作者: D. E. Baranano , M. Rao , C. D. Ferris , S. H. Snyder
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摘要: Bilirubin, an abundant pigment that causes jaundice, has long lacked any clear physiologic role. It arises from enzymatic reduction by biliverdin reductase of biliverdin, a product heme oxygenase activity. Bilirubin is potent antioxidant we show can protect cells 10,000-fold excess H2O2. We report bilirubin major cytoprotectant. Thus, cellular depletion RNA interference markedly augments tissue levels reactive oxygen species and apoptotic cell death. Depletion glutathione, generally regarded as cytoprotectant, elicits lesser increases in The actions reflect amplification cycle whereby bilirubin, acting antioxidant, itself oxidized to then recycled back bilirubin. This redox may constitute the principal function