Heme oxygenase induction by cadmium chloride: evidence for oxidative stress involvement

doi:10.1016/0300-483X(95)03157-B

Toxicology

Volume 104, Issues 1–3, 15 December 1995, Pages 141-147

https://doi.org/10.1016/0300-483X(95)03157-B Get rights and content

Abstract

Cadmium chloride (CdCl₂), a well-known inducer of heme oxygenase, produced a strong increase in ‘in vivou’ rat liver chemiluminescence (QLV) 3 h after administration. Heme oxygenase activity increased 5 h after treatment, reaching a maximum value around 12–15 h after CdO₂ administration. Such induction was preceded by a decrease in the intrahepatic GSH pool and an increase in hydrogen peroxide steady-state concentration, both effects taking place several hours before induction of heme oxygenase. The activity of antioxidant enzymes, Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) was found to be significantly decreased S h after CdCl₂ injection. Administration of bilirubin, the end product of heme catabolism in mammals, and α-tocopherol, a widely employed antioxidant, prevented heme oxygenase induction as well as the decrease in hepatic GSH and the increase in chemiluminescence when administered 2 h before CdCl₂ treatment. These results obtained with CdCl₂ treatment support our recent reports correlating heme oxygenase induction with oxidative stress.

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Heme oxygenase induction by cadmium chloride: evidence for oxidative stress involvement

Abstract

J. Biol. Chem.

Toxicol. Appl. Pharmacol.

Arch. Biochem. Biophys.

Biochem. Pharmacol.

Toxicol. Appl. Pharmacol.

FEBS Lett.

J. Biol. Chem.

J. Biol. Chem.

Exp. Cell Res.

Biochim. Biophys. Acta

Biochim. Biophys. Acta

J. Biol. Chem.

J. Biol. Chem.

Mutat. Res.

J. Biol. Chem.

Arch. Biochem. Biophys.

Life Sci.

FEBS Lett.

J. Biol. Chem.

Arch. Biochem. Biophys.

Fundam. Appl. Toxicol.