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It has been proposed that depletion of hepatic GSH, particularly mitochondrial GSH, is one of the early changes associated with chronic alcohol consumption and is a critical contributor to ALD pathogenesis 11

Similarly, the expression of H

De Andrade RR, De Oliveira-Neto OB, Barbosa LT, Santos IO, De Sousa-Rodrigues CF, Barbosa FT

These effects were accompanied by elevated ROS levels, linking oxidative stress to Hcy-mediated endothelial dysfunction [53, 85, 124, 130]