Please use this identifier to cite or link to this item:
Title: Dioxygen reduction, reduced oxygen species, oxygen toxicity and antioxidants — A commentary
Authors: Ramasarma, T
Keywords: Ascorbic acid;Autoxidation;Glutathione;Hydrogen peroxide;Oxyl radicals;α-Tocopherol;Ubiquinol
Issue Date: Nov-2016
Publisher: NISCAIR-CSIR, India
Abstract:   Molecular oxygen, a diradical, needs intervention of redox metal ions or other radicals to receive electrons for its reduction. The oxygen radicals thus produced are responsible for oxygen toxicity and oxidative stress. But, autoxidation, relevant in ischemia-reperfusion injury, is absent in any discussion on oxygen toxicity. Naturally occurring compounds which prevent formation or action of the reactive oxygen species (ROS) are generally referred as antioxidants. The reduced oxygen species, superoxide, peroxide and hydroxyl radicals, are formed in a variety of systems in the cell and are useful in selective oxidations. Currently, the popular method for assaying ROS with fluorescence of dichlorofluorescein actually measures a hemeprotein-Fe-oxo complex. The Fe-oxyl radicals are the likely oxidants in damaging proteins, nucleic acids and lipids. Such major lesions are normally repaired or replaced in the cells.
  The antioxidants counter the damaging oxidant actions. Among these, occurring in large concentration, are glutathione and ubiquinol, synthesized in the body and ascorbic acid and α-tocopherol, drawn from the food. A large number of plant-derived phenolic compounds, especially the flavonoid variety, are also absorbed, albeit poorly, from the food. At the natural low concentrations, these compounds show wide ranging biological effects. Increased benefit on increasing them in circulating blood needs individual verification. The polyphenolic compounds demonstrated powerful antioxidant effects in laboratory experiments. But the clinical studies did not support the consequent expectations of countering the oxidative stress, the purported crucial factor in pathology in several diseases. Antioxidant action against ROS causing oxygen toxicity needs to be reassessed.
  This commentary is a reappraisal of formation and reactivity of ROS in different cells, the active cellular oxidant forms, products of oxidant action on proteins, nucleic acids and lipids as marker of oxidant injury, bulk antioxidants of endogenous and exogenous origin, limited absorption occurrence and functions of polyphenolic classes.
Page(s): 688-699
ISSN: 0975-1009 (Online); 0019-5189 (Print)
Appears in Collections:IJEB Vol.54(11) [November 2016]

Files in This Item:
File Description SizeFormat 
IJEB 54(11) 688-699.pdf318.47 kBAdobe PDFView/Open

Items in NOPR are protected by copyright, with all rights reserved, unless otherwise indicated.