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Abstract
Liver microsomal functions related to xenobiotic biotransformation and free radical production were studied in control rats and in animals subjected to L-3,3′,5-triiodothyronine (T3) and/or lindane administration as possible mechanisms contributing to oxidative stress, in relation to the activity of enzymes (superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glucose-6-phosphate dehydrogenase (G-6PDH)) and content of lipid-soluble vitamins (α-tocopherol, β-carotene, and lycopene) affording antioxidant protection. Lindane treatment in euthyroid rats at a dosage of 20 mg/kg did not modify the content of liver microsomal cytochromes P450 and b5, the activity of NADPH-cytochrome P450 reductase and NADH-cytochrome b5 reductase, and the production of superoxide radical (O·-2), as well as antioxidant systems, except for the reduction in lycopene levels. Hyperthyroidism elicited a calorigenic response and increased specific and molecular activities of NADPH-cytochrome P450 reductase, O·-2 generation, and G-6PDH activity, concomitantly with diminution in liver SOD and catalase activities and in α-tocopherol, β-carotene, and lycopene levels. The administration of lindane to hyperthyroid animals led to a further increase in the molecular activity of NADPH-cytochrome P450 reductase and in the O·-2 production/SOD activity ratio, and decrease of hepatic α-tocopherol content, in a magnitude exceeding the sum of effects elicited by the separate treatments, as previously reported for reduced glutathione depletion. Collectively, these data support the contention that the increased susceptibility of the liver to the toxic effects of acute lindane treatment in hyperthyroid state is conditioned by potentiation of the hepatic oxidative stress status.
