Enhanced brain regional lipid peroxidation in developing rats exposed to low level lead acetate

Neurotoxicity associated with lead exposure may be the result of a series o f small perturbations in brain metabolism, and, in particular, of oxidative stress. Some studies have suggested a lead-induced enhancement on lipid pe roxidation as a possible mechanism for some toxic effects of lead. However, there are no reports about the association between lipid peroxidation enha ncement and brain lead content. In this study, we determined the concentrat ion of lead and the formation of lipid fluorescence products in the blood, as well as in the parietal cortex, striatum, hippocampus, thalamus, and cer ebellum of rats exposed prenatally and postnatally to variable concentratio ns of lead acetate through drinking water. Pregnant Wistar rats were intoxi cated throughout gestation with solutions containing either 320 or 160 ppm of lead. The pups were treated after birth in the same way until 45 days of age. Control animals received deionized water for the same period of time. The developing rats were sacrificed at postnatal day 45 and lead level was assessed biochemically in the blood and different brain regions. Results s howed that blood lead levels were increased in a dose-dependent manner. In the brain, lead accumulated preferentially in the parietal cortex, striatum , and thalamus as compared to the control group, while lipid fluorescence p roducts were significantly increased in the striatum, thalamus, and hippoca mpus of the treated animals. These data suggest that in the brain of rats e xposed to lead acetate, lead produces a neurotoxic effect with a complex co rrelation with both lead regional content and lipid peroxidation. (C) 2001 Elsevier Science Inc.