Toxic effects of hexaammine cobalt(III) chloride on liver and kidney in mice: Implication of oxidative stress

Abstract

Hexaammine cobalt (III) chloride is a trivalent complex cation of Co(III) and amine that has previously been shown to act as an inhibitor of insulin secretion, radiosensitizing agent, and an antiviral agent. We have recently reported the anticancer potential of the compound against diethylnitrosamine-induced carcinogenesis in mice. However, there is no report on the potential toxicity of the compound. The present study was conducted to evaluate the tissue distribution of the compound and its potential toxicity following acute administration of the compound through intraperitoneal route in Balb/c mice. Our results showed that cobalt accumulated maximally in kidney, followed by liver, spleen, blood, and lung in a decreasing order and in a dose-dependent manner. Evaluation of liver and kidney function tests revealed that the compound exerted a relatively higher toxicity in kidney, as compared to liver, as evidenced by the sharp enhancement in the serum levels of urea and creatinine in a dose-dependent manner. Examination of levels of lipid peroxidation and selected oxidative stress–related parameters in kidney, liver, and lung suggest that higher accumulation of cobalt in kidney may promote higher oxidative stress in the organ, as compared to liver and lung, which may eventually impair kidney function.

Keywords::

• Hexaammine cobalt(III) chloride
• liver
• kidney toxicity
• oxidative stress

Acknowledgments

This study was supported by grant no. 01(1864)/03/EMR-II from the Council of Scientific and Industrial Research (CSIR; New Delhi, India). The authors thank Raj Pal Sharma, Ph. D. Professor of Chemistry at Panjab University, for providing hexaammine cobalt(III) chloride for the present study.

Declaration of interest: The authors report no financial conflicts of interest. The authors alone are responsible for the content and writing of this paper.