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Table 3 Oxidative stress indicator, glutathione, and antioxidant enzyme activities in plasma and S3I-201 supplier liver Plasma and hepatic PLP significantly negatively correlated with plasma (r=?0.74, pQuinapyramine B6 diet or a B6-supplemented diet but was aggravated by a vitamin B6-deficient diet. Vitamin B6 has been shown to prevent the oxygen radical generation and lipid peroxidation caused by H2O2 in U937 monocytes (10) and endothelial cells (25). Keles et al., (6) evaluated lipid peroxidation and free selleck products radical scavenging activities in kidney tissue of vitamin B6-deficient rats; the results showed that levels of total and non-enzymatic superoxide scavenger activity and antioxidant potential in kidney tissue of vitamin B6-deficient rats were significantly lower than those of the control rats. A study of human indicated that lower plasma PLP was associated with higher urinary 8-hydroxydeixyguanosine (an oxidative damage marker) concentration in older Puerto Rican adults (26), which also supports the association between lower vitamin B6 status and higher oxidative stress. In the present study, a significant relationship between vitamin B6-deficient status and higher lipid peroxidation was observed in mice livers. Although we could not demonstrate whether vitamin B6 had a free radical scavenging activity in this study, a possible direct antioxidant mechanism of vitamin B6 might be that vitamin B6 compounds have both the hydroxyl and amine group substitution on a pyridine ring which can react with the peroxy radicals and thereby scavenge radicals and inhibit lipid peroxidation (6�C10). In addition to the potential direct free radical scavenging capability of vitamin B6, vitamin B6 status might affect cysteine and GSH synthesis and be indirectly involved in the antioxidant defense system.