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. 2001 Mar 15;354(Pt 3):493-500.
doi: 10.1042/0264-6021:3540493.

Epicatechin and its in vivo metabolite, 3'-O-methyl epicatechin, protect human fibroblasts from oxidative-stress-induced cell death involving caspase-3 activation

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Epicatechin and its in vivo metabolite, 3'-O-methyl epicatechin, protect human fibroblasts from oxidative-stress-induced cell death involving caspase-3 activation

J P Spencer et al. Biochem J. .

Abstract

There is considerable current interest in the cytoprotective effects of natural antioxidants against oxidative stress. In particular, epicatechin, a major member of the flavanol family of polyphenols with powerful antioxidant properties in vitro, has been investigated to determine its ability to attenuate oxidative-stress-induced cell damage and to understand the mechanism of its protective action. We have induced oxidative stress in cultured human fibroblasts using hydrogen peroxide and examined the cellular responses in the form of mitochondrial function, cell-membrane damage, annexin-V binding and caspase-3 activation. Since one of the major metabolites of epicatechin in vivo is 3'-O-methyl epicatechin, we have compared its protective effects with that of epicatechin. The results provide the first evidence that 3'-O-methyl epicatechin inhibits cell death induced by hydrogen peroxide and that the mechanism involves suppression of caspase-3 activity as a marker for apoptosis. Furthermore, the protection elicited by 3'-O-methyl epicatechin is not significantly different from that of epicatechin, suggesting that hydrogen-donating antioxidant activity is not the primary mechanism of protection.

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References

    1. Biochem J. 2000 Apr 15;347(Pt 2):543-51 - PubMed
    1. Carcinogenesis. 1998 Sep;19(9):1583-9 - PubMed
    1. Biochem J. 1969 Dec;115(4):831-6 - PubMed
    1. Free Radic Biol Med. 1997;22(4):669-78 - PubMed
    1. J Nutr. 1998 Jul;128(7):1172-8 - PubMed

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