Objective To study the effect of lead acetate on the apoptosis 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 prevention and treatment of poisoning by lead.
Methods Mature and health Sprague-Dawley rats were divide dinto four groups randomly, six rats every group. Lead acetate was given at the dosage of 25, 50, 100mg/(kg·weight) throughip for 5 days, respectively. The determination of apoptosis in hippocampus and cerebral cortex was made by terminal-deoxy nucleotidyl transferase mediated d-UTP nick and labeling (TUNEL). The expression of fos, jun, genes in hippocanlpus and cerebral cortex were observed by using immuno-histochemical method.
Results Lead acetate induced apoptosis of cells from hippocampus, cerebral cortex in every lead acetate induced apoptosis of cells from hip pocampus, cerebral cortex in every treatment group (P < 0.05), and there was a significant dose-response relationship.(2)The expression of fos, jun increased in neural cells from hippocanlpus, cerebral cortex in every lead acetate treatment group compared with the control, and there was a significant dose-response relationship. (3)Correlation analysis demonstrated that the apoptosis were positively correlated with the expression of fos, jun.
Conclusion (1) Lead may elicit apoptosis of rat neural cells form hippocampus, cerebral conex, and the apoptosis was positive correlative with 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.
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