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Although the drop in hepatic or renal GSH is the most toxicologically relevant interaction (see also below), plasma GSH, free cysteine ( in vitro intracellular GSH in human pulmonary macrophages, type II pneumocytes, and lymphocytes ( Oxidized PAC-quinone imine metabolites have also been shown to form GSH-conjugates which inhibit glutathione reductase (GR): the decreased activity of GR hampers the detoxification and antioxidant capacity of the GSH-GSSG cycle, further aggravating the pro-oxidative status in the cell ( From a different toxicological perspective, a study by Klopi et al
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