镍致小鼠中枢神经毒性机制的研究

对小鼠脑内微量注射硫酸镍0．2mg／kg，0．4mg／kg，0．8mg／kg一次性染毒，制备脑突触小体。检测脑组织Ca^2 -ATP ase活性、钙调素(CaM)以及丙二醛(MDA)、还原型谷胱甘肽(GSH)含量和超氧化物歧化酶(SOD)活性。结果显示，硫酸镍明显抑制脑突触小体膜Ca^2 -ATP ase活性，使CaM含量降低；脑组织中MDA含量井高的同时SOD活性受抑制，并引起GSH含量减少。说明硫酸镍可导致钙稳态失衡，同时引起神经细胞脂质过氧化作用增强而致脑损伤。

A study on the mechanism of central nervous system toxicity caused by nickel in mice

Nickel sulfate at varied doses of 0.2 mg/kg,0.4mg/kg and 0.8mg/kg,respectively,was injected intracerebrally for mice.The cerebral synaptosome was prepared.Activity of Ca 2+-ATPase,the contents of calmodulin(CaM),malondialdehyde(MDA),GSH and activity of SOD in the brain were measured with enzyme and biochemical analysis.Results showed that activities of Ca 2+-ATPase and SOD in the cerebral synaptosome were inhibited significantly,its contents of CaM and GSH decreased and its content of MDA increased in the mice treated with nickel sulfate,indicating nickel sulfate could cause imbalance of stable state of calcium and enhancement of lipid peroxidation in nerve cells leading to brain damage.