What is Oxidative Stress? The Health Impact of Free Radicals

Free radicals, antioxidants and functional foods: Impact on human health

What is Oxidative Stress? The Health Impact of Free Radicals

1. Aruoma OI. Methodological consideration for characterization for potential antioxidant actions of bioactive components in plants foods. Mutat Res. 2003;532:9–20. [PubMed] [Google Scholar]

2. Mohammed AA, Ibrahim AA. Pathological roles of reactive oxygen species and their defence mechanism. Saudi Pharm J. 2004;12:1–18. [Google Scholar]

3. Bagchi K, Puri S. Free radicals and antioxidants in health and disease. East Mediterranean Health Jr. 1998;4:350–60. [Google Scholar]

4. Aruoma OI. Nutrition and health aspects of free radicals and antioxidants. Food Chem Toxicol. 1994;32:671–83. [PubMed] [Google Scholar]

5. Cheeseman KH, Slater TF. An introduction to free radicals chemistry. Br Med Bull. 1993;49:481–93. [PubMed] [Google Scholar]

6. Young IS, Woodside JV. Antioxidants in health and disease. J Clin Pathol. 2001;54:176–86. [PMC free article] [PubMed] [Google Scholar]

7. Liu T, Stern A, Roberts LJ. The isoprostanes: Novel prostanglandin- products of the free radical catalyzed peroxidation of arachidonic acid. J Biomed Sci. 1999;6:226–35. [PubMed] [Google Scholar]

8. Ebadi M. Antioxidants and free radicals in health and disease: An introduction to reactive oxygen species, oxidative injury, neuronal cell death and therapy in neurodegenerative diseases. Arizona: Prominent Press; 2001. [Google Scholar]

9. Lea AJ. Dietary factors associated with death rates from certain neoplasms in man. Lancet. 1966;2:332–3. [PubMed] [Google Scholar]

10. Harman D. Role of free radicals in aging and disease. Ann N Y Acad Sci. 1992;673:126–41. [PubMed] [Google Scholar]

11. Sies H. Oxidative stress: Introductory remarks. In: Sies H, editor. Oxidative Stress. San Diego: Academic Press; 1985. pp. 1–7. [Google Scholar]

12. Docampo R. Antioxidant mechanisms. In: Marr J, Müller M, editors. Biochemistry and Molecular Biology of Parasites. London: Academic Press; 1995. pp. 147–60. [Google Scholar]

13. Rice-Evans CA, Gopinathan V. Oxygen toxicity, free radicals and antioxidants in human disease: Biochemical implications in atherosclerosis and the problems of premature neonates. Essays Biochem. 1995;29:39–63. [PubMed] [Google Scholar]

14. Rock CL, Jacob RA, Bowen PE. Update o biological characteristics of the antioxidant micronutrients- Vitamin C, Vitamin E and the carotenoids. J Am Diet Assoc. 1996;96:693–702. [PubMed] [Google Scholar]

15. Mc Cord JM. The evolution of free radicals and oxidative stress. Am J Med. 2000;108:652–9. [PubMed] [Google Scholar]

16. Rao AL, Bharani M, Pallavi V. Role of antioxidants and free radicals in health and disease. Adv Pharmacol Toxicol. 2006;7:29–38. [Google Scholar]

17. Stefanis L, Burke RE, Greene LA. Apoptosis in neurodegenerative disorders. Curr Opin Neurol. 1997;10:299–305. [PubMed] [Google Scholar]

18. Esterbauer H, Pubi H, Dieber-Rothender M. Effect of antioxidants on oxidative modification of LDL. Ann Med. 1991;23:573–81. [PubMed] [Google Scholar]

19. Neuzil J, Thomas SR, Stocker R. Requirement for promotion, or inhibition of α- tocopherol of radical induced initiation of plasma lipoprotein lipid peroxidation. Free Radic Biol Med. 1997;22:57–71. [PubMed] [Google Scholar]

20. Poppel GV, Golddbohm RA. Epidemiologic evidence for β – carotene and cancer prevention. Am J Clin Nutr. 1995;62:1393–5. [PubMed] [Google Scholar]

21. Glatthaar BE, Horing DH, Moser U. The role of ascorbic acid in carcinogenesis. Adv Exp Med Biol. 1986;206:357–77. [PubMed] [Google Scholar]

22. Sokol RJ. Vitamin E deficiency and neurologic diseses. Annu Rev Nutr. 1988;8:351–73. [PubMed] [Google Scholar]

23. Ashok BT, Ali R. The aging paradox: Free radical theory of aging. Exp Gerontol. 1999;34:293–303. [PubMed] [Google Scholar]

24. Sastre J, Pellardo FV, Vina J. Glutathione, oxidative stress and aging. Age. 1996;19:129–39. [Google Scholar]

25. Cantuti-Castelvetri I, Shukitt-Hale B, Joseph JA. Neurobehavioral aspects of antioxidants in aging. Int J Dev Neurosci. 2000;18:367–81. [PubMed] [Google Scholar]

26. Freeman BA, Crapo JD. Biology of disease: Free radicals and tissue injury. Lab Invest. 1982;47:412–26. [PubMed] [Google Scholar]

27. Lovell MA, Ehmann WD, Buffer BM, Markesberry WR. Elevated thiobarbituric acid reactive substances and antioxidant enzyme activity in the brain in Alzemers disease. Neurology. 1995;45:1594–601. [PubMed] [Google Scholar]

28. Woo RA, Melure KG, Lee PW. DNA dependent protein kinase acts upstream of p53 in response to DNA damage. Nature. 1998;394:700–4. [PubMed] [Google Scholar]

29. Hattori Y, Nishigori C, Tanaka T, Ushida K, Nikaido O, Osawa T. 8 Hydroxy-2-deoxyguanosine is increased in epidermal cells of hairless mice after chronic ultraviolet B exposure. J Invest Dermatol. 1997;89:10405–9. [PubMed] [Google Scholar]

30. Halliwell B. How to characterize an antioxidant- An update. Biochem Soc Symp. 1995;61:73–101. [PubMed] [Google Scholar]

31. Shi HL, Noguchi N, Niki N. Comparative study on dynamics of antioxidative action of α- tocopheryl hydroquinone, ubiquinol and α- tocopherol, against lipid peroxidation. Free Radic Biol Med. 1999;27:334–46. [PubMed] [Google Scholar]

32. Levine M, Ramsey SC, Daruwara R. Criteria and recommendation for Vitamin C intake. JAMA. 1991;281:1415–23. [PubMed] [Google Scholar]

33. Matill HA. Antioxidants. Annu Rev Biochem. 1947;16:177–92. [PubMed] [Google Scholar]

34. German J. Food processing and lipid oxidation. Adv Exp Med Biol. 1999;459:23–50. [PubMed] [Google Scholar]

35. Jacob R. Three eras of vitamin C discovery. Subcell Biochem. 1996;25:1–16. [PubMed] [Google Scholar]

36. Knight J. Free radicals: Their history and current status in aging and disease. Ann Clin Lab Sci. 1998;28:331–46. [PubMed] [Google Scholar]

37. Moreau, Dufraisse Comptes Rendus des Séances et Mémoires de la Société de Biologie. 1922;86:321. [Google Scholar]

38. Wolf G. The discovery of the antioxidant function of vitamin E: The contribution of Henry A. Mattill. J Nutr. 2005;135:363–6. [PubMed] [Google Scholar]

39. Frie B, Stocker R, Ames BN. Antioxidant defences and lipid peroxidation in human blood plasma. Proc Natl Acad Sci. 1988;37:569–71. [Google Scholar]

40. Rice-Evans CA, Diplock AT. Current status of antioxidant therapy. Free Radic Biol Med. 1993;15:77–96. [PubMed] [Google Scholar]

41. Krinsky NI. Mechanism of action of biological antioxidants. Proc Soc Exp Biol Med. 1992;200:248–54. [PubMed] [Google Scholar]

42. Niki E. Antioxidant defenses in eukaryotic cells. In: Poli G, Albano E, Dianzani MU, editors. Free radicals: From basic science to medicine. Basel, Switzerland: Birkhauser Verlag; 1993. pp. 365–73. [Google Scholar]

43. Sies H. Oxidative stress: Oxidants and antioxidants. Exp Physiol. 1997;82:291–5. [PubMed] [Google Scholar]

44. Magnenat JL, Garganoam M, Cao J. The nature of antioxidant defense mechanisms: A lesson from transgenic studies. Environ Health Perspect. 1998;106:1219–28. [PMC free article] [PubMed] [Google Scholar]

45. Zelko I, Mariani T, Folz R. Superoxide dismutase multigene family: A comparison of the CuZn-SOD (SOD1), Mn-SOD (SOD2), and EC-SOD (SOD3) gene structures, evolution, and expression. Free Radic Biol Med. 2002;33:337–49. [PubMed] [Google Scholar]

46. Banniste J, Bannister W, Rotilio G. Aspects of the structure, function, and applications of superoxide dismutase. CRC Crit Rev Biochem. 1987;22:111–80. [PubMed] [Google Scholar]

47. Johnson F, Giulivi C. Superoxide dismutases and their impact upon human health. Mol Aspects Med. 2005;26:340–52. [PubMed] [Google Scholar]

48. Wuerges J, Lee JW, Yim YI, Yim HS, Kang SO, Djinovic Carugo K. Crystal structure of nickel-containing superoxide dismutase reveals another type of active site. Proc Natl Acad Sci. 2004;101:8569–74. [PMC free article] [PubMed] [Google Scholar]

49. Corpas FJ, Barroso JB, del Río LA. Peroxisomes as a source of reactive oxygen species and nitric oxide signal molecules in plant cells. Trends Plant Sci. 2001;6:145–50. [PubMed] [Google Scholar]

50. Corpas FJ, Fernández-Ocaña A, Carreras A, Valderrama R, Luque F, Esteban FJ, et al. The expression of different superoxide dismutase forms is cell-type dependent in olive (Olea europaea L.) leaves. Plant Cell Physiol. 2006;47:984–94. [PubMed] [Google Scholar]

51. Cao X, Antonyuk SV, Seetharaman SV, Whitson LJ, Taylor AB, Holloway SP, et al. Structures of the G85R variant of SOD1 in familial amyotrophic lateral sclerosis. J Biol Chem. 2008;283:16169–77. [PMC free article] [PubMed] [Google Scholar]

52. Chelikani P, Fita I, Loewen PC. Diversity of structures and properties among catalases. Cell Mol Life Sci. 2004;61:192–208. [PubMed] [Google Scholar]

53. Gaetani G, Ferraris A, Rolfo M, Mangerini R, Arena S, Kirkman H. Predominant role of catalase in the disposal of hydrogen peroxide within human erythrocytes. Blood. 1996;87:1595–9. [PubMed] [Google Scholar]

54. Eisner T, Aneshansley DJ. Spray aiming in the bombardier beetle: Photographic evidence. Proc Natl Acad Sci USA. 1999;96:9705–9. [PMC free article] [PubMed] [Google Scholar]

55. Meister A, Anderson M. Glutathione. Annu Rev Biochem. 1983;52:711–60. [PubMed] [Google Scholar]

56. Brigelius-Flohe R. Tissue-specific functions of individual glutathione peroxidases. Free Radic Biol Med. 1999;27:951–65. [PubMed] [Google Scholar]

57. Hayes J, Flanagan J, Jowsey I. Glutathione transferases. Annu Rev Pharmacol Toxicol. 2005;45:51–88. [PubMed] [Google Scholar]

58. Smirnoff N. L-ascorbicacid biosynthesis. Vitam Horm. 2001;61:241–66. [PubMed] [Google Scholar]

59. Meister A. Glutathione-ascorbic acid antioxidant system in animals. J Biol Chem. 1994;269:9397–400. [PubMed] [Google Scholar]

60. Padayatty S, Katz A, Wang Y, Eck P, Kwon O, Lee J, et al. Vitamin C as an antioxidant: Evaluation of its role in disease prevention. J Am Coll Nutr. 2003;22:18–35. [PubMed] [Google Scholar]

61. Shigeoka S, Ishikawa T, Tamoi M, Miyagawa Y, Takeda T, Yabuta Y, et al. Regulation and function of ascorbate peroxidase isoenzymes. J Exp Bot. 2002;53:1305–19. [PubMed] [Google Scholar]

62. Meister A, Anderson A. Glutathione. Annu Rev Biochem. 1983;52:711–60. [PubMed] [Google Scholar]

63. Meister A. Glutathione metabolism and its selective modification. J Biol Chem. 1988;263:17205–8. [PubMed] [Google Scholar]

64. Fairlamb AH, Cerami A. Metabolism and functions of trypanothione in the Kinetoplastida. Annu Rev Microbiol. 1992;46:695–729. [PubMed] [Google Scholar]

65. Nassar E, Mulligan C, Taylor L, Kerksick C, Galbreath M, Greenwood M, et al. Effects of a single dose of N-Acetyl-5-methoxytryptamine (Melatonin) and resistance exercise on the growth hormone/IGF-1 axis in young males and females. J Int Soc Sports Nutr. 2007;4:14. [PMC free article] [PubMed] [Google Scholar]

66. Caniato R, Filippini R, Piovan A, Puricelli L, Borsarini A, Cappelletti E. Melatonin in plants. Adv Exp Med Biol. 2003;527:593–7. [PubMed] [Google Scholar]

67. Reiter RJ, Carneiro RC, Oh CS. Melatonin in relation to cellular antioxidative defense mechanisms. Horm Metab Res. 1997;29:363–72. [PubMed] [Google Scholar]

68. Tan DX, Manchester LC, Reiter RJ, Qi WB, Karbownik M, Calvo JR. Significance of melatonin in antioxidative defense system: Reactions and products. Biol Signals Recept. 2000;9:137–59. [PubMed] [Google Scholar]

69. Herrera E, Barbas C. Vitamin E: Action, metabolism and perspectives. J Physiol Biochem. 2001;57:43–56. [PubMed] [Google Scholar]

70. Brigelius-Flohe R, Traber M. Vitamin E: Function and metabolism. FASEB J. 1999;13:1145–55. [PubMed] [Google Scholar]

71. Traber MG, Atkinson J. Vitamin E, antioxidant and nothing more. Free Radic Biol Med. 2007;43:4–15. [PMC free article] [PubMed] [Google Scholar]

72. Wang X, Quinn P. Vitamin E and its function in membranes. Prog Lipid Res. 1999;38:309–36. [PubMed] [Google Scholar]

73. Jaeschke H, Gores GJ, Cederbaum AI, Hinson JA, Pessayre D, Lemasters JJ. Mechanisms of hepatotoxicity. Toxicol Sci. 2002;65:166–76. [PubMed] [Google Scholar]

74. Papas AM. Diet and antioxidant status. Food Chem Toxicol. 1999;37:999–1007. [PubMed] [Google Scholar]

75. Brown JE, Rice-Evan CA. Luteolin-rich Artichoke extract protects low density lipoprotein from oxidation in vitro. Free Radic Res. 1998;29:247–255. [PubMed] [Google Scholar]

76. Furuta S, Nishiba Y, Suda I. Fluorometric assay for screening antioxidative activities of vegetables. J Food Sci. 1997;62:526–8. [Google Scholar]

77. Wang H, Cao G, Prior RL. Total antioxidant capacity of fruits. J Agric Food Chem. 1996;44:701–5. [Google Scholar]

78. Lin JK, Lin CH, Ling YC, Lin-Shian SY, Juan IM. Survey of catechins, gallic acid and methylxantines in green, oolong, puerh and black teas. J Agric Food Chem. 1998;46:3635–42. [Google Scholar]

79. Devasagayam TP, Tilak JC, Boloor KK, Sane KS, Ghaskadbi SS, Lele RD. Free radicals and antioxidants in Human Health: Current status and future prospects. J Assoc Physicians India. 2004;52:794–803. [PubMed] [Google Scholar]

80. López-Varela S, González-Gross M, Marcos A. Functional foods and the immune system: A review. Eur J Clin Nutr. 2002;56:S29–33. [PubMed] [Google Scholar]

81. Roberfroid MB. What is beneficial for health? The concept of functional food. Food Chem Toxicol. 1999;37:1034–41. [PubMed] [Google Scholar]

82. Krishnaswamy K. Indian functional food: Role in prevention of cancer. Nutr Rev. 1996;54:127–31. [PubMed] [Google Scholar]

83. DeFelice SL. Nutraceuticals: Opportunities in an Emerging Market. Scrip Mag. 1992;9:14–5. [Google Scholar]

84. Dillard CJ, German JB. Phytochemicals: Nutraceuticals and human health. J Sci Food Agric. 2000;80:1744–56. [Google Scholar]

85. Tapas AR, Sakarkar DM, Kakde RB. Review article flavonoids as nutraceuticals: A review. Trop J Pharm Res. 2008;7:1089–99. [Google Scholar]

86. Vidya AD, Devasagayam TP. Current status of Herbal drug in India: An overview. J Clin Biochem Nutr. 2007;41:1–11. [PMC free article] [PubMed] [Google Scholar]

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249911/

Antioxidant and Oxidative Stress: A Mutual Interplay in Age-Related Diseases

What is Oxidative Stress? The Health Impact of Free Radicals

The average life expectancy has increased rapidly over the past decades, with an average of around 71.4 years in 2015 worldwide (World Health Organization, 2018).

In view of the demographics of the world population in between 2000 and 2050, the population over 60 years is expected to grow from 605 million to 2 billion people (World Health Organization, 2014). Although the increasing life expectancy reflects a positive human development, a new challenge is arising.

In fact, growing older is positively linked to cognitive and biological degeneration such as physical frailty, psychological impairment, and cognitive decline (Jin et al., 2015).

Age-related diseases have become the greatest health threats in the twenty-first century.

Aging is an intrinsic, universal, multifactorial, and progressive process characterized as degenerative in nature, accompanied by progressive loss of function and ultimately increased mortality rate (Dabhade and Kotwal, 2013; López-Otín et al., 2013; Shokolenko et al., 2014; Chang et al., 2017).

Among the theories that explain the aging process, the free radical theory of aging is long-established (Harman, 1956).

This theory speculates that aging is a consequence of the failure of several defensive mechanisms to respond to the reactive oxygen species (ROS)-induced damage, particularly at the mitochondria (Islam, 2017).

Age-related diseases are related to structural changes in mitochondria, accompanied by the alterations of biophysical properties of the membrane including alteration in the electron transport chain complexes activities, decreased fluidity, and subsequently resulted in energy imbalance and mitochondrial failure.

These perturbations impair cellular homeostasis and mitochondrial function and enhance vulnerability to oxidative stress (Eckmann et al., 2013; Chistiakov et al., 2014). Elderly people are susceptible to oxidative stress due to a decline in the efficiency of their endogenous antioxidant systems. Organs such as brain and heart, with high rates of oxygen consumption and limited respiration levels, are particularly vulnerable to this phenomenon, hence partially explaining the high prevalence of cardiovascular diseases (CVD) and neurological disorders in elderly (Corbi et al., 2008).

Oxidative stress plays a crucial role in the development of age-related diseases including arthritis, diabetes, dementia, cancer, atherosclerosis, vascular diseases, obesity, osteoporosis, and metabolic syndromes (Tan et al., 2015a; Liu et al., 2017).

ROS are generated within the biological system to modulate the cellular activities such as cell survival, stressor responses, and inflammation (He and Zuo, 2015; Zuo et al., 2015). Elevation of ROS has been associated with the onset and progression of aging. Although ROS generation may not be an essential factor for aging (López-Otín et al.

, 2013), they are more ly to exacerbate age-related diseases progression via oxidative damage and interaction with mitochondria (Dias et al., 2013). Due to their reactivity, high concentrations of ROS can cause oxidative stress by disrupting the balance of antioxidant and prooxidant levels (Zuo et al., 2015).

Emerging research evidence has suggested that natural compounds can reduce oxidative stress and improve immune function (Ricordi et al., 2015). Indeed, oxidation damage is highly dependent on the inherited or acquired defects in enzymes involved in the redox-mediated signaling pathways.

Therefore, the role of molecules with antioxidant activity that promote healthy aging and counteract oxidative stress is worth to discuss further. Of particular interest in (II) ions and glutathione. RSC Adv. 6, 103169–103177. doi: 10.1039/C6RA21309J

CrossRef Full Text | Google Scholar

Lu, S. C., Mato, J. M., Espinosa-Diez, C., and Lamas, S. (2016). MicroRNA-mediated regulation of glutathione and methionine metabolism and its relevance for liver disease. Free Radic. Biol. Med. 100, 66–72. doi: 10.1016/j.freeradbiomed.2016.03.021

PubMed Abstract | CrossRef Full Text | Google Scholar

Lu, T. M., Chiu, H. F., Shen, Y. C., Chung, C. C., Venkatakrishnan, K., and Wang, C.-K. (2015). Hypocholesterolemic efficacy of quercetin rich onion juice in healthy mild hypercholesterolemic adults: a pilot study. Plant Foods Human Nutr.

Source: https://www.frontiersin.org/articles/10.3389/fphar.2018.01162/full

What is Oxidative Stress? The Health Impact of Free Radicals

What is Oxidative Stress? The Health Impact of Free Radicals

One theory suggests that oxidative stress may underlie different diseases, including mental health and brain disorders, heart disease, diabetes, and more. Is there scientific ground to this theory and what exactly is oxidative stress? We go into the science behind it to explain how the body strikes a balance between free radicals and antioxidants to maintain good health.

Definition

Scientists commonly use the term “oxidative stress.” It refers to a relative dominance of free radicals over antioxidants. It means that more free radicals are being produced than can be neutralized or removed from the cells, tissues, or the body as a whole [1, 2].

To a certain extent, free radicals are normally produced in the body. They support immune defense and help cells communicate. But an excess of free radicals, such as from toxin exposure and pollution, may lead to tissue damage [2].

Reactive oxygen species (ROS) is an umbrella term for a variety of highly reactive molecules or oxidants. The most prominent members include superoxide (O2·−), hydroxyl (OH·), and peroxy radical (ROO). The mitochondria are their main production site [1, 3].

Reactive oxygen species (ROS) are produced by all cell types that line blood vessels, muscles, and connective tissue with the help of numerous enzymes. They are also produced by neutrophils and macrophages during inflammation, which is needed short-term to help the body fight off infections [4, 3].

The rate and magnitude of oxidant formation are usually balanced by the rate of oxidant elimination. Oxidative stress is when prooxidants override antioxidant defense [5].

What Increases Free Radicals?

Some research suggests that oxidants can also be generated by:

  • Different types of radiation, with X-irradiation generating the hydroxyl radical [6, 3].
  • Excess UV light [6, 3].
  • Ultrasound and microwave radiation [6].
  • Mineral excess or heavy metals (including iron, copper, chromium, cobalt, vanadium, cadmium, arsenic, nickel) [3].
  • Pollutants [3].

“Free Radical Defense”

It has become apparent to scientists that plants actively produce ROS as a way to control processes such as programmed cell death, stress responses, defense against microbes and cellular communication [7].

Research suggests that we might use free radicals in a similar way.
That means that our bodies don’t only have “antioxidant defense,” as most people see it. We also seem to have “free radical defense.”

In humans, free radical reactions are essential for defense against microbes. Neutrophils, macrophages and other cells of the immune system produce them. However, their overproduction can have a counter-effect, leading to tissue injury and cell death [1].

ROS within cells act as communication molecules. In low concentrations, they appear to increase the growth, reproduction, and survival of cell types. In high concentrations, they may induce cell death. This is being researched as a potential cancer-fighting approach [3].

Researchers point to their other roles in the body, such as regulating cellular calcium, protein phosphorylation, and transcription factors – all of which are seen as crucially important for human health [3, 2].

Research Limitations

The majority of studies covered in this section deal with associations only, which means that a cause-and-effect relationship hasn’t been established.

For example, just because heart disease has been linked with high oxidative stress doesn’t mean that heart disease is caused by oxidative stress. Data are lacking to make such claims.

Also, even if a study did find that free radicals can contribute to heart disease, they are highly unly to be the only cause. Complex disorders heart disease always involve multiple possible factors – including biochemistry, environment, health status, and genetics – that may vary from one person to another.

Disease Associations

According to limited research, as many as 200 human diseases have been associated with increased levels of oxidative stress. These include the following [8]:

  • Cardiovascular disease [9], Stroke [4], Heart failure [4], Hypertension [9, 4]
  • High cholesterol [9, 4]
  • Cancer [9]
  • Parkinson’s disease [9]
  • Alzheimer’s disease [9]
  • Diabetes [4]
  • Kidney disease [4]

Some studies had conflicting findings. More research is needed.

Cellular Damage

Scientists found that high concentrations of ROS can damage structures within cells, including fats (in membranes), proteins, and nucleic acids that build RNA and DNA. What constitutes “high levels” in our day-to-day life has yet to be determined, though [3].

According to one hypothesis, oxidative damage accumulates during the life cycle, and it may play a role in the development of age-related diseases such as arthritis, dementia, and others. Although possible, large-scale evidence is still lacking to firmly establish this hypothesis [3, 2].

Diabetes

People with both type 1 and 2 diabetes seem to have high levels of free radicals, according to some estimates. The onset of diabetes has been associated with oxidative stress, but its exact role is still unclear [1].

Too much oxidative stress relevant to antioxidant levels is also hypothesized to impair sugar balance [1].

In one study, oxidative stress was suggested to accelerate diabetes complications by damaging proteins. Another study suggests that oxidative stress byproducts contribute to insulin resistance, a hallmark of type 2 diabetes. Large scale data are needed [1].

COPD

Oxidative stress damages and impairs the functioning of several kinds of proteins, harming the lungs in ways that can induce COPD, a chronic lung disease. The main cause of COPD is smoking, a major source of toxic chemicals and trigger of excess free radicals in the body [10].

The harmful effects of oxidative stress in COPD include excessive mucus, membrane damage, and lung cell death [10].

It may start off a vicious cycle in COPD patients: oxidative stress causes inflammation, and inflammation, in turn, causes more oxidative stress [11].

Scientists think this cycle is hard to break because oxidation makes various proteins lose function, and that hinders the body’s ability to restore a healthy oxidant/antioxidant balance [11].

Cancer Controversy

The link between free radicals and cancer is still unclear.

Researchers explain that DNA mutation is a critical step in cancer formation. Excessive DNA damage caused by free radicals (as measured by 8-OH-G) has been found in tumors. One unproven hypothesis states that this type of damage may underlie cancer initiation, but solid evidence is lacking [3].

High levels of oxidative stress are toxic to cells and ultimately kill them. Thus, increasing oxidative stress has been studied as a potential cancer-fighting strategy [2].

Low levels of oxidative stress are thought to stimulate cell division in the promotion stage. Some scientists think that this might, along with many other complex factors, stimulate tumor growth. This hasn’t been proven in humans either, but [3].

these findings, though, an excess of antioxidants might theoretically increase the growth of existing tumors. This hasn’t been confirmed in large-enough studies, but some human findings are available.

In one study of breast cancer patients, antioxidant use during chemotherapy or radiation therapy was associated with worsened breast cancer prognosis in postmenopausal women [12].

A mice study published in 2019 even casts doubt on regularly using well-known antioxidants to improve health. The antioxidant N-acetylcysteine protected from COPD (lung emphysema) but induced lung cancer in mice [13].

It seems that tilting the balance in either direction – toward free radical excess or deficiency – may be detrimental.

It’s no surprise that antioxidant supplements aren’t a panacea – studies suggest that they are more ly to be harmful. But future research should clarify whether – and to what extent – antioxidant status and supplementation affect cancer risk.

Natural Antioxidant Defense

Living organisms have evolved a number of antioxidant defenses to maintain their survival against excessive oxidative stress [4].

To avoid free radical overproduction from oxidative stress, tissues naturally have antioxidants at their disposal. These antioxidants can neutralize free radicals [1].

Some common antioxidants include vitamins A, C, and E, glutathione, and the enzymes superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase [14].

Other antioxidants include lipoic acid, mixed carotenoids, coenzyme Q10, several bioflavonoids, antioxidant minerals (copper, zinc, manganese, and selenium), and various cofactors (folic acid, vitamins B1, B2, B6, B12) [14].

They work in synchrony when balanced. The body can produce some of them, while we can get the others in adequate amounts from a healthy diet [14].

Antioxidant Supplements

The optimal source of antioxidants seems to come from our diet, not from antioxidant supplements, especially in well-nourished populations [15].

Vegetables and fruits are great sources of antioxidants. There is good evidence that eating a diet rich in vegetables and fruits is healthy [16].

Antioxidant supplements, on the other hand, have no known health benefits.

They have not been approved by the FDA for medical use. Supplements generally lack solid clinical research. Regulations set manufacturing standards for them but don’t guarantee that they’re safe or effective.

According to the National Center for Complementary and Alternative Health [16]:

“Rigorous scientific studies involving more than 100,000 people combined have tested whether antioxidant supplements can help prevent chronic diseases, such as cardiovascular diseases, cancer, and cataracts. In most instances, antioxidants did not reduce the risks of developing these diseases.”

Additionally, antioxidant supplements were not associated with a lower risk of dying in other studies [17, 18].

Concerns have been raised about associations between high doses of certain antioxidants and health risks. Beta-carotene supplementation has been linked with lung cancer in smokers, vitamin E with prostate cancer, and vitamin A with a higher risk of dying [17, 18].

Additionally, antioxidant supplements may interact with some medicines. Supplement-drug interactions can be dangerous and, in rare cases, even life-threatening.

Always consult your doctor before supplementing or making major changes to your diet and let them know about all drugs and supplements you are using or considering.

Source: https://selfhacked.com/blog/oxidative-stress-101/

What Are Free Radicals?

What is Oxidative Stress? The Health Impact of Free Radicals

The body is under constant attack from oxidative stress. Oxygen in the body splits into single atoms with unpaired electrons. Electrons to be in pairs, so these atoms, called free radicals, scavenge the body to seek out other electrons so they can become a pair. This causes damage to cells, proteins and DNA. 

Free radicals are associated with human disease, including cancer, atherosclerosis, Alzheimer's disease, Parkinson's disease and many others. They also may have a link to aging, which has been defined as a gradual accumulation of free-radical damage, according to Christopher Wanjek, the Bad Medicine columnist for Live Science. 

Substances that generate free radicals can be found in the food we eat, the medicines we take, the air we breathe and the water we drink, according to the Huntington's Outreach Project for Education at Stanford University. These substances include fried foods, alcohol, tobacco smoke, pesticides and air pollutants.

Free radicals are the natural byproducts of chemical processes, such as metabolism. Dr. Lauri Wright, a registered dietitian and an assistant professor of nutrition at the University of South Florida, said, “Basically, I think of free radicals as waste products from various chemical reactions in the cell that when built up, harm the cells of the body.” 

Yet, free radicals are essential to life, Wanjek wrote in 2006. The body's ability to turn air and food into chemical energy depends on a chain reaction of free radicals. Free radicals are also a crucial part of the immune system, floating through the veins and attacking foreign invaders.

The danger of free radicals

According to Rice University, once free radicals are formed, a chain reaction can occur.

The first free radical pulls an electron from a molecule, which destabilizes the molecule and turns it into a free radical.

That molecule then takes an electron from another molecule, destabilizing it and tuning it into a free radical. This domino effect can eventually disrupt and damage the whole cell.

The free radical chain reaction may lead to broken cell membranes, which can alter what enters and exits the cell, according to the Harvard School of Public Health. The chain reaction may change the structure of a lipid, making it more ly to become trapped in an artery. The damaged molecules may mutate and grow tumors. Or, the cascading damage may change DNA code. 

Oxidative stress occurs when there are too many free radicals and too much cellular damage. Oxidative stress is associated with damage of proteins, lipids and nucleic acids, according to an article in the Pharmacognosy Review.

Several studies throughout the last few decades have suggested that oxidative stress plays a role in the development of many conditions, including macular degeneration, cardiovascular disease, certain cancers, emphysema, alcoholism, Alzheimer's disease, Parkinson's disease, ulcers and all inflammatory diseases, such as arthritis and lupus. 

Free radicals are also associated with aging. “The free radical theory of aging states that we age because of free radical damage over time,” said Wright. Free radicals can damage DNA's instructional code, causing our new cells to grow incorrectly, leading to aging. 

Symptoms of oxidative stress

According to a 2010 article in Methods of Molecular Biology, there are no officially recognized symptoms of oxidative stress. According to naturopathic doctor Donielle Wilson’s website, however, symptoms include fatigue, headaches, noise sensitivity, memory loss and brain fog, muscle and joint pain, wrinkles and gray hair, vision trouble and decreased immunity.  

Testing for free radicals

It is not possible to directly measure the amount of free radicals in the body, according to Rice University.

According to a 2000 article in theAmerican Journal of Clinical Nutrition, there are indirect methods of measuring oxidative stress, usually involving analysis of the byproducts of lipid peroxidation.

The article warns that all methods should “should be used with caution because of the lack of accuracy, validity or both.” 

The more recent article in Methods of Molecular Biology states that kits for testing oxidative stress are increasingly available, though their accuracy and validity are still under scrutiny. 

Antioxidants and free radicals

Antioxidants keep free radicals in check. Antioxidants are molecules in cells that prevent free radicals from taking electrons and causing damage. Antioxidants are able to give an electron to a free radical without becoming destabilized themselves, thus stopping the free radical chain reaction.

“Antioxidants are natural substances whose job is to clean up free radicals. Just fiber cleans up waste products in the intestines, antioxidants clean up the free radical waste in the cells,” said Wright.

Well-known antioxidants include beta-carotene and other carotenoids, lutein, resveratrol, vitamin C, vitamin E, lycopene and other phytonutrients.

Our body produces some antioxidants on its own, but an insufficient amount. Oxidative stress occurs when there is an imbalance of free radicals and antioxidants (too many free radicals and too few antioxidants), according to the Pharmacognosy Review. 

Antioxidants can be acquired through diet. “Antioxidants are plentiful in fruits and vegetables, especially colorful fruits and vegetables,” said Wright. “Some examples include berries, tomatoes, broccoli, spinach, nuts and green tea.” 

Antioxidants became well known in the 1990s when scientists began to realize the possible effects of free radicals on cancer development, atherosclerosis and other chronic conditions.

During the subsequent decades, scientists have conducted many studies on the effects of antioxidants with mixed results. Wright gave a few examples.

“A six-year trial, the Age-Related Eye Disease Study (AREDS), found that a combination of vitamin C, vitamin E, beta-carotene and zinc offered some protection against the development of advanced age-related macular degeneration,” she said. 

On the other hand, Wright mentioned that a beta-carotene trial among Finnish men who were heavy smokers found an increase in lung cancer among those taking beta-carotene supplements. 

Scientists do not completely understand the mixed results from the trials or the exact mechanism that makes antioxidants effective or ineffective against free radicals, but according to Wright, the study results suggest that it is more effective and potentially safer to get antioxidants through whole foods rather than supplements.

Free radicals and exercise

According to an article in Biochemical Society Transactions, intense aerobic exercise can induce oxidative stress. Burning fuel in high-intensity cardio exercise causes chemical reactions that make free radicals form at a faster rate.

This isn't an excuse to skip the gym, however. According to an article in the American Journal of Clinical Nutrition, frequent exercise training seems to reduce the oxidative stress initially brought on by exercise.

This is because regular physical exercise enhances antioxidant defenses.

Spurred by the concern that intense exercise could cause oxidative stress, several studies were conducted to look at the effects of antioxidant supplementation for athletes.

The American Journal of Clinical Nutrition article said that supplementing high intensity exercise with antioxidant supplements produced no beneficial effects, however.

Regular exercise alone was enough to build up antioxidant defenses against the initial exercise-induced oxidative stress. 

Therefore, shape and infrequent exercisers who do a spontaneous b intense physical activity may invoke oxidative stress, while those who are consistently active should not worry. 

Additional resources

Source: https://www.livescience.com/54901-free-radicals.html

Natural Remedies for Fighting Oxidative Stress

What is Oxidative Stress? The Health Impact of Free Radicals
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  1. Pizzino G, Irrera N, Cucinotta M, et al.

    Oxidative stress: harms and benefits for human health. Oxid Med Cell Longev. 2017;2017:8416763. doi:10.1155/2017/8416763

  2. Devine JF. Chronic obstructive pulmonary disease: an overview. Am Health Drug Benefits. 2008;1(7):34–42.

  3. Weinreb RN, Aung T, Medeiros FA. The pathophysiology and treatment of glaucoma: a review. JAMA. 2014;311(18):1901–1911. doi:10.1001/jama.2014.3192

  4. Seyyedebrahimi S, Khodabandehloo H, Nasli esfahani E, Meshkani R. The effects of resveratrol on markers of oxidative stress in patients with type 2 diabetes: a randomized, double-blind, placebo-controlled clinical trial. Acta Diabetol. 2018;55(4):341-353. doi:10.1007/s00592-017-1098-3

  5. Birben E, Sahiner UM, Sackesen C, Erzurum S, Kalayci O. Oxidative stress and antioxidant defense. World Allergy Organ J. 2012;5(1):9–19. doi:10.1097/WOX.0b013e3182439613

Additional Reading

  • Allen CL, Bayraktutan U. “Oxidative stress and its role in the pathogenesis of ischaemic stroke.” Int J Stroke. 2009 Dec;4(6):461-70.
  • Hininger-Favier I, Benaraba R, Coves S, Anderson RA, Roussel AM. “Green tea extract decreases oxidative stress and improves insulin sensitivity in an animal model of insulin resistance, the fructose-fed rat.” J Am Coll Nutr.

    2009 Aug;28(4):355-61.

  • Kairisalo M, Bonomo A, Hyrskyluoto A, Mudò G, Belluardo N, Korhonen L, Lindholm D. “Resveratrol reduces oxidative stress and cell death and increases mitochondrial antioxidants and XIAP in PC6.3-cells.” Neurosci Lett. 2011 Jan 25;488(3):263-6. Epub 2010 Nov 19.
  • Kirkham P, Rahman I.

    “Oxidative stress in asthma and COPD: antioxidants as a therapeutic strategy.” Pharmacol Ther. 2006 Aug;111(2):476-94. Epub 2006 Feb 3.

  • Logan AC, Wong C. “Chronic fatigue syndrome: oxidative stress and dietary modifications.” Altern Med Rev. 2001 Oct;6(5):450-9.
  • Madamanchi NR, Vendrov A, Runge MS. “Oxidative stress and vascular disease.

    ” Arterioscler Thromb Vasc Biol. 2005 Jan;25(1):29-38. Epub 2004 Nov 11.

  • Maritim AC, Sanders RA, Watkins JB 3rd. “Diabetes, oxidative stress, and antioxidants: a review.” J Biochem Mol Toxicol. 2003;17(1):24-38.
  • Reiter RJ. “Oxidative damage in the central nervous system: protection by melatonin.” Prog Neurobiol. 1998 Oct;56(3):359-84.

  • Sasazuki S, Hayashi T, Nakachi K, Sasaki S, Tsubono Y, Okubo S, Hayashi M, Tsugane S. “Protective effect of vitamin C on oxidative stress: a randomized controlled trial.” Int J Vitam Nutr Res. 2008 May;78(3):121-8.
  • Thyagarajan A, Jiang J, Hopf A, Adamec J, Sliva D.

    “Inhibition of oxidative stress-induced invasiveness of cancer cells by Ganoderma lucidum is mediated through the suppression of interleukin-8 secretion.” Int J Mol Med. 2006 Oct;18(4):657-64.

Source: https://www.verywellhealth.com/oxidative-stress-and-your-health-89492

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