ACUTE LINDANE INTOXICATION - A STUDY ON LINDANE TISSUE CONCENTRATION AND OXIDATIVE STRESS-RELATED PARAMETERS IN LIVER AND ERYTHROCYTES

Treatment of rats with daily dosis of 20 mg of lindane/kg for 3 consec utive days led to the accumulation of the insecticide in several tissu es, including erythrocytes and liver. Lindane did not alter the hemato crit and hemoglobin concentration but reduced methemoglobin levels by 17%. Red blood cells from controls and lindane-treated rats, exposed t o t-butyl hydroperoxide, exhibited comparable rates of oxygen uptake a nd visible chemiluminescence, whereas the induction period that preced es oxygen uptake was significantly enhanced in the latter group. Linda ne treatment did not modify the activity of erythrocyte glutathione pe roxidase, glucose-6-phosphate dehydrogenase, catalase, and methemoglob in reductase, being the total content of glutathione and superoxide di smutase activity significantly increased. The liver from lindane-treat ed rats showed an enhanced microsomal pro-oxidant activity, evidenced by higher cytochrome P450 content and NADPH-cytochrome c reductase and NADPH oxidase activities. The higher enzyme activities led to an incr eased superoxide anion generation (adrenochrome formation) and lipid p eroxidation (measured either by the production of thiobarbituric acid reactants and spontaneous visible chemiluminescence). Concomitantly, l iver glutathione content and the activity of glutathione peroxidase-gl utathione reductase couple were augmented by lindane treatment, withou t any change in superoxide dismutase activity, together with a reducti on in that of catalase. Results suggest that lindane does not alter th e prooxidant/antioxidant status of the erythrocyte in conditions of a significant cellular accumulation of the insecticide, which might exer t direct action on enzymatic systems leading to enhanced superoxide di smutase activity and glutathione content. In the liver, lindane-induce d pro-oxidant condition was not accompanied by cell injury, probably d ue to the adaptative increase in some antioxidant mechanisms of the he patocyte.