Attenuation of porphyrinogen oxidation by glutathione in vitro and reversal by porphyrinogenic trace metals.
We have employed a model in vitro system for iron-peroxide-catalyzed oxidation of porphyrinogens to investigate the potential role of glutathione (GSH) in trace metal-induced porphyrias. GSH strongly attenuates porphyrinogen oxidation at biologically relevant concentrations in a dose-dependent manner. Porphyrinogenic trace metals reduce the effectiveness of GSH as a porphyrinogen antioxidant, leading to significantly higher rates of porphyrinogen oxidation to porphyrins. These observations may, in part, underlie the etiology of porphyrinurias induced during prolonged trace metal exposures.
D001149:Arsenates / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004492:Edetic Acid / Q000494:pharmacology; D005978:Glutathione / Q000031:analogs & derivatives / Q000494:pharmacology*; D019803:Glutathione Disulfide; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007501:Iron / Q000494:pharmacology; D008628:Mercury / Q000494:pharmacology; D008670:Metals / Q000494:pharmacology*; D010084:Oxidation-Reduction; D011165:Porphyrinogens / Q000378:metabolism*; D014131:Trace Elements / Q000494:pharmacology*
D001149:Arsenates; D008670:Metals; D011165:Porphyrinogens; D014131:Trace Elements; D004492:Edetic Acid; D006861:Hydrogen Peroxide; D007501:Iron; D008628:Mercury; D005978:Glutathione; D019803:Glutathione Disulfide