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Vol. 283, Issue 3, 1529-1533, 1997

Enhanced Renal Toxicity by Inorganic Mercury in Metallothionein-Null Mice

Masahiko Satoh, Noriko Nishimura, Yoshitaka Kanayama, Akira Naganuma, Tsuguyoshi Suzuki and Chiharu Tohyama

Environmental Health Sciences Division (M.S., C.T.), National Institute for Environmental Studies (T.S.), Tsukuba, Ibaraki 305, Japan; Department of Veterinary Pathology (N.N.), University of Sydney, Sydney 2006, Australia; and Department of Molecular and Biochemical Toxicology (Y.K., A.N.), Faculty of Pharmaceutical Sciences, Tohoku University, Aobayama, Sendai 980-77, Japan

To elucidate a protective role of metallothionein (MT) in the manifestation of inorganic mercury toxicity, we studied the susceptibility of MT-null mice to the renal toxicity of mercuric chloride. Because the MT-null (J) mice are a genetic background of 129/Sv strain, the 129/Sv mice were used as wild-type controls. Nine-week-old male MT-null (J) and 129/Sv mice were given subcutaneous injections of mercuric chloride at doses of 10 to 40 µmol/kg. The basal MT level in the kidney of MT-null (J) mice was undetectable (<0.2 µg/g of tissue) and ~2.5 µg/g of tissue in 129/Sv mice. The sensitivity to the renal toxicity of mercuric chloride was markedly enhanced in the MT-null (J) mice compared with the 129/Sv mice. The renal mercury level was similar for the MT-null (J) and 129/Sv mice at 4 hr after the injection of mercuric chloride (20 µmol/kg) but became significantly lower in MT-null (J) mice than in 129/Sv mice at 24 and 72 hr. Based on the present results, we conclude that MT is an important protective factor against the renal toxicity caused by inorganic mercury and that it may play a major role in the retention of mercury in the kidney.

0022-3565/97/2833-1529$03.00/0
Copyright © 1997 by The American Society for Pharmacology and Experimental Therapeutics


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