Effect of lead on apoptosis,c-fos and c-jun expression of rat's brain

Objective To study the effect of lead acetate on the apop tosis and the expression of fos,jun and to provide some scientific basis for the thorough revealment of neurotoxic mechanism of lead as well as for the preventi on and treatment of poisoning by lead.Methods Mature and health Sprague-Dawley rats were divide d into four groups randomly,six rats every group.Lead acetate was given at the d osage of 25,50,100?mg/(kg·weight) through ip for 5 days,respectively.The deter min ation of apoptosis in hippocampus and cerebral cortex was made by terminal-deoxy nucleotidyl transferase mediated d-UTP nick and labeling(TUNEL).The expression o f fos,jun,genes in hippocanlpus and cerebral cortex were observed by using immun o-histochemical method.Results Lead acetate induced apoptosis of cells from hipp ocampus,cerebral cortex in every lead acetate induced apoptosis of cells from hi p pocampus,cerebral cortex in every treatment group ( P 0.05),and there was a s ignificant dose-response relationship.(2)The expression of fos,jun increased in neural cells from hippocanlpus,cerebral cortex in every lead acetate treatment g roup compared with the control ,and there was a significant dose-response relati onship.(3)Correlation analysis demonstrated that the apoptosis were positively c orrelated with the expression of fos,jun.Conclusion (1)Lead may elicit apoptosis of rat neural cel ls form hippocampus,cerebral conex,and the apoptosis was positive correlative wi th the lead dosage.(2) Lead acetate may promote the expression of fos,jun genes ,and there was a good dose-response relationship,respectively.The results above suggested that fos,jun,as a regular factor of apoptosis,may participate in the neurotoxical damage to the central nervous system by lead.