Nevertheless, experimental data suggest that the altered intracellular redox status associated with hyperhomo-cysteinemia-induced oxidant stress is the major molecular mechanism responsible for the atherothrombogenicity of moderately elevated circulating homocysteine
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Several investigators have shown that orally administered GSH increases plasma concentrations of reduced and protein-bound GSH through intestinal absorption in animal models 10,13,15 and humans
doi: 10.1007/s11920-015-0574-0 65 SeveranceEGYolkenRHEatonWW
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