Mercury vapor uptake and hydrogen peroxide detoxification in human and mouse red blood cells.
The uptake of Hg vapor (Hg0) by suspensions of human and BALB-c mouse erythrocytes was studied in a closed exposure system. The formation of catalase-compound-I and thereby the oxidation of Hg0 was initiated by microinfusion of hydrogen peroxide. The degradation of H2O2 by the glutathione (GSH)/GSH peroxidase system was reduced by t-butyl-hydroperoxide (t-BOOH) or by 1-chloro-2,4-dinitrobenzene (CDNB). In human red blood cells, CDNB and t-BOOH increased the rate of Hg vapor oxidation at the low and intermediate H2O2 supplementation rates. In mouse erythrocytes, Hg uptake was increased by CDNB over the entire H2O2 infusion range. In human cells, t-BOOH (0.1 mM) produced a remarkably high Hg uptake even without added H2O2. This Hg uptake in absence of exogenous H2O2 was inhibited by aminotriazole as was the activity of catalase. Hence, the Hg uptake was likely to have been induced by endogenous hydrogen peroxide. These findings support the view that the intact GSH/GSH peroxidase system can diminish the efficiency of compound-I-induced Hg vapor oxidation in erythrocytes.
Halbach
S
S
Institut für Toxikologie, Gesellschaft für Strahlen- und Umweltforschung, Neuherberg, West Germany.
Ballatori
N
N
Clarkson
T W
TW
D000818:Animals; D004137:Dinitrochlorobenzene / Q000494:pharmacology; D004912:Erythrocytes / Q000378:metabolism*; D005978:Glutathione / Q000097:blood; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism / Q000494:pharmacology*; D066298:In Vitro Techniques; D008658:Inactivation, Metabolic; D008628:Mercury / Q000493:pharmacokinetics*; D051379:Mice; D008807:Mice, Inbred BALB C; D010545:Peroxides / Q000494:pharmacology; D014835:Volatilization; D020122:tert-Butylhydroperoxide
D004137:Dinitrochlorobenzene; D010545:Peroxides; D020122:tert-Butylhydroperoxide; D006861:Hydrogen Peroxide; D008628:Mercury; D005978:Glutathione