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Inhibition of Induction of Benzpyrene Hydroxylase by Nickel Carbonyl¹

Pathology Department, University of Florida College of Medicine, Gainesville, Florida 32603

Exposure of rats to nickel carbonyl by inhalation (0.2 mg Ni/liter of air/15 min) or intravenous injection (2 mg Ni/100 gm) was found to inhibit the induction of benzpyrene hydroxylase in lung and liver. Phenothiazine induction and fluorometric measurements of benzpyrene hydroxylase were performed by the methods of Wattenberg and co-workers (31, 32). Benzpyrene hydroxylase activities in lungs and livers of control rats were 9.5 (S.D. ± 4.3) and 295 (S.D. ± 123) units, respectively. Benzpyrene hydroxylase activities began to diminish 3 hours after administration of nickel carbonyl, reached a minimum at 2 to 3 days, and remained diminished up to 1 week. For example, 52 hours after injection of nickel carbonyl, benzpyrene hydroxylase activities in lungs and livers were 1.1 ± 1.0 (P < 0.01) and 113 ± 24 (P < 0.01) units, respectively. The inhibition of benzpyrene hydroxylase activity was apparently mediated either by diminished synthesis or increased catabolism of the enzyme, inasmuch as nickel carbonyl did not have any direct effect upon benzpyrene hydroxylase activity, in vivo or in vitro. It is suggested that by inhibiting benzpyrene hydroxylation, nickel carbonyl may prolong the tissue retention of 3,4-benzpyrene and thereby promote carcinogenesis.

¹ This investigation was supported by U. S. Atomic Energy Commission Grant No. AT-(40-1)-3461, by American Cancer Society Grant No. E-374A, and by a USPHS research grant from the National Cancer Institute, No. CA-08783-01.

Received 9/19/66. Accepted 1/ 5/67.