Neurotoxicity associated with lead exposure may be the result of a series of small
perturbations in brain metabolism, and, in particular, of oxidative stress. Some studies
have suggested a lead-induced enhancement on lipid peroxidation as a possible mechanism
for some toxic effects of lead. However, there are no reports about the association
between lipid peroxidation enhancement and brain lead content. In this study, we determined
the concentration of lead and the formation of lipid fluorescence products in the
blood, as well as in the parietal cortex, striatum, hippocampus, thalamus, and cerebellum
of rats exposed prenatally and postnatally to variable concentrations of lead acetate
through drinking water. Pregnant Wistar rats were intoxicated 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 showed 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 products were significantly
increased in the striatum, thalamus, and hippocampus of the treated animals. These
data suggest that in the brain of rats exposed to lead acetate, lead produces a neurotoxic
effect with a complex correlation with both lead regional content and lipid peroxidation.