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Changes in zinc and copper homeostasis in human livers and kidneys associated with exposure to environmental cadmium

National Research Centre for Environmental Toxicology, Brisbane, Australia; National Research Centre for Environmental Toxicology, 39 Kessels Road, Coopers Plains, Brisbane 4108, Queensland, Australia

J R Baker

National Research Centre for Environmental Toxicology, Brisbane, Australia

P Eb Reilly

Department of Biochemistry, University of Queensland, Brisbane, Australia

M R Moore

National Research Centre for Environmental Toxicology, Brisbane, Australia; Queensland Health Scientific Services, John Tonge Centre for Forensic Pathology, Queensland Department of Health, Brisbane, Australia

D J Williams

Queensland Health Scientific Services, John Tonge Centre for Forensic Pathology, Queensland Department of Health, Brisbane, Australia

This study was undertaken to assess changes in zinc and copper homeostasis in human tissues that could be attributed to human exposure to environmental cadmium, using samples of lung, liver and kidney cortex of 61 Queensland residents, aged 2 to 89 years, who had died of accidental causes. None of the subjects were exposed to cadmium in the workplace. Levels of zinc in liver and kidney cortex samples showed inverse associations with donor age whereas zinc in lung only showed inverse association with gender. Lung zinc levels in females were 14% lower than in males. Zinc in liver and kidney cortex samples were found to exist in at least two pools; one was associated with cadmium that bound to metallothionein (MT) and the other was associated with non-MTbound copper. Inliver, the amounts ofzinc inthe MT pool were smaller compared to those in non-MT pool given that only 7% of zinc variations were explained by cadmium whereas 22% of the liver zinc variations were accounted for by non-MTbound copper. In sharp contrast, larger amounts of zinc in kidney cortex samples were in the MT pool, compared to those in the non-MT pool given that cadmium was found to explain 69% of total zinc variation whereas copper explained only 17% of kidney zinc variations. The levels of copper in liver were found to be increased by 45-50% in subjects with high cadmium exposure level, compared to subjects ofsimilar ages with medium exposure level. The levels of zinc and copper in kidney cortex samples in the subjects with high cadmium exposure were both found to be significantly elevated compared to those found in the medium-exposure group whereas copper contents were about 19-23% greater than in medium-as well as low-exposure groups. Taken together these results indicate increased sequestration of zinc and copper in liver and kidney cortex samples. The increases in metal sequestra-tions were observed in liver samples having cadmium contents of greater than 1 µg/g wet weight and in kidney cortex having cadmium contents of greater than 26 µg/g wet weight. Zinc and copper contents in lung of this sample group, however, were not associated with cadmium due probably to lower exposure levels compared to those of liver and kidney.

Key Words: cadmium body burden • human autopsy • zinc • copper • metal homeostasis • metal toxicity • chronic low-level exposure • liver • kidne

Human & Experimental Toxicology, Vol. 20, No. 4, 205-213 (2001)
DOI: 10.1191/096032701678766787


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