Free radicals: what they are and how they work

Free Radicals

Free radicals are molecules formed by our body, or generated by external factors that cause them to form in the human body1. Our bodies form or acquire those molecules2 and they are then involved in a range of chemical reactionsor in changes that can alter how the body is regulated.

How free radicals work

Free radicals are involved in important functions that are essential for good health. These actions include the production, fertilisation and maturation of cell movement, eliminating toxic products and protecting us from microbes, viruses and even tumor cells2.

Free radicals and oxidants have both toxic and beneficial effects, so they can be either harmful or useful to the body1. When these substances are produced in excess they can cause tissue lesions, which play a role in a range of health problems2.

Where are free radicals found?

Several factors contribute to the production of free radicals. Lifestyle, stress and the environment can cause excessive formation of free radicals, resulting in the creation of oxidative stress.

Examples of these factors are air pollution3, cigarette smoke3, alcohol consumption4, high blood sugar levels5, high intake of polyunsaturated fatty acids3, radiation3, too much or too little oxygen in your body6, intense and prolonged exercise7, excessive intake of antioxidants, or antioxidant deficiency8.

Free radicals, oxidative stress and antioxidants

When our body generates an overload of free radicals that we cannot destroy over time, oxidative stress occurs1.

The term oxidative stress refers to oxidative damage that occurs when the production of free radicals and antioxidant compounds is unbalanced9. This instability is associated with damage to various molecular entities such as lipids, proteins and nucleic acids10, leading to the development of chronic and degenerative health problems1.

In the short term, oxidative stress can occur in tissues injured by trauma, infection or excessive exercise1. These injured tissues produce an increase in free radical-generating enzymes (e.g. xanthine oxidase, lipoxygenase or cyclooxygenase), phagocyte activation, the release of free iron, copper ions or an interruption of the electron transport chains of oxidative phosphorylation, resulting in excess reactive oxygen species (ROS)1. The onset and development of diseases has been linked to an imbalance between the number of reactive oxygen species and antioxidant molecules1

Oxidative stress

Scientific research has studied the ability of the human body to counteract oxidative stress by producing antioxidants1 through food and/or supplements1. It is therefore essential to maintain healthy bodily function by achieving a balance between free radicals and antioxidants1.

How to eliminate free radicals

Science suggests that one factor contributing to the proper functioning of our bodies is determined by the rate of free radical-induced degradation11. However, free radicals can be regulated in the human body:

By antioxidant molecules

  • Vitamins A, C and E12: antioxidants such as beta-carotene, ascorbic acid and alpha tocopherol neutralise the oxidation caused by free radicals in vitro and in vivo12. These antioxidants are ideally obtained from natural sources such as fruits and vegetables13
  • Taurine, bilirubin and uric acid: these are the three natural antioxidant molecules found in breast milk, the liver and kidneys. They can neutralise the production of free radicals14.

By natural supplements 

Several antioxidants have been shown to be effective15 in improving humoral and cellular immune responses in elderly people. Using natural antioxidant supplements can help enhance our body’s response to free radicals, reduce oxidative stress, and prevent age-related immune system weakening. For example:

  • Pro DNA, which contributes to normal DNA synthesis and the cell division process16
  • Multivitamin formula, a balanced synergy of vitamins and minerals whose composition has been carefully researched and controlled, providing 100% of the nutrient reference values of the majority of the micro-nutrients necessary for a healthy diet.
  • Organic Acerola, a fruit high in natural vitamin C (60 times more than orange) that helps protect cells from oxidative damage.

By free radical-destroying enzymes17

  • Superoxide dismutase (SOD): found in ‘energy plants’ or the mitochondria of human cells, this enzyme converts superoxide radicals into much less reactive hydrogen peroxides18.
  • Catalase: Catalase breaks down hydrogen peroxides into water molecules to prevent the formation of hydroxyl radicals19.
  • Glutathione peroxidase: this enzyme catalyses the ability of reduced glutathione (GSH) to release hydrogen to a hydroxyl, or of hydrogen peroxide to form water 20.
  • Thioredoxin: TRX plays a protective role against oxidative stress, thanks to its free radical elimination properties21.

Striking a balance between free radicals and antioxidants is advised, to prevent or minimise the duration of oxidative stress, contributing to better health. 

Free radicals as a cause of ageing

A relationship has also been observed between free radicals and the origin of some health problems and the ageing trajectory22.

According to the theory proposed by D. Harman in 195623, cellular ageing is linked to chronic oxidative stress24. This theory is still applied and accepted by current research25, which states that ageing is linked to oxidative stress produced by free radicals and other reactive oxygen species (ROS)13

How many free radicals are there?1

There are different types of free radicals: hydroxyl radical, superoxide radical anion, hydrogen peroxide, singlet oxygen, hypochlorite, nitric oxide radical and radical peroxynitrite1. These are the main radicals generated by the human body26

  • Superoxide (O-2) radicals: produced in cellular metabolic reactions, either because of auto-oxidation or by the action of enzymes such as oxidases. In our body, superoxide radicals are the main agents involved in the bactericidal action of phagocytes (a type of immune cell)27, but can also be a harmful mediator in inflammation and cause normal body tissues to be damaged28
  • Hydroxyl (OH-) radicals: formed in different cellular chemical reactions involving hydrogen. These are the most reactive free radicals, as one of the main mediators of cellular damage29.
  • Nitric oxide (NO): is a highly diffusible, lipid-soluble and short-lived radical (6). NO is involved in immune defence, which makes it a free radical highly important to the body30.

Free radicals can also be classified into the following types31

  • Primary free radicals: these are formed from the transfer of electrons on the oxygen atom. They have a very short half-life10.
  • Secondary free radicals: these are formed from the transfer of a primary radical to an atom of an organic molecule, or by the reaction of two primary radicals with each other. They typically have a longer half-life than primary free radicals10.
  • Stable free radical intermediates: these are stable molecules that are not radical, but from which the latter are formed10.

Both classifications illustrate the multiple different forms and physical properties of free radicals and reactive species within the body. This diverse range of forms and properties extends throughout our human body. 

Although the biological half-life of free radicals last microseconds, it is enough time for them to react with everything around them. Cellular, molecular and even tissue damage can occur due to external or internal contaminants.


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  1. Pham-Huy LA, He H, Pham-Huy C. Free radicals, antioxidants in disease and health. Int J Biomed Sci. 2008 Jun;4(2):89-96. PMID: 23675073; PMCID: PMC3614697.
  2. Deadly nanoparcel for cancer cells: free radical generating hybrid nanomaterial for the oxidative destruction of hypoxic cancer cells. Saudi Med J. 2017 Jun; 38(6): 670. PMCID: PMC5541195.
  3. Turpeinen AM, Basu S, Mutanen M. A high linoleic acid diet increases oxidative stress in vivo and affects nitric oxide metabolism in humans. Prostaglandins Leukot Essent Fatty Acids. 1998 Sep;59(3):229-33. doi: 10.1016/s0952-3278(98)90067-9. PMID: 9844997.
  4. Albano E. Alcohol, oxidative stress and free radical damage. Proc Nutr Soc. 2006 Aug;65(3):278-90. doi: 10.1079/pns2006496. PMID: 16923312.
  5. Marfella R, Quagliaro L, Nappo F, Ceriello A, Giugliano D. La hiperglucemia aguda induce un estrés oxidativo en sujetos sanos. J Clin Invest. Agosto de 2001; 108 (4): 635-6. doi: 10.1172 / JCI13727. PMID: 11518739; PMCID: PMC209408.
  6. Liu Y, Fiskum G, Schubert D. Generation of reactive oxygen species by the mitochondrial electron transport chain. J Neurochem. 2002 Mar;80(5):780-7. doi: 10.1046/j.0022-3042.2002.00744.x. PMID: 11948241.
  7. Powers SK, Jackson MJ. Exercise-induced oxidative stress: cellular mechanisms and impact on muscle force production. Physiol Rev. 2008 Oct;88(4):1243-76. doi: 10.1152/physrev.00031.2007. PMID: 18923182; PMCID: PMC2909187.
  8. Rahal A, Kumar A, Singh V, Yadav B, Tiwari R, Chakraborty S, Dhama K. Oxidative stress, prooxidants, and antioxidants: the interplay. Biomed Res Int. 2014;2014:761264. doi: 10.1155/2014/761264. Epub 2014 Jan 23. PMID: 24587990; PMCID: PMC3920909.
  9. Pharmacogn Rev. 2010 Jul-Dec; 4(8): 118–126. doi: 10.4103/0973-7847.70902. PMCID: PMC3249911. PMID: 22228951.
  10. Avello, Marcia, & Suwalsky, Mario. (2006). Radicales libres, antioxidantes naturales y mecanismos de protección. Atenea (Concepción), (494), 161-172.
  11. Pharmacogn Rev. 2010 Jul-Dec; 4(8): 118–126. doi: 10.4103/0973-7847.70902. PMCID: PMC3249911. PMID: 22228951.
  12. Tucker JM, Townsend DM. Alpha-tocopherol: roles in prevention and therapy of human disease. Biomed Pharmacother. 2005 Aug;59(7):380-7. doi: 10.1016/j.biopha.2005.06.005. PMID: 16081238; PMCID: PMC6361124.
  13. Le Prell CG, Hughes LF, Miller JM. Free radical scavengers vitamins A, C, and E plus magnesium reduce noise trauma. Free Radic Biol Med. 2007 May 1;42(9):1454-63. doi: 10.1016/j.freeradbiomed.2007.02.008. Epub 2007 Feb 20. PMID: 17395018; PMCID: PMC1950331.
  14. C. de Teresa Galván et al. / Rev Andal Med Deporte 2008;1(2): 61-72.
  15. 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 Oct;52:794-804. PMID: 15909857.
  16. COMMISSION REGULATION (EU) No 432/2012 of 16 May 2012 establishing a list of permitted health claims made on foods, other than those referring to the reduction of disease risk and to children’s development and health.
  17. © 2017 Alexandria University Faculty of Medicine. Production and hosting by Elsevier B.V.
  18. CRC Experimental Chemotherapy Group, Department of Pharmacy, University of Aston in Birmingham, Birmingham B4 7ET.
  19. Sahnoun Z, Jamoussi K, Zeghal KM. Radicaux libres et antioxydants: physiologie, pathologie humaine et aspects thérapeutiques [Free radicals and antioxidants: human physiology, pathology and therapeutic aspects]. Therapie. 1997 Jul-Aug;52(4):251-70. French. PMID: 9437876.
  20. I. F. Bonola Gallardo, M. E. Irigoyen Camacho, L. I. Vera Robles, A. Campero Celis, A. Hamdan Partida. Oxidative stress: the glutathione enzyme system and oral health. Vol. 15. Núm. 1. páginas 2-8 (Enero - Junio 2014).
  21. Schallreuter KU, Wood JM. The role of thioredoxin reductase in the reduction of free radicals at the surface of the epidermis. Biochem Biophys Res Commun. 1986 Apr 29;136(2):630-7. doi: 10.1016/0006-291x(86)90487-0. PMID: 2423087.
  22. Rock CL, Jacob RA, Bowen PE. Update on the biological characteristics of the antioxidant micronutrients: vitamin C, vitamin E, and the carotenoids. J Am Diet Assoc. 1996 Jul;96(7):693-702; quiz 703-4. doi: 10.1016/S0002-8223(96)00190-3. PMID: 8675913.
  23. HARMAN D. Aging: a theory based on free radical and radiation chemistry. J Gerontol. 1956 Jul;11(3):298-300. doi: 10.1093/geronj/11.3.298. PMID: 13332224.
  24. Influencia de los radicales libres en el envejecimiento celular, Fernando Paredes Salido, Juan José Roca Fernández. Vol. 21. Núm. 7. páginas 96-100 (Julio 2002).
  25. Integration of theories of ageing J. Miquel. Vol. 41. Núm. 1. Páginas 55-63 (Enero 2006).
  26. Gutiérrez-Salinas J, Mondragón-Terán P, García-Ortíz L, et al. Breve descripción de los mecanismos moleculares de daño celular provocado por los radicales libres derivados de oxígeno y nitrógeno. Rev Esp Med Quir. 2014;19(4):446-454.
  27. Rosen GM, Pou S, Ramos CL, Cohen MS, Britigan BE. Free radicals and phagocytic cells. FASEB J. 1995 Feb;9(2):200-9. doi: 10.1096/fasebj.9.2.7540156. PMID: 7540156.
  28. McCord JM. The superoxide free radical: its biochemistry and pathophysiology. Surgery. 1983 Sep;94(3):412-4. PMID: 6310808.
  29. Ward JF (1988). "DNA damage produced by ionizing radiation in mammalian cells: identities, mechanisms of formation, and reparability". Progress in Nucleic Acid Research and Molecular Biology. 35 (3): 95–125. doi:10.1016/s0079-6603(08)60611-x. ISBN 9780125400350. PMID 3065826.
  30. Inmunidad y nutrición, Adela-Emilia Gómez Ayala. Vol. 20. Núm. 3. páginas 52-57 (Marzo 2006).
  31. Venereo Gutiérrez, Justo R.. (2002). Daño oxidativo, radicales libres y antioxidantes. Revista Cubana de Medicina Militar, 31(2), 126-133. Recuperado el 23 de noviembre de 2020.

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