Abstract: Purpose：To provide some scientific basis for the revealment of neurotoxic mechanism of lead ,The present study was undertake to the effect of lead acetate on the apoptosis and the expression of P53. Methods: Mature and health Sprague- Dawley rats were divided into four groups randomly, six rats in every group. Lead acetate was given at the dosage of 25,50,100 mg/kg through ip for 5 days, respectively . The determination of apoptosis in hippocampus and cerebral cortex was made by terminal- deoxynucleotidyl transferase mediated d- UTP nick and labeling(TUNEL). The expression of P53 genes in hippocampus and cerebral cortex was observed by using immuno- histochemical method . Results: The results of TUNEL showed that lead acetate induced apoptosis f cells from hippocampus, cerebral cortex in every treatment group (P < 0.05), and there was a significant dose- response relationship.The expression of P53 increased in neural cells from hippocampus, cerebral cortex in every lead acetate treatment group compared with the control , and there was a significant dose- response relationship. Correlation analysis demonstrated that the apoptosis were positively correlated with the expression of P53. Conclusion: Lead may elicit apoptosis of rat neural cells from hippocampus, cerebral cortex , and the apoptosis was positive correlative with the lead dosage. Lead acetate may promote the expression of P53 genes， and there was a good dose- response relationship。 The results above suggested that P53 as a regular factor of apoptosis， may participate in the neurotoxical damaging to the central nervous system by lead. The overexpression of P53 induced the apoptosis of neural cells. Lead acetate may initiate the expression of P53 followed by he apoptosis of neural cells .

Key words: lead, rat, neurotoxicity, apoptosis, P53 gene