Free radicals and antioxidants in food andin vivo:What they do and how they work

Abstract

A wide variety of oxygen free radicals and other reactive oxygen species can be formed in the human body and in food systems. Transition metal ions accelerate free-radical damage. Antioxidant defenses, both enzymic and nonenzymic, protect the body against oxidative damage, but they are not 100% efficient, and so free-radical damage must be constantly repaired. Nonenzymatic antioxidants are frequently added to foods to prevent lipid peroxidation. Several lipid antioxidants can exert prooxidant effects toward other molecules under certain circumstances, and so antioxidants for food and therapeutic use must be characterized carefully. Methods of measuring oxidative damage and trapping free radicals in vivo are briefly discussed. Such methods are essential in checking proposals that increased intake of food-derived antioxidants (such as antioxidant vitamins) would be beneficial to humans.

Bioactive potential of the wild mushroom Astraeus hygrometricus in South-west India

“…Such results might be due to polysaccharides present in A. hygrometricus as depicted by Zhang et al (2011). Lipid peroxidation due to catalytic activity of metal-ions is responsible for deterioration of food stuffs leading to cause arthritis and cancer (Gordon 1990; Halliwell et al 1995). The pro-oxidant metals will be converted into stable compounds by metal chelators, which are responsible to reduce the damaging effect (Leopoldini et al 2006; Soares et al 2009).…”

Green Tea Polyphenol Protection Against 4-Nitroquinoline 1-Oxide-Induced Bone Marrow Lipid Peroxidation and Genotoxicity in Wistar Rats

“…Oxidative stress can result in adaptation or cell injury due to lipid peroxidation (Halliwell et al, 1995). Lipid peroxidation is a free radical mediated process.…”

Antioxidants: Basis concepts in relation to the eye

“…The predominant mechanisms by which superoxide radical is ger~ated in the cells is by catalytic reduction of oxygen by membrane bound enzymes (mitochondrial, microsomal and endoplasmic reticular) as well as by enzymes located in the cytosol; by the auto-oxidation of haemoglobin, catecholamines, flavins, glutathione, ascorbate, melanin etc. (5,6). The maximum superoxide production occurs at the level of cellular membranes and this probably accounts for the increased propensity of these membranes to beco~ i~= affected early and more severely during any form of damage by oxidative stress.…”