Increased lipid peroxidation in tissues of the catfish Clarias batrachus following vanadium treatment: in vivo and in vitro evaluation
1994
Bishayee, A. | Chatterjee, M.
This paper deals with the underlying biochemical mechanism of the cytotoxicity of vandadium (as ammonium monovanadate) in a warm water teleost, Clarias batrachus (Linn). Lipid peroxidation, a well-known biochemical marker for cell injury, was found to be significantly enhanced in fish liver, kidney, and brain after 12 hr and maximally induced after 72 hr exposure of this compound (10 mg/L). When the fish were exposed to 5, 10, 15, and 20 mg/L of vanadium compound for 72 hr, lipid peroxidation in these three organs were elevated dose-dependently but the degree of increase varied between organs. The induction of both enzymatic (paraquat-NADPH) and non-enzymatic (ascorbate-Fe2+) in vitro lipid peroxidation was enhanced by this vanadium salt when added in micromolar concentrations (42 or 85 micromolar) to the liver, kidney, and brain microsomal preparations. Both in vivo and in vitro studies revealed that kidney tissue was most severely affected with acute vanadium intoxication, followed by liver and brain.
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