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Thus, in selenoenzymes, selenium does not serve as a cofactor, which is different than most minerals required for enzyme function

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Considering that this compound has been demonstrated to expand the GSH system along with a reduction in oxidative injury by the AKT/Nrf2 signaling pathway in the hearts of rats and H9C2 cells, the abovementioned enhanced TAC may cover GSH and GSH-dependent antioxidant enzymes [150,151,152]