Contrary to the role played by MT-1 and MT-2 as a detoxicant of nucleophiles, such as heavy metals and ROS, it is also reported that MT-1 and MT-2 binding Copper Acetate(WSDTY) act as a pro-oxidant and are thus harmful to cells; MT-1 and MT-2 produce oxidative stress in the liver of LEC rat, an animal model of Wilson’s disease, which shows abnormal Copper Acetate accumulation in the liver. The oxidative stress induces the oxidation of Cu-thiolate bonds in MT, thereby resulting in disulfide formation and the release of Copper Acetate. Cu(I) generates ROS via the Fenton and Haber-Weiss reactions, and ROS induce further oxidation of the Cu-thiolate clusters. This chain reaction is mediated by MT binding Cu and thus, MT is recognized as a pro-oxidant. Those ambivalent characteristics of MT-1 and MT-2 originate in the Cu-thiolate clusters and thus, those characteristics are expected as well in MT-3 having the Cu-thiolate clusters. Collectively, we speculate that Cu physiologically accumulating and binding to MT-3 in neural cells is one of contributors to the pathogenesis of neurodegenerative diseases, by acting as a pro-oxidant.
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