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In addition, GSH was shown to exert negative regulation on cellular PKC isozymes which have cysteine residues at, or near, the active site of the enzyme and this control was removed when GSH pools were depleted by exposure to ROS [25]

(Our example here is hypothetical

Schisandrin B prevents doxorubicin-induced cardiotoxicity via enhancing glutathione redox cycling

It is important to note that a recent study revealed the opposite result with high doses of atorvastatin (40 m) in human cardiomyocytes and murine skeletal muscle cells, which is consistent with the adverse muscle effects of atorvastatin [229]