Vitamin radical quenching capability

In ischemia, the endogenous free radical quenching capability of the neurons diminishes further adding to cell stress. Consequently, free radical scavengers such as extract of Ginkgo biloba (Szabo et al., 1991), a-lipoic acid (Block and Schwarz 1997), vitamin E (Celebi et al., 2002), thioredoxin (Shibuki et al., 2000), an ascorbic acid derivative (Kuriyama et al., 2001), mannitol (Gupta and Marmor, 1993), and the iron chelator desferrioxamine (Ophir et al., 1994) have all been shown to be neuroprotective in ischemia-reperfusion injury. 

Vitamin E has been shown, in a wide range of studies, to be capable of affording considerable protection to cells exposed to free radical attack, either from pathological or drug-induced sources. In injured nervous tissue, vitamin E probably exerts its protective effect by scavenging free radicals, stabilizing cellular membranes and quenching the cascade of biochemical events that... 

The free radical reaction may be accelerated and propagated via chain branching or homolytical fission of hydroperoxides formed to generate more free radicals (equations (11.4), (11.5)). Free radicals formed can initiate or promote fatty acid oxidation at a faster rate. Thus, once initiated, the free radical reaction is self-sustaining and capable of oxidizing large amounts of lipids. On the other hand, the free radical chain reaction may be terminated by antioxidants (AH) such as vitamin E (tocopherols) that competitively react with a peroxy radical and remove a free radical from the system (equation (11.6)). Also, the chain reaction may be terminated by self-quenching or pol)rmerization of free radicals to form non-radical dimers, trimers and polymers (equation (11.7)). 

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