Prenatal Action of Lead Acetate on the Antioxidant Glutathione System of the Brain of Newborn Rats in Vivo and on Neurite Growth in Vitro

We studied the state of the antioxidant glutathione system ( activity of glutathione peroxidase, glutathione reductase, and content of GSH and GSSG) and the level of lipid peroxidation in the brain of newborn rats, as well as the intensity of neurite growth in the cultured spinal ganglia of these animals after prenatal treatment with lead acetate. Daily addition ( 6 mg/kg) or single addition on the 18th day of pregnancy ( 200 mg/kg) of lead acetate to food of pregnant females resulted in a considerable decrease in the activity of the glutathione system and increase in the levels of GSSG and malonic dialdehyde in the brain tissue. The lead intoxication also inhibited neurite growth in cultured ganglia. In addition, the permanent presence of lead acetate (0.02 mM) in the cultures of ganglia of intact rats on the second and third days in vitro also led to inhibition of neurite growth. The data obtained indicate that oxidative stress, which results in decreased antioxidant activity, may be one of the main mechanisms that underlie toxic injury of central and peripheral neurons after prenatal action of lead.