il\VOLVEMENT OF RETII\OIC ACID II{ - MSpace at the University of ...
il\VOLVEMENT OF RETII\OIC ACID II{ - MSpace at the University of ...
il\VOLVEMENT OF RETII\OIC ACID II{ - MSpace at the University of ...
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<strong>of</strong> a large array <strong>of</strong> cellular abnormalities (Mukai and Goldstein 1976; Shamberger et al.<br />
1974;Teebor et al. 1988).<br />
<strong>II</strong>.c. Antioxidant reserve<br />
Every living form is constantly <strong>at</strong>tacked by <strong>the</strong> exogenous and endogenously<br />
gener<strong>at</strong>ed free radicals. However, physiological systems are in place to ensure <strong>the</strong><br />
protection against <strong>the</strong>se damaging molecules. This is achieved by <strong>the</strong> activity <strong>of</strong> several<br />
enzym<strong>at</strong>ic and nonenzym<strong>at</strong>ic intracellular antioxidant protective systems (Freeman and<br />
Crapo 1982). Three intracellular enzymes play a crucial role in <strong>the</strong> endogenous<br />
antioxidant enzl'rn<strong>at</strong>ic protection: superoxide dismutase (SOD), glut<strong>at</strong>hione peroxidase<br />
(GSHPx) and c<strong>at</strong>alase. This b<strong>at</strong>tery <strong>of</strong> endogenous antioxidants, also known as<br />
antioxidant reserve, ensure <strong>the</strong> maintenance <strong>of</strong> optimal milieu for <strong>the</strong> functioning <strong>of</strong><br />
essential physiological processes (Singal and Kirshenbaum 1990). Ano<strong>the</strong>r group <strong>of</strong><br />
intracellular antioxidants are nonenzym<strong>at</strong>íc compounds such as tocopherol (vitamin E),<br />
carotenoids (provitamin A compounds), retinol (vitamin A), mel<strong>at</strong>onin, ubiquinol,<br />
ascorbic acid (vitamin C) and glut<strong>at</strong>hione (Kaul et al. 1993; Palace et al. 1999). Despite<br />
<strong>the</strong> differences between <strong>the</strong>ir mechanisms <strong>of</strong> action, one general mechanism <strong>of</strong><br />
antioxidant protection is proposed. Antioxid<strong>at</strong>ive protection is achieved by <strong>the</strong><br />
nonenzSrm<strong>at</strong>ic antioxidant's ability to quench potentialiy damaging free radicals and<br />
prevent <strong>the</strong> propag<strong>at</strong>ion <strong>of</strong> free-radical induced cellular damage. This reactive oxidant is<br />
<strong>the</strong>n converted into a new non-reactive product (Halliwell and Gutteridge i990; Palace et<br />
aL 1999; Tesoriere et al. 1 993).<br />
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