The Hepatotoxicity and Nephrotoxicity of Hexachlorobutadiene

摘要: ABSTRACT Hexachloro 1:3 butadiene (HCBD) is formed as a by-product during the chlorination of hydrocarbons for manufacture chlorinated ethylenes and carbon tetrachloride. Administration HCBD (300 mg/kg, ip) to rats produces mild reversible hydropic swelling liver. This change associated with mitochondria in hepatocytes located periportal region However, major target organ toxicity kidney where necrosis pars recta proximal tubule. Treatment inducers or inhibitors hepatic and/or renal drug metabolising enzymes followed by administration does not markedly alter HCBD-induced liver injury. In male rats, causes depletion but non-protein sulphydryl content (NP-SH) pretreatment animals diethylmaleate, which reduces tissue glutathione content, enhances nephrotoxicity HCBD. Our findings date indicate that plays protective role against tubular suggests metabolic activation reaction may be involved nephrotoxicity.