioning antioxidant enzymes, which may cause damage or even death to cells [6]. Given the potentials implication of Free radical damage in numerous human ailments, extensive research explores the utility of antioxidants in pharmacology, particularly in treating stroke and neurodegenerative disorder [7]. Nonetheless, whether oxidative stress acts as the cause or consequence of diseases remains unclear. Antioxidants are extensively utilized in dietary supplements, aiming to sustain health and avert conditions like cancer and coronary heart disease. While early studies suggested potential health benefits of antioxidant supplements, subsequent large clinical trials failed to validate such advantages and instead hinted at potential harm with excessive supplementation. Additionally, antioxidants find broad industrial applications, functioning as chemicals in food and Corrective and inhibiting condescension in latex and petrol [8, 9]. Chemists have long acknowledged the ability of antioxidants to mitigate oxidation caused by free radicals, essential for maintaining stability in various substances, including lubrication oils and plastics. Human biological processes, encompassing respiration, metabolism, digestion, and energy conversion, generate reactive oxygen and nitrogen species (RONs), which can manifest as free radicals or readily generate them [10]. RONs, at moderate concentrations, play pivotal roles in biological pathways but can cause considerable damage at elevated levels, leading to disruptions in cellular signaling and Free radical damage [11]. This imbalance can lead to irreversible alterations in cell compounds, affecting cellular health and contributing to major chronic ailments such as cancer, cardiovascular, liver, and neurological disorders. Antioxidant defense mechanisms encompass a spectrum of approaches, including inhibiting free radical production, scavenging free radicals, converting free radicals into less dangerous substances, postponing the emergence of more hazardous species and halting the spread of chains reactions, bolstering the endogenous antioxidant defense system through synergistic action, and chelation. These multifaceted mechanisms collectively contribute to cellular resilience against Free radical damage and its detrimental moment [12].
1.2 Generalization of Antioxidant
Antioxidants is compounds that protect cells from oxidative damage caused by free radicals and reactive oxygen species (ROS). Oxidative stress resulting from an inequality between the production of these harmful molecules and the body’s ability to neutralize them has been linked to various chronic diseases, including cardiovascular diseases, cancer, neurodegenerative disorders, and aging [13]. The main types of antioxidants are those that use a single electron transfer (ET) mechanism or hydrogen atom donation (HAT) to eliminate free radicals. Antioxidant catalysts that are prooxidant are neutralized by secondary antioxidants [14]. These include compounds that deactivate reactive species like singlet oxygen (beta-carotene) or chelate prooxidant metal ions (such iron and copper), such as (EDTA) and citric acid (CA) [10]. Mechanism of antioxidants -Scavenging Free Radicals: Antioxidants, through various enzymes and molecules, can neutralize free radicals by donating electrons [15]. This process mitigates the harmful chain reactions initiated by free radicals.
Enzymatic Scavengers: as reverse fibrosis, catalase, and GPx1, act as the first line of defense against free radical damage, reverse fibrosis. For example, catalyzes the dismutation of superoxide radicals into less harmful species.
Non-enzymatic Antioxidants:
Non-enzymatic antioxidants encompass a wide range of molecules, including vit (e.g., vitamin E,C), lignans (e.g., flavonoids and resveratrol), and trace elements (e.g., selenium and zinc). These antioxidants exert their effects by quenching ROS directly or indirectly
[16]
.
Chelation of Metal Ions:
Some antioxidants, like metal-binding proteins and chelators, combat oxidative stress by binding to metal ions (e.g., iron and copper) that catalyze the formation of highly reactive radicals. This prevents metal-mediated ROS generation
[17]
.
Regulation of Transcription Factors:
Some antioxidants activate transcription variables, like the nuclear factor erythroid 2-associated factor 2 (Nrf2), to modify how cells react to oxidative stress. Nrf2 controls the expression of numerous antioxidant genes, enhancing the body’s overall antioxidant capacity
[18]
.
Mitochondrial Protection:
Mitochondria are major sources of ROS production. Antioxidants, particularly those targeted to the mitochondria, reduce mitochondrial ROS generation and maintain mitochondrial function [19].
The mechanisms of action of natural antioxidants and oxidative processes. When polyunsaturated lipids are exposed to light, heat, ionizing radiation, metal ions, or metalloprotein catalysts, a free radical chain reaction is set off, which causes the autoxidation of the lipids in food. Oxidation can also be initiated by the enzyme lipoxygenase. Photooxidation can occur when exposed to light, and high-temperature thermal oxidation—which occurs when food is cooked, grilled, or fried—produces polar and polymeric compounds. The oxidation that happens to food most frequently is called autoxidation. The initiation (creation of lipid free radicals), propagation, and termination (generation of nonradical products) reactions are part of the traditional route of autoxidation, as shown in Figure 1.1[20].
Figure 1.1 Autoxidation process [20].
1.3 Reactive Oxygen Species (ROS) and Free Radicals
Reactive oxygen species (ROS) and free radicals are fundamental components of cellular physiology, denoting chemically reactive molecular entities that harbor unpaired electrons in their outer orbits [21, 22] Reactive Oxygen Species surround a contrast array of oxygen-derived species, including superoxide anion (O2•−), hydroxyl radical (•OH), hydrogen peroxide (H2O2), and singlet oxygen (1O2), among others. On the other hand, free radicals, a subset of ROS, exhibit exceptional reactivity due to their unpaired electron, which drives them to readily engage in oxidative reactions [23].
These molecules are generated within the cell during various physiological processes, including aerobic respiration, immune responses, and cellular signaling [24, 25]. However, when their production exceeds the capacity of endogenous antioxidant defenses, it can lead to free radical damage.
The causes of ROS and free radical formation are multifaceted, encompassing both endogenous and exogenous sources [26]. Endogenously, ROS are produced during mitochondrial respiration, where electrons escape from the ETC [27]. Additionally, cellular enzyme such as nicotinamide adenine dinucleotide hydrogen phosphate oxidases and xanthine oxidoreductase contribute to ROS production as part of normal cellular functions [28]. Exogenously, exposure to outside influences like ionizing rays, pollutants, and heavy metals can increase ROS generation. The consequences of elevated ROS and free radicals are profound and multifarious. Oxidative stress, characterized by an inequality between ROS production and the body’s ability to detoxify these species, is a common result [29]. This imbalance can lead to oxidative damage to biological molecules found in cells, such as proteins, fats, and DNA and RNA ultimately contributing to the pathogenesis of various diseases, such as cancer, neurodegenerative disorders, cardiovascular diseases, and inflammation-related conditions.
In response to the challenge posed by ROS and free radicals, the body has evolved a sophisticated defense system, employing endogenous antioxidants like superoxide dismutase, catalase, and glutathione peroxidase [30]. However, exogenous antioxidants from the diet, including vit E,C as well as polyphenols, play a pivotal role in bolstering the cellular defense against oxidative stress. Antioxidants function by donating electrons to free radicals without becoming destabilized themselves, thereby neutralizing these potentially harmful species By counteracting the detrimental effects of reactive oxidative stress and free radicals, antioxidants serve as an essential safeguard against the progression of diseases rooted in oxidative stress Understanding the intricate interplay between ROS, free radicals, and antioxidants is central to elucidating the molecular underpinnings of health and disease and may offer novel avenues for therapeutic intervention [31].
Pathology related to antioxidants: Pathology related to antioxidants is fundamentally centered on the intricate interplay between the protective role of antioxidants and the detrimental consequences of free radical damage [32] free radical damage, marked by an imbalance between the generation of reactive oxygen species and the bodies power to detoxify or repair the resultant damage, underpins numerous pathological conditions spanning various organ systems [33–37]. Oxidative stress stands as a linchpin in a plethora of ailments, ranging from cardiovascular diseases, neurodegenerative disorders, and cancer to diabetes, inflammatory conditions, and the process of aging itself [38]. At its core, oxidative stress is perpetuated by free radicals, which include highly reactive molecules such as superoxide anion (O2-), hydroxyl radicals (OH·), and hydrogen peroxide (H2O2) [39]. These agents wreak havoc on cellular components, inflicting harm upon DNA, proteins, and lipids [40]. In this intricate biological battle, antioxidants emerge as the valiant defenders of cellular integrity. These compounds come in two categories [41]: enzymatic antioxidants like superoxide dismutase, catalase, and glutathione peroxidase, and non-enzymatic antioxidants including vit C and E, glutathione, and flavonoids [42]. Acting in unison, these antioxidants mount a concerted effort to eliminate radicals and maintain the delicate balance of cellular redox equilibrium [43]. The pathological implications of oxidative stress are far-reaching and multi-faceted [44]. Cardiovascular diseases, encompassing conditions like atherosclerosis, hypertension, ischemia-reperfusion injury, and heart failure, bear the heavy burden of oxidative stress-induced damage [45]. Emerging evidence suggests that diets rich in antioxidants and antioxidant supplementation hold promise in mitigating cardiovascular pathology by alleviating oxidative damage [46]. Neurodegenerative disorders, such as Alzheimer’s disease, Parkinson’s disease, ALS, and multiple sclerosis, have their origins intertwined with oxidative stress-induced damage, contributing to their onset and progression [47]. Antioxidant therapy offers hope in delaying neurodegeneration and enhancing cognitive function. Cancer development, a multifaceted process governed by cellular and molecular alterations driven by a variety of endogenous and exogenous factors, is marked by oxidative DNA damage [48]. This damage serves as a key hallmark of carcinogenesis, instigating the initiation and promotion of cancer through chromosomal defects and the activation of oncogenes by free radicals. Diabetes and metabolic disease, characterized by free radical damage as a defining feature, underscore the potential of antioxidants in preventing diabetic complications, such as mononeuropathy, and retinopathy, by counteracting oxidative stress-induced damage. Furthermore, inflammatory disorders, particularly those of a chronic nature, are often perpetuated by oxidative stress [49]. Antioxidants, equipped with their anti-inflammatory properties, present a potential avenue for attenuating conditions like rheumatoid arthritis and inflammatory bowel disease [50]. The repercussions of antioxidant deficiency are dire, as insufficient intake or impaired antioxidant defense mechanisms significantly heighten the susceptibility to oxidative damage [51]. This exacerbates the pathology associated with various diseases, reinforcing the paramount importance of maintaining an adequate antioxidant defense system. In summary, the intricate web of oxidative stress, antioxidants, and their pathological implications underscores the critical role of these molecules in maintaining cellular health and the prevention of numerous diseases across various systems in the body [52]. Understanding this delicate balance is pivotal in the ongoing pursuit of novel therapeutic interventions and lifestyle modifications aimed at mitigating the burden of oxidative stress-related diseases [53–58].
Natural origin of Antioxidant: Reactive Oxygen Species (ROS) and free radicals are dynamic entities known for their potential to cause cellular damage, contributing to a range of diseases, including cancer and cardiovascular conditions [59]. In response to this challenge, antioxidants found in various foods play a crucial role in maintaining health. These antioxidants are abundant in fruits, vegetables, nuts, seeds, and select beverages, offering a multifaceted defense against oxidative stress. Fruits and vegetables, for instance, are rich sources of antioxidants, including vitamin C, E [60], elements such as selenium, and phytochemicals, such as flavonoids and carotenoids [61] as shown in Figure 1.2.
Figure 1.2 Sources of antioxidants.
These compounds are synthesized by plants as a defense mechanism against environmental stressors and as a means to attract pollinators [62]. In the realm of cereals and legumes, polyphenols, particularly phenolic acids, feature prominently. Ferulic acid, monohydroxybenzoic acid and (E)-3-(4-Hydroxyphenyl)-2-propenoic acid [63] are vital components, while buckwheat stands out with its abundant rutin content [64]. These polyphenolic compounds exist in both ester [65] and glycoside forms [66], with their chemical structure and concentration directly influencing their antioxidant activity [67, 68]. Additionally, catechins are found in cereal grains, with buckwheat, oats, and rye containing noteworthy amounts. Beverages [69] and spices also contribute significantly to antioxidant intake [70]. Coffee, tea, cocoa, red wine, and herbs and spices are rich sources of antioxidants [71]. In tea, catechins are prominent, particularly in green tea, which boasts over 2-times higher antioxidant activity compared to black or red tea. Roasted coffee, on the other hand, features chlorogenic acid as the dominant polyphenolic compound [73]. Flavonoids [72], a diverse group of naturally occurring compounds, offer strong antioxidant properties and can be found in various plant-based foods. Citrus fruits, berries, and dark chocolate are rich sources of specific flavonoids like hesperidin, naringin, anthocyanins, and epicatechin. Flavonoids combat oxidative stress through mechanisms such as free radical scavenging, metal chelation, and the enhancement of antioxidant enzymes [74]. Furthermore, marine environments are emerging as novel sources of antioxidants, with microalgae [75] and seaweed offering valuable contributions. Fucoxanthin from Sargassum siliquastrum[76], for example, has been found to protect human fibroblasts from UV-B-induced oxidative stress, thereby reducing intracellular [77] ROS, enhancing cell survival, and minimizing DNA damage. Additionally, compounds like fragilamide from Martensia fragilis exhibit moderate antioxidant activity, further expanding the scope of potential natural sources for antioxidants. Mechanism of action of various antioxidants is shown in Figure 1.3.
Figure 1.3 Mechanism of action of antioxidants.
Research has explored the connection between the color spectrum of fruits and vegetables and their antioxidant capacity, categorizing them into three groups based on Total Antioxidant Capacity (TAC). The first group includes high-TAC fruits like black grapes and strawberries. The second group comprises medium-TAC fruits such as blueberries and green apples. The third group consists of fruits with low-medium TAC, including mangoes and bananas, revealing the diversity of antioxidants in nature and emphasizing the health benefits of dietary variety. This classification is derived from computer vision-based image analysis of color hues related to TAC.
1.4 Importance of Antioxidant in Medicine
Antioxidants, the molecular heroes that combat the destructive forces of oxidative stress, play a pivotal role in the field of medicine. As the human body relentlessly generates reactive oxygen species (ROS) and free radicals through metabolic processes, it faces a constant battle against cellular damage, inflammation and causes the rise of various diseases. The importance of antioxidants in medicine lies in their remarkable ability to neutralize these harmful molecules and safeguard cellular health. Antioxidants have become a formidable asset in the field of medical science, presenting a potent means for not only preventing chronic ailments such as cancer, cardiovascular diseases, and neurodegenerative disorders but also for fortifying the body’s immune defenses. Their emergence marks a promising pathway for interventions that encompass both preventive measures and therapeutic strategies. This introduction sets the stage to explore the multifaceted impact of antioxidants in medicine, underscoring their significance in the quest for better health and well-being. Here we are going to discuss on uses of antioxidant in various conditions and diseases [78, 79].
In Pregnancy -Pregnancy imposes heightened nutritional demands on mothers to support fetal development, with several micronutrients serving as essential cofactors or antioxidants. Normal placental development generates oxidative stress, which intensifies in the absence of sufficient antioxidant micronutrients, adversely affecting both the placenta and maternal circulation. Selenium, a crucial component of selenoproteins, including antioxidant enzymes like glutathione peroxidase, experiences reduced concentrations and activity during pregnancy (1st trimester: 65 μg/L; 3rd trimester: 50 μg/L). In pregnant women prone to postpartum thyroid dysfunction (PPTD), supplementation with 200 μg/d selenomethionine significantly lowers PPTD and permanent hypothyroidism incidence, attributed to enhanced selenoprotein activities mitigating postpartum immunological rebound [80].
Shifting to heart health, carotenoids, responsible for the vibrant hues of fruits and vegetables, showcase potent antioxidant properties. Beyond adding color, they contribute to lowering heart disease and cancer risks, boosting the immune system, and safeguarding against age-related macular degeneration – a leading cause of irreversible blindness in adults [81].
Neurological effect -A study has demonstrated Vit A neuroprotective effects against cytotoxicity associated with amyloid fibrillation. Given its capacity to interact with the Aβ-42 peptide, vitamin A emerges as a potential candidate for the therapy of Alzheimer’s and Parkinson’s diseases, countering systemic amyloidosis [82]. Various studies have established a correlation between vitamin C deficiencies and neurodegenerative disorders, including Parkinson’s, Alzheimer’s, Huntington’s diseases, and amyotrophic sclerosis. Notably, a clinical study indicated that the administration of vitamin C and/or E supplements resulted in a reduced risk of cognitive decline in individuals aged ≥65 years. Furthermore, proanthocyanidins, a class of natural flavonoids, demonstrated efficacy in alleviating rotenone-induced oxidative stress in human neuroblastoma SH-SY5Y dopaminergic cells, serving as a model for Parkinson’s disease [83, 84]. Co-administration of astaxanthin and fucoxanthin exhibited neuroprotective effects on pheochromocytoma neuronal cells, presenting a potential treatment approach for Alzheimer’s disease.
In cancer, oleuropein has been identified as a compound that not only hampers cell proliferation but also triggers apoptosis in breast cancer cells. Its antiproliferative impact extends to human hepatocellular carcinoma cells, breast cancer cells, various human tumor cells, and human colon carcinoma cells [85]. Additionally, pectin, extracted from Citrus peels, serves as a widely employed gelling agent in diverse food industrial processes prevent cancer. In MTT assays, the exposure to 6-OHDA resulted in a concentration-dependent reduction in cell viability in PC12 cells, corroborated by apoptosis confirmation Particularly, concentrations ranging from 50 μM to 400 μM revealed the enhanced protective potential of EGCG, leading to a substantial reduction in apoptotic cells and the prevention of apoptosis-related nuclear changes. Mechanism of action of different natural antioxidants are shown in Figure 1.4.
Toxicity of antioxidant: Antioxidants are substances that help protect the body from the damaging effects of free radicals, which are unstable molecules that can damage cells and contribute to the aging process and various diseases, including cancer and cardiovascular diseases [96]. While antioxidants are generally beneficial for health, like many compounds, they can have potential toxic effects if consumed in excessive amounts. Here are some aspects to consider regarding the potential toxicity of antioxidants:
Excessive Supplementation: Consuming high doses of antioxidant supplements, such as vit A, C, E, and beta-carotene, beyond the recommended daily allowances (RDAs), can lead to toxicity. Excessive intake of these supplements may cause nausea, diarrhea, stomach cramps, and in severe cases, can lead to organ damage [
97
–
99
].
Vitamin A (Retinol) Toxicity: Vitamin A is an essential nutrient, but excessive intake, especially in the form of supplements, can lead to vitamin A toxicity
[100]
. This can cause dizziness, nausea, headaches, blurred vision, bone pain, and in severe cases, it can affect the liver and even be life-threatening.
Selenium Toxicity: Selenium is an essential trace element and antioxidant. However, excessive intake can lead to selenosis, causing symptoms like hair loss, nausea, diarrhea, skin rashes, and in severe cases, it can result in nerve damage and liver and kidney problems.
Iron and Copper Overload: Iron and copper are essential minerals with antioxidant properties. However, excessive levels of these minerals in the body can lead to toxicity
[101]
. Iron overload (hemochromatosis) can cause fatigue, joint pain, and eventually, damage to the liver, heart, and pancreas. Copper toxicity can lead to gastrointestinal symptoms and neurological issues.
Interference with Chemotherapy: High doses of antioxidants during cancer treatment, especially chemotherapy, may interfere with the treatment’s effectiveness [
102
–
104
]. Some studies suggest that antioxidants can protect cancer cells from the damaging effects of chemotherapy.
Interaction with Medications: Antioxidants can interact with certain medications, affecting their efficacy or potentially causing harmful effects. For example, vitamin E can interact with blood thinners, and high doses of vitamin C may interfere with certain cancer treatments.
Potential Pro-Oxidant Effects: In certain conditions and at high concentrations, antioxidants can switch from being protective to potentially harmful by acting as pro-oxidants
[105]
. This paradoxical effect can lead to cellular damage rather than protection.
Figure 1.4 Mechanism of action of different natural antioxidants [89, 90].
S. no.
Antioxidant
Impact on health
References
1
Anthocyanin
Dietary antioxidants have the potential to offer health benefits by aiding in the prevention of various diseases, including neuronal disorders, cardiovascular conditions, cancer, diabetes, inflammation, and more.
[86]
2
Carotenoids
Carotenoid intake may lower the risk of cancer, cardiovascular diseases, and other chronic conditions, and some also serve as provitamin A.
[87]
3
Lycopene
Lycopene administration improved cognition, reduced oxidative stress markers, increased MDA and 8-OHdG and prevented neuroinflammation and apoptosis.
[88]
4
Amurensin and cosmosiin
Research findings indicate that amurensin and cosmosin, both flavonoids extracted from
Trigonella foenum
, display promising potential in hindering neurodegeneration induced by NaNO2 in the hippocampus and cortex regions of mice brains.
[89]
5
Tiliroside
Research has demonstrated the anti-neuroinflammatory potential of tiliroside, a glycosidic flavonoid, in increasing Nrf2, HO-1, and NQO1 protein levels, suggesting Nrf2 protective pathway activation in microglia.
[90]
6
vit E, α-lipoic acid and Vit. C
In a study these three antioxidant combination preserved arachidonic acid levels and positively impacted the D-6 desaturase system and unsaturated fatty acid levels in both diabetic and non-diabetic rats.
[91]
7
vitamin c
Vitamin C supplementation effectively reduces the accumulation of (sugar alcohol) sorbitol RBC’s of diabetic patient, normalizes sorbitol levels in T1DM within 30 days, reduces capillary fragility, and improves glucose and lipid metabolism as well as glycemic control.
[92]
8
lipoic acid
Lipoic acid enhances glucose transport in muscle cells, safeguards the insulin receptor in adipocytes, and increases insulin-mediated glucose uptake in patients with T2DM, potentially improving insulin sensitivity.
[93]
9
Fucoidan
Fucoidan inhibited H2O2-triggered PC12 cell apoptosis by scavenging ROS and enhancing SOD and GSH-Px activity.
[94]
10
Fucotriphlorethol A
Fucotriphlorethol A, derived from the consumable brown alga
Fucus vesiculosus
L., demonstrates inhibition of cytochrome P450 1A, exhibiting IC50 values within the range of 17 to 33.5 μg/ml.
[95]
S. no.
Antioxidant
Side effect
References
1
Vit E
The study found that in some cases, high-dose antioxidant supplementation, particularly vitamin E, was associated with an increased risk of mortality. It suggested that excessive antioxidant intake might not always be beneficial and could potentially have adverse effects.
[106]
2
Vitamin C
The research found that excessive vitamin C intake was linked to an increased risk of developing kidney stones, highlighting the importance of moderation in antioxidant supplementation.
[107]
3
selenium
Furthermore, increased seminal plasma levels of selenium (≥80 ng/ml) were reported to be associated with decreased motility, asthenozoospermia and elevated abortion rates, whereas selenium levels between 40 and 70 ng/ml were reported to be optimal for re-productive performance.
[108]
4
Resveratrol
This study show that Gastrointestinal issues, interactions with medications.
[109]
5
Beta-Carotene
In individuals who smoked and were administered a daily supplementation of 20 mg β-carotene (Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group, 1994), or 30 mg β-carotene along with 25,000 IU retinyl palmitate, a noteworthy elevation in the likelihood of developing lung cancer was observed during an efficacy trial involving 29,133 and 18,314 subjects, respectively, in comparison to a placebo.
[110]
1.5 Conclusion
Antioxidants, the stalwart defenders against the ravages of oxidative stress, have cemented their significance in the realm of medicine. In the bustling city of our body’s biological processes, where metabolic activities produce reactive oxygen species (ROS) and free radicals, antioxidants act as vigilant protectors. They neutralize these harmful molecules, thus safeguarding cellular health and contributing to the prevention of a multitude of diseases. Their importance extends across the medical spectrum, from thwarting the progression of chronic conditions like cancer, cardiovascular diseases, and neurodegenerative disorders to enhancing the body’s natural defense mechanisms.
In the realm of cancer, antioxidants play an important role, with their ability to inhibit cell proliferation and induce apoptosis, potentially transforming the landscape of cancer treatment. However, the delicate balance between their benefits and potential toxicity must be maintained. Excessive supplementation can lead to adverse effects, including nausea, organ damage, and even life-threatening conditions. Vitamin A, selenium, iron, and copper are all susceptible to toxicity when consumed in excess. Furthermore, the interaction of antioxidants with chemotherapy and medications can influence their efficacy, and their pro-oxidant effects, especially at high concentrations, can paradoxically lead to cellular damage. Therefore, moderation in antioxidant consumption is key to reaping their benefits while mitigating potential risks. In a world where oxidative stress and the resulting diseases pose a significant threat to human health, antioxidants stand as formidable allies, offering protection, prevention, and the potential to revolutionize the landscape of modern medicine. Their significance in maintaining health and well-being underscores the need for continued research and responsible consumption, paving the way for a healthier, more resilient future.
References
1. Sies, H., Oxidative stress: oxidants and antioxidants.
Exp. Physiol. Transl. Integr.
,
82
, 2, 291–295, 1997.
2. Bjelakovic, G., Nikolova, D., Gluud, L.L., Simonetti, R.G., Gluud, C., Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis.
Jama
,
297
, 8, 842–857, 2007.
3. Pizzino, G., Irrera, N., Cucinotta, M., Pallio, G., Mannino, F., Arcoraci, V., Squadrito, F., Altavilla, D., Bitto, A., Oxidative stress: harms and benefits for human health.
Oxid. Med. Cell. Longevity
, 2017, 1–13, 2017.
4. Forman, H.J. and Zhang, H., Targeting oxidative stress in disease: Promise and limitations of antioxidant therapy.
Nat. Rev. Drug Discov.
,
20
, 9, 689–709, 2021.
5. Rudrapal, M., Khairnar, S.J., Khan, J., Dukhyil, A.B., Ansari, M.A., Alomary, M.N., Alshabrmi, F.M., Palai, S., Deb, P.K., Devi, R., Dietary polyphenols and their role in oxidative stress-induced human diseases: Insights into protective effects, antioxidant potentials and mechanism(s) of action.
Front. Pharmacol.
,
13
, 283, 2022.
6. Adwas, A.A., Elsayed, A., Azab, A.E., Quwaydir, F.A., Oxidative stress and antioxidant mechanisms in human body.
J. Appl. Biotechnol. Bioeng.
,
6
, 1, 43–47, 2019.
7. Costa, M., Losada-Barreiro, S., Paiva-Martins, F., Bravo-Díaz, C., Polyphenolic Antioxidants in Lipid Emulsions: Partitioning Effects and Interfacial Phenomena.
Foods
, 10, 539, 2021.
8. Pisoschi, A.M., Pop, A., Iordache, F., Stanca, L., Predoi, G., Serban, A.I., Oxidative stress mitigation by antioxidants-an overview on their chemistry and influences on health status.
Eur. J. Med. Chem.
,
209
, 112891, 2021.
9. Forrester, S.J., Kikuchi, D.S., Hernandes, M.S., Xu, Q., Griendling, K.K., Reactive oxygen species in metabolic and inflammatory signaling.
Circ. Res.
,
122
, 6, 877–902, 2018.
10. Singh, A., Kukreti, R., Saso, L., Kukreti, S., Oxidative stress: a key modulator in neurodegenerative diseases.
Molecules
,
24
, 8, 1583, 2019.
11. Murphy, M.P., Bayir, H., Belousov, V., Chang, C.J., Davies, K.J., Davies, M.J., Dick, T.P., Finkel, T., Forman, H.J., Janssen-Heininger, Y., Gems, D., Guidelines for measuring reactive oxygen species and oxidative damage in cells and
in vivo. Nat. Metab.
,
4
, 6, 651–662, 2022.
12. Losada-Barreiro, S., Sezgin-Bayindir, Z., Paiva-Martins, F., Bravo-Díaz, C., Biochemistry of antioxidants: Mechanisms and pharmaceutical applications.
Biomedicines
,
10
, 12, 3051, 2022.
13. Miller, G.J. and Quackenbush, F.W., A comparison of alkylated phenols as antioxidants for lard.
J. Am. Oil Chem. Soc.
,
34
, 5, 249–250, 1957.
14. Heim, K.E., Tagliaferro, A.R., Bobilya, D.J., Flavonoid antioxidants: chemistry, metabolism and structure-activity relationships.
J. Nutr. Biochem.
,
13
, 10, 572–584, 2002.
15. Heijnen, C.G., Haenen, G.R., Vekemans, J.A., Bast, A., Peroxynitrite scavenging of flavonoids: structure activity relationship.
Environ. Toxicol. Pharmacol.
,
10
, 4, 199–206, 2001.
16. Mirończuk-Chodakowska, I., Witkowska, A.M., Zujko, M.E., Endogenous non-enzymatic antioxidants in the human body.
Adv. Med. Sci.
,
63
, 1, 68–78, 2018.
17. Gulcin, İ. and Alwasel, S.H., Metal ions, metal chelators and metal chelating assay as antioxidant method.
Processes
,
10
, 1, 132, 2022.
18. Aycan, M., Nahar, L., Baslam, M., Mitsui, T., B-type response regulator hst1 controls salinity tolerance in rice by regulating transcription factors and antioxidant mechanisms.
Plant Physiol. Biochem.
,
196
, 542–555, 2023.
19. Kumar, S., Sharma, S., Vasudeva, N., Review on antioxidants and evaluation procedures.
Chin. J. Integr. Med.
, 2017, 1–12, 2017.
20. Helberg, J. and Pratt, D.A., Autoxidation vs. antioxidants–the fight for forever.
Chem. Soc. Rev.
,
50
, 13, 7343–7358, 2021.
21. Hancock, J.T., Desikan, R., Neill, S.J., Role of reactive oxygen species in cell signalling pathways.
Biochem. Soc. Trans.
,
29
, 2, 345–349, 2001.
22. Sharma, A., Mohapatra, H., Arora, K., Babbar, R., Arora, R., Arora, P., Kumar, P., Algın Yapar, E., Rani, K., Meenu, M.
et al.
, Bioactive Compound-Loaded Nanocarriers for Hair Growth Promotion: Current Status and Future Perspectives.
Plants
,
12
, 3739, 2023.
23. Sies, H., Oxidative stress: Eustress and distress in redox homeostasis, in:
Stress: physiology, biochemistry, and pathology
, pp. 153–163, Academic Press, Cambridge, Massachusetts, United States, 2019.
24. El-Bahr, S.M., Biochemistry of free radicals and oxidative stress.
Biochemistry
,
1
, 5567/5cjiŋt, 11–11, 2013.
25. Lane, N.,
Oxygen. The Molecule That Made the World
, revised ed., Oxford University Press, Oxford, UK, 2016.
26. Winterbourn, C.C., The biological chemistry of hydrogen peroxide.
Methods Enzymol.
,
528
, 3–25, 2013.
27. Martemucci, G., Costagliola, C., Mariano, M., D’andrea, L., Napolitano, P., D’Alessandro, A.G., Free radical properties, source and targets, antioxidant consumption and health.
Oxygen
,
2
, 2, 48–78, 2022.
28. Choe, E. and Min, D.B., Mechanisms and factors for edible oil oxidation.
Compr. Rev. Food Sci. Food Saf.
,
5
, 169–186, 2006.
29. Parcheta, M., Świsłocka, R., Orzechowska, S., Akimowicz, M., Choińska, R., Lewandowski, W., Recent developments in effective antioxidants: The structure and antioxidant properties.
Materials
,
14
, 8, 1984, 2021.
30. Kohen, R. and Nyska, A., Invited review: oxidation of biological systems: oxidative stress phenomena, antioxidants, redox reactions, and methods for their quantification.
Toxicol. Pathol.
,
30
, 6, 620–650, 2002.
31. Habib, S. and Ali, A., Biochemistry of nitric oxide.
Indian J. Clin. Biochem.
,
26
, 3–17, 2011.
32. Blaise, G.A., Gauvin, D., Gangal, M., Authier, S., Nitric oxide, cell signaling and cell death.
Toxicology
,
208
, 2, 177–192, 2005.
33. Ray, R. and Shah, A.M., NADPH oxidase and endothelial cell function.
Clin. Sci.
,
109
, 3, 217–226, 2005.
34. Moncada, S.R.M.J., Palmer, R.M.L., Higgs, E., Nitric oxide: physiology, pathophysiology, and pharmacology.
Pharmacol. Rev.
,
43
, 2, 109–142, 1991.
35. Repetto, M., Semprine, J., Boveris, A., Lipid peroxidation: Chemical mechanism, biological implications and analytical determination, in:
Lipid Peroxidation
, D.A. Catala (Ed.), pp. 3–30, InTech, Rijeka, Croatia, 2012.
36. Alshehri, M.M., Quispe, C., Herrera-Bravo, J., Sharifi-Rad, J., Tutuncu, S., Aydar, E.F., Topkaya, C., Mertdinc, Z., Ozcelik, B., Aital, M., Kumar, N.V., A review of recent studies on the antioxidant and anti-infectious properties of Senna plants.
Oxid. Med. Cell. Longev.
, 2022, 6025900, 2022.
37. Elahi, M.M., Kong, Y.X., Matata, B.M., Oxidative stress as a mediator of cardiovascular disease.
Oxid. Med. Cell. Longev.
,
2
, 5, 259–269, 2009.
38. Taverne, Y.J., Bogers, A.J., Duncker, D.J., Merkus, D., Reactive oxygen species and the cardiovascular system.
Oxid. Med. Cell. Longev.
, 2013, 862423, 2013.
39. Sharifi-Rad, J., Sharifi-Rad, M., Salehi, B., Iriti, M., Roointan, A., Mnayer, D., Soltani-Nejad, A., Afshari, A.,
In vitro
and
in vivo
assessment of free radical scavenging and antioxidant activities of Veronica persicaPoir.
Cell. Mol. Biol.
,
64
, 8, 57–64, 2018.
40. Singh, R.B., Mengi, S.A., Xu, Y.J., Arneja, A.S., Dhalla, N.S., Pathogenesis of atherosclerosis: A multifactorial process.
Exp. Clin. Cardiol.
,
7
, 1, 40, 2002.
41. Perrotta, I. and Aquila, S., The role of oxidative stress and autophagy in atherosclerosis.
Oxid. Med. Cell. Longev.
, 2015, 1–10, 2015.
42. Salehi, B., Martorell, M., Arbiser, J.L., Sureda, A., Martins, N., Maurya, P.K., Sharifi-Rad, M., Kumar, P., Sharifi-Rad, J., Antioxidants: positive or negative actors?
Biomolecules
,
8
, 4, 124, 2018.
43. Tsatsakis, A., Docea, A.O., Calina, D., Tsarouhas, K., Zamfira, L.M., Mitrut, R., Sharifi-Rad, J., Kovatsi, L., Siokas, V., Dardiotis, E., Drakoulis, N., A mechanistic and pathophysiological approach for stroke associated with drugs of abuse.
J. Clin. Med.
,
8
, 9, 1295, 2019.
44. Wang, X. and Michaelis, E.K., Selective neuronal vulnerability to oxidative stress in the brain.
Front. Aging Neurosci.
,
2
, 1224, 2010.
45. Delcambre, S., Nonnenmacher, Y., Hiller, K., Dopamine metabolism and reactive oxygen species production, in:
Mitochondrial mechanisms of degeneration and repair in Parkinson’s disease
, pp. 25–47, 2016.
46. Docea, A.O., Gofita, E., Goumenou, M., Calina, D., Rogoveanu, O., Varut, M., Olaru, C., Kerasioti, E., Fountoucidou, P., Taitzoglou, I., Zlatian, O., Six months exposure to a real life mixture of 13 chemicals’ below individual NOAELs induced non monotonic sex-dependent biochemical and redox status changes in rats.
Food Chem. Toxicol.
,
115
, 470–481, 2018.
47. Saha, S.K., Lee, S.B., Won, J., Choi, H.Y., Kim, K., Yang, G.M., AbdalDayem, A., Cho, S.G., Correlation between oxidative stress, nutrition, and cancer initiation.
Int. J. Mol. Sci.
,
18
, 7, 1544, 2017.
48. Mishra, A.P., Salehi, B., Sharifi-Rad, M., Pezzani, R., Kobarfard, F., Sharifi-Rad, J., Nigam, M., Programmed cell death, from a cancer perspective: an overview.
Mol. Diagn. Ther.
,
22
, 281–295, 2018.
49. Smith, M.T., Guyton, K.Z., Gibbons, C.F., Fritz, J.M., Portier, C.J., Rusyn, I., DeMarini, D.M., Caldwell, J.C., Kavlock, R.J., Lambert, P.F., Hecht, S.S., Key characteristics of carcinogens as a basis for organizing data on mechanisms of carcinogenesis.
Environ. Health Perspect.
,
124
, 6, 713–721, 2016.
50. Glasauer, A. and Chandel, N.S., Targeting antioxidants for cancer therapy.
Biochem. Pharmacol.
,
92
, 1, 90–101, 2014.
51. Li, W., Cao, L., Han, L., Xu, Q., Ma, Q., Superoxide dismutase promotes the epithelial-mesenchymal transition of pancreatic cancer cells via activation of the H2O2/ERK/NF-κB axis.
Int. J. Oncol.
,
46
, 6, 2613–2620, 2015.
52. Andersson, K.E., Oxidative stress and its possible relation to lower urinary tract functional pathology.
