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Alcoholic liver disease: Chronic alcohol consumption severely depletes hepatic glutathione through multiple mechanisms: increased ROS production during ethanol metabolism, reduced cysteine availability, and impaired mitochondrial glutathione transport

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This special binding could be explained by the colocalization of mGluR1 and A and the presence of A and GluN2B immunoreactivities in neurites [35, 36] In AD, AO prevents physiological activation of the cellular prion protein-mGluR5 (PrPC-mGluR5) complex by glutamate