Reactive products of oxygen are among the most potent and omnipresent threats faced by the living organism. Intracellular accumulation of reactive oxygen species such as superoxide anion, hydrogen peroxide, hydroxyl radical, and peroxy radical, can arise from toxic insults or normal metabolic processes. These species may perturb the cell's natural antioxidant defence systems, resulting in damage to all of the major classes of biological macromolecules, including nuclear acids, proteins, carbohydrates and lipids. Oxidative stress has been defined as a disturbance in the prooxidant-antioxidant balance, resulting in potential cell damage. It has been implicated in several biological and pathological processes like ageing, inflammation, carcinogenesis, ischemia-reperfusion and in diseases including diabetes mellitus, atherosclerosis, and/or neurodegenerative diseases
Abuja PM, Albertini R. Methods for monitoring oxidative stress, lipid peroxidation and oxidation resistance of lipoproteins. Clin Chim Acta. 306:1–17.
2.
Pryor WA, Squadrito GL. The chemistry of peroxynitrite in vivo from nitric oxide and superoxide. Chem Biol Interact. 96:203–6.
3.
Rossi F, Bellavite P, Barton G. Mechanism of production of toxic oxygen radicals by granulocytes and macrophages and their function in the inflammatory process. Pathol Res Pract. 180:136–42.
Jacobson MD. Reactive oxygen species and programmed cell death. Trends Biochem Sci. 24(3):81–119.
6.
Dalton TP, Shertzer HG, Puga A. Regulation of gene expression by reactive oxygen. Annu Rev Pharmacol Toxicol. 39:67–101.
7.
Hancock JT, Desikan R, Neill SJ. Role of reactive oxygen species in cell signalling pathways. Biochem Soc Trans. 29:345–50.
8.
Niki E, Yoshida Y, Saito Y, Noguchi N. Lipid peroxidation: Mechanisms, inhibition and biological effects. Biochem Biophys Res Commun. 338:668–76.
9.
Zwart LL, J M, J C, N V. Biomarkers of free radical damage: applications in animals and in humans. Free Radic Biol Med. 26:202–26.
10.
Cooke JP. Flow, NO, and atherogenesis. PNAS. 100(3):768–70.
11.
Brigelius-Flohe R. Tissue-specific functions of individual glutathione peroxidases. Free Radic Biol Med. 27:951–65.
12.
Steinberg D. Low density lipoprotein oxidation and its pathological significance. J Biol Chem. 272:20963–6.
13.
Hawkins CL, Davies MJ. Generation and propagation of radical reactions on proteins. Biochim Biophys Acta. 1504:196–219.
14.
Chen J, Mehta JL. Role of oxidative stress in coronary heart disease. Indian Heart J. 56:47–75.
15.
Duikan S, Farewell A, Ballestores M, Taddei F, Radman M. Protein oxidation in response to increased transcriptional or translation errors. Proc Natl Acad Sci USA. 97:5746–9.
16.
Witko-Sarsat V, Friedlander M, Capeilliere-Blandin C. Advanced oxidation protein products as a novel marker of oxidative stress in uremia. Kidney Int. 49:1304–13.
17.
Marnet LJ. Lipid peroxidation-DNA-damage by malondialdehyde. Mutat Res. 424:83–95.
18.
Đorđević V, Pavlović D, Kocić G. Biohemija slobodnih radikala.
19.
Price DT, Vita JA, JF K. Redox control of vascular nitric oxide bioavailability. Antioxid Redox Signal. 2(4):919–35.
20.
Stuehr D, Pou S, Rosen GM. Oxygen Reduction by Nitric oxide synthases. J Biol Chem. 276(18):14533–6.
21.
Moncada S, L-Arginine HA. Nitric Oxide Pathway. The New Engl J Med. 329(27):2002–12.
22.
Harris LR, Cake MA, Macey DJ. Iron release from ferritin and its sensitivity to superoxide ions differs among vertebrates. Biochem J. 301:385–9.
23.
Halliwell B. Antioxidant defense mechanisms: from the beginning to the end. Free Radic Res. 31:261–72.
24.
Mates JM, Perez-Gomez C, Castro I. Antioxidant enzymes and human diseases. Clin Biochem. 32:595–603.
25.
Fridovich J. Superoxide anion radical (O2•−), superoxide dismutases and related matters. J Biol Chem. 272:18515–7.
26.
Nordberg J, Arner ESJ. Reactive oxygen species, antioxidants and the mammalian thioredoxin system. Free Radic Biol Med. 31(11):1287–312.
27.
Liochev SI, Fridovich I. Role of O2 in the production of OH• in vitro and in vivo. Free Radic Biol Med. 16:29–33.
The statements, opinions and data contained in the journal are solely those of the individual authors and contributors and not of the publisher and the editor(s). We stay neutral with regard to jurisdictional claims in published maps and institutional affiliations.
