EFFECT OF METHIONINE ON CADMIUM-PROVOKED OXIDATIVE STRESS IN RATS

Modulators of SH-reserve influence the liver oxidant status in Cd-trea ted rats (1 mg Cd/kg): diethylmaleate (1 ml/kg), SH-depleting agent, a ggravated impairement of catalase and cytochrome P-450 and hepatotoxic effect, whereas methionine (1 g/kg, twice), a precursor of cysteine, increased glutathione (GSH) level and attenuated hepatotoxic effect of cadmium, Protective effect of methionine against Cd-provoked oxidativ e stress was assessed in rats repeatedly exposed to CdCl2 (cumulative dose of 20 mg Cd/kg over 12 weeks) and simultaneously given 0,1% DL-me thionine in drinking water (daily supply ca. 100 mg/kg body weight). R epeated Cd-exposure produced following prooxidative effect in the live r and kidneys: enhanced lipid peroxidation, destruction of cytochrome P-350, and compensating activation of GSH-S-transferase. Distinct targ et organ changes included: induction of heme oxygenase and impairment of GSH peroxidase in the liver and lowered superoxide dismutase (SOD) and enhanced GSH-peroxidase activities with increment of GSH level in the kidneys. Increase of serum lipid peroxidation rate and values of t arget organ injury markers, serum sorbitol dehydrogenase (SDH) for liv er, and urinary N-acetyl-beta-D-glucosaminidase (NAG) for kidney confi rmed the Cd-provoked oxidative stress. Methionine in general did not p rotect against prooxidative effect of Cd in the liver and kidney yet e nhanced GSH level and ameliorated symptoms of oxidative stress as infe rred from normalization of the oxidative stress markers, i.e. lipid pe roxidation in the serum and activities of serum SDH and urinary NAG, t he markers of hepatotoxic and nephrotoxic effects, respectively.