The effect of chloroacetonitrile on the liver and kidney of adult male rats: a light and electron microscopic study

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Chloroacetonitrile (CAN) is a by-product of chlorination of drinking water. It might present a hazard to human health. It has mutagenic and carcinogenic activity. It is metabolized to cyanide in the body. CAN is ∼10 times more toxic compared with acetonitrile. Occupational exposure to CAN may occur through inhalation or dermal contact at workplaces where CAN is used or produced. There is scanty information on CAN hepatotoxicity and nephrotoxicity.


The present study was designed to investigate the effects of CAN on the liver and kidney of adult male rats using light and electron microscopic studies to avoid any hazard to human health.

Materials and methods

A total of 120 adult male Sprague–Dawley rats were divided into two groups (60 rats/group). The rats of the control group were given corn oil orally through a gastric tube for 21 days. The rats of the treated group were given CAN at a dose of 25 mg/kg/day orally through a gastric tube for 21 days. The animals of both groups were sacrificed. The livers and kidneys were dissected immediately. The specimens of each group were processed for light and transmission electron microscopic studies. The specimens for light microscopic studies were stained with H&E, Masson’s trichrome, and toluidine blue. Quantitative morphometric and statistical studies were performed.


In light and electron microscopic studies on treated liver and kidney sections, cytotoxicity manifested in the form of disorganized architecture of the liver, damaged endothelial lining of the hepatic sinusoids, Von Kupffer cells, and hepatocytes. The kidney showed partial and complete damage of the glomeruli and proximal convoluted tubules, and obliterated space of Bowman’s capsule.


CAN is both hepatotoxic and nephrotoxic in adult male rats. Hence, it may be hazardous to human health.

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