ubiquinol and Lead-Poisoning

Oxidative damage associated with the presence of lead (Pb) in the brain has been proposed as one possible mechanism involved in Pb toxicity. To investigate this hypothesis, we examined the long-term effects of Pb2+ on parameters of oxidative stress in the brain from rats chronically exposed to the metal (1 g Pb acetate/1 drinking water). After 8 weeks of treatment, Pb2(+)-intoxicated rats (blood Pb concentration > 100 microg/dl) showed lower body weight, and lower hematocrit and 5-aminolevulinic acid dehydratase activity as compared to controls. The content of brain 2-thiobarbituric acid-reactive substances (TBARS), an indicator of lipid oxidation, was significantly (P < 0.05) higher in the Pb2(+)-intoxicated animals than in controls. Higher activities of the antioxidant enzymes glutathione reductase and glutathione peroxidase, and a lower (44%) level of ubiquinol 10 were found in the brain of the Pb2(+)-treated rats, compared to controls. A negative correlation between brain ubiquinol 9 (r2 = 0.79), 10 (r2 = 0.84) and blood Pb concentration was observed. Brain alpha-tocopherol levels, superoxide dismutase activity and parameters of oxidative damage to proteins were similar between control and Pb2(+)-treated rats. The present results indicate that chronic Pb2+ intoxication induces an oxidative stress situation in rat brain.

Topics: Animals; Antioxidants; Body Weight; Brain; Glutathione Peroxidase; Glutathione Reductase; Hematocrit; Lead; Lead Poisoning; Lipid Peroxidation; Male; Porphobilinogen Synthase; Proteins; Rats; Rats, Wistar; Superoxide Dismutase; Thiobarbituric Acid Reactive Substances; Ubiquinone; Vitamin E