Abstract
The hepatotoxic and nephrotoxic effects of CBr 4 were studied in male Sprague—Dawley rats following a single i.p. administration in a dose range of 25 to 125 μl/kg to animals maintained for 15 days either on normal diet or a diet containing 10 ppm chlordecone (CD). At these doses, CBr 4 did not cause hepatotoxic effects when given alone or in combination with prior exposure to CD. CBr 4 caused renal dysfunction characterized by oliguria, aciduria and hypo-osmolality, and these effects were abolished by dietary CD pretreatment. In vitro incubation of renal cortical slices obtained from CBr 4-treated animals revealed a significant depression of organic anion transport, i.e., decreased transport of p-aminohippurate (PAH). Organic cation transport was unaffected as judged by accumulation of tetraethylammonium (TEA). CBr 4-induced renal dysfunction appeared unrelated to depressed PAH transport since CD pretreatment which abolished renal dysfunction failed to restore PAH transport. These results show that CD does not potentiate CBr 4 hepatotoxicity and the nephrotoxic effects of this halomethane are abolished by prior exposure to CD.
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