Volume 106, Issue 4 pp. 348-355

Increased Hepatic and Decreased Urinary Metallothionein in Rats after Cessation of Oral Cadmium Exposure

Yihuai Liang

Yihuai Liang

Department of Occupational Health and Toxicology, School of Public Health, Fudan University, Shanghai, China

Environmental Medicine, Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden

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Huiqi Li

Huiqi Li

Department of Occupational Health and Toxicology, School of Public Health, Fudan University, Shanghai, China

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Cuiqin Xiang

Cuiqin Xiang

Shanghai Municipal Center For Disease Control and Prevention, Shanghai, China

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Lijian Lei

Lijian Lei

Department of Occupational Health and Toxicology, School of Public Health, Fudan University, Shanghai, China

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Taiyi Jin

Taiyi Jin

Department of Occupational Health and Toxicology, School of Public Health, Fudan University, Shanghai, China

Environmental Medicine, Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden

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Monica Nordberg

Monica Nordberg

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden

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Gunnar F. Nordberg

Gunnar F. Nordberg

Environmental Medicine, Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden

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First published: 12 March 2010
Citations: 4
Author for correspondence: Taiyi Jin, Department of Occupational Health and Toxicology, School of Public Health, Fudan University, Shanghai, 200032, China (fax +86 21 6417 8160, e-mail [email protected]).

Abstract

Abstract: We investigated the role of metallothionein (MT) in tissues after cessation of cadmium (Cd) exposure. Wistar rats of both genders were given CdCl2 in drinking water at daily doses of 0, 2.5, 5.0 or 10.0 mg Cd/kg body-weight for 12 weeks. Half of the animals were then killed; the others were given Cd-free water for the following 16 weeks, i.e. until 28 weeks after start of the experiment (28-week rats). We observed dose-dependent increases in the levels of MT in the tissues of rats 12 weeks after beginning the experiment (12-week rats). After the exposure ceased, levels of MT in the 28-week rats changed in three ways: an increase in the liver, persistence in the kidney cortex and a decrease in the medulla, relative to those levels in their 12-week counterparts. Biomarkers of kidney dysfunction were determined to be urinary MT (UMT) and urinary N-acetyl-β-d-glucosaminidase (UNAG). After 12 weeks, we observed dose-related statistically significant increases in UMT and UNAG in all of the Cd-exposed groups. A statistically significant decrease for UNAG between the 12- and 28-week rats occurred among males at the lowest Cd dose and for UMT in all of the Cd-exposed groups. The unchanged tissue levels of MT in the kidney cortex suggest that decreased UMT is a sign either of (i) decreased transport of Cd-MT from the liver via blood plasma to the renal tubules or (ii) increased tubular reabsorption and recovery of renal tubular function.

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