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Hepatic Cytochrome P-450 and Microsomal Heme Oxygenase in Copper-Deficient Rats^1,2,

Department of Internal Medicine and the Department of Biochemistry and Molecular Biology, Louisiana State University School of Medicine in Shreveport, Shreveport, LA 71130

Copper deficient and control rats were pair-fed from weaning a milk-based diet. Each animal received 25 mg of iron parenterally. After 6 weeks of dietary manipulation the animals were killed. As expected, rats fed the copper-deficient diet were anemic. Copper-dependent enzyme activities and copper content of plasma and liver confirmed that copper deficiency was present in these rats. Hepatic microsomal cytochrome P-450 specific contents were similar in control and copper-deficient animals in the uninduced state and following induction of cytochrome P-450 by treatment with phenobarbital. However, microsomal heme oxygenase was increased in copper-deficient animals compared with controls whether they were treated with phenobarbital or not. No differences were observed in splenic microsomal heme oxygenase between dietary groups. These studies suggest that hepatic heme catabolism is enhanced in copper deficiency. The explanation for this enhancement may be related to increased hepatic iron accumulation in copper-deficient animals or to the associated defect of selenium metabolism in copper deficiency.

KEY WORDS: • copper deficiency • cytochrome P-450 • heme oxygenase

¹ Part of this work was presented at the Federation of American Societies of Experimental Biology meeting April 1980.

² Supported in part by NIH grants ES 01992 and AM 23004.

³ Present address: Gastroenterology Division, Dept. of Internal Medicine, University of Texas Health Sciences Center, San Antonio, TX 78284.

Manuscript received 17 November 1980.