Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2012;1(1):1-4.
doi: 10.5455/oams.080612.ed.001.

Oxidants and antioxidants: friends or foes?

Sukru Oter  1 , Si Jin  2 , Luca Cucullo  3 , H J Damien Dorman  4
Affiliations

Oxidants and antioxidants: friends or foes?

Sukru Oter et al. Oxid Antioxid Med Sci. 2012.
No abstract available

Keywords: Antioxidants; Free radicals; Oxidants; Reactive species; Redox signalling.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Major known oxidant/antioxidant pathways in living organisms. Many pathologic processes including inflammation, ischemia, irradiation, etc. as well as physiological functions such as cellular respiration can trigger or increase superoxide radical (O2•−) production. The antioxidant enzyme superoxide dismutase (SOD) facilitates the dismutation reaction of O2•− to hydrogen peroxide (H2O2). H2O2 can be reduced to water (H2O) via different ways: the glutathione cycle in which the reduced form of glutathione (GSH) was oxidized to glutathione disulfide (GSSG) and then will again be reduced to GSH plays the major role; mainly glutathione peroxidase (GPX) glutathione reductase (GR) and glutathione-S-transferase (GST), but also glutathione synthethase (GS), glutaredoxin (GRX) and glutamate cysteine ligase (GCL) are involved in this system. Catalase (CAT), thioredoxin (TRX) and peroxiredoxin (PRX) are also fighting against H2O2 overproduction; heme oxygenase-1 (HO-1) and several metal chelators are other important members of the endogenous redox state regulatory systems. If free Fe3+ or Cu2+ are present around H2O2, another possible - but unwanted - pathway is the production of the hydroxyl radical (•OH), one of the most reactive species known, via the Fenton and following Haber-Weiss reactions; •OH have the ability to oxidize almost all biomolecules. Another unwanted pathway is, in the presence of excessive amounts of nitric oxide (NO•) produced mainly by the inducible isotype of nitric oxide synthase (iNOS), the outcompeting of SOD for its substrate O2•−. In this case the reaction of NO• with O2•− will produce peroxynitrite (ONOO−), a highly reactive molecule; S-nitrothiols (RSNOs) such as S-nitrosoglutathione (GSNO) can be produced in following steps. On the other hand, the radical or non-radical reactive species can trigger the activation of ‘redox sensitive transcription factors’ such as nuclear factor kappa B (NF-κB) or activator protein-1 (AP-1) which can mediate both a lot of physiological functions or inflammatory responses via several cytokines. Particularly in chronic pathologies, the re-activation of reactive molecules can lead to a vicious circle. Please note that ‘antioxidants’ cover a large broad of molecules and they can act in much more steps of redox reactions than simply shown in the figure; e.g. inhibiting ROS generating enzymes, supporting the production of endogenous defense molecules, scavenging free radicals. [Other abbreviations: ROS, reactive oxygen species; RNS, reactive nitrogen species; TNFα, tumor necrosis factor alpha; IL-1β, interleukin 1-beta; COX-2, cyclooxygenase 2; Nrf2, Nuclear factor erythroid 2-related factor 2]
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Harman D. Aging: a theory based on free radical and radiation chemistry. J Gerontol. 1956;11:298–300. - PubMed
    1. Harman D. The biologic clock: the mitochondria? J Am Geriatr Soc. 1972;20:145–7. - PubMed
    1. Harman D. Free radical theory of aging: consequences of mitochondrial aging. Age. 1983;6:86–94.
    1. Harman D. Free radical theory of aging: the “free radical” diseases. Age. 1984;7:11–31.
    1. Cross CE, Halliwell B, Borish ET, Pryor WA, Ames BN, Saul RL, McCord JM, Harman D. Oxygen radicals and human disease. Ann Intern Med. 1987;107:526–45. - PubMed

LinkOut - more resources