Effects on Nitric Oxide Synthase Expression in Rat Brain Induced by Lead
Lan An
Abstract
Lan An
Abstract
Objective To study the effects of lead exposure on NOS expression in rat brain, and provide scientific basis for the revealment of neurotoxic mechanisms of lead. Methods Adult male SD rats were divided into four groups randomly, six male rats each group. The rats were exposed to lead acetate at doses of 25, 50, 100 mg/kg bw respectively through IP. for 5 days. The expression of nNOS and iNOS in hippocampus and cerebral cortex were observed using immunohistochemical method. Results The expression of iNOS in the hippocampus and the cerebral cortex of each lead exposure group were significantly increased compared with the control group and showed significant dose,response relationships. The expression of nNOS in hippocampus of each lead exposure group increased significantly, while the expression of nNOS in the cerebral cortex showed no significant differences between the lead exposure groups and the control group. Conclusion Lead exposure may induce the over,expression of NOS, which cause the production of excessive amount of NO and damage the neural cells.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Objective To study the effects of lead exposure on NOS expression in rat brain, and provide scientific basis for the revealment of neurotoxic mechanisms of lead. Methods Adult male SD rats were divided into four groups randomly, six male rats each group. The rats were exposed to lead acetate at doses of 25, 50, 100 mg/kg bw respectively through IP. for 5 days. The expression of nNOS and iNOS in hippocampus and cerebral cortex were observed using immunohistochemical method. Results The expression of iNOS in the hippocampus and the cerebral cortex of each lead exposure group were significantly increased compared with the control group and showed significant dose,response relationships. The expression of nNOS in hippocampus of each lead exposure group increased significantly, while the expression of nNOS in the cerebral cortex showed no significant differences between the lead exposure groups and the control group. Conclusion Lead exposure may induce the over,expression of NOS, which cause the production of excessive amount of NO and damage the neural cells.
Key concepts: Lead acetate, Hippocampus, Nitric oxide synthase, Cerebral cortex, Nitric oxide, Immunohistochemistry, Internal medicine, Endocrinology