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作 者:贾克[1] 徐兆发[1] 徐斌[1] 贺安宁[1] 李晶[1] 邓宇[1] 张芳林[1]
机构地区:[1]中国医科大学公共卫生学院环境卫生教研室,沈阳110001
出 处:《中国公共卫生》2008年第3期346-347,共2页Chinese Journal of Public Health
基 金:辽宁省教育厅科学研究基金资助项目(2004C025)
摘 要:目的研究不同剂量锰对大鼠纹状体谷氨酰胺合成酶(GS)、谷氨酰胺酶(PAG)和脑皮质琥珀酸脱氢酶(SDH)、钠钾三磷酸腺苷酶(Na+-K+-ATPase)活性的影响,以探讨锰的兴奋性毒性的细胞分子学机制。方法大鼠按体重随机分成4组,每组6只。第1组为对照组,腹腔注射0.9%的氯化钠,第2~4组为锰染毒组,分别腹腔注射8,40,200μmol/kg的氯化锰溶液,注射容量为5ml/kg。染毒25d后,测定纹状体GS和PAG的活性和脑皮质SDH和Na+-K+-ATPase的活性。结果随着染锰剂量的增加,脑皮质SDH和Na+-K+-ATPase活性降低,200μmol/kg染锰组与对照组比较,SDH和Na+-K+-ATPase活性明显降低(P<0.01);随着染锰剂量的增加,GS活性降低,PAG活性升高,200μmol/kg染锰组与对照组比较,GS活性明显降低(P<0.01),PAG活性明显升高(P<0.05)。结论锰可引起大鼠脑SDH、Na+-K+-ATPase和GS活性降低以及PAG活性升高,造成谷氨酸代谢失衡。Objective To study the effects of different doses of manganese on activities of GS and PAG in the rat striatum and the activities of SDH and Na^+-K^+-ATPase in pallium in order to explore the cell molecular mechanism of manganese-induced exeitotoxicity.Methods The Wistar rats were divided into four groups by weight at random.The first group was the control group which was given peritoneal injection(i.p)of 0.9% NaC1;the second to fourth groups were respectively given i.p of 8,40,200 μtmol/kg MnCl2.The capacity of injection was all 5ml/kg.After 25-days administration,the activities of GS and PAG in the rat striatum and the activities of SDH and Na^+-K^+-ATPase in pallium were determined.Results Accompanied with the incrasing of treated Mn dosage,the activities of SDH and Na^+-K^+-ATPase in pallium decreased,the activities of SDH and Na^+-K^+-ATPase in pallium in 200?μmol/kg MnCl2 group decreased significantly with a dose-response relationship;the activity of PAG in corpora striatum increased and the activity of GS in corpora striatum decreased in 200μmol/kg MnCl2 group;the activity of GS in corpora striatum decreased significantly,however,the activity of PAG in corpora striatum increased significantly.Conclusion Mn may decrease the activities of SDH and Na^+-K^+-ATPase in pallium and the activity of GS in corpora striatum,and increase the activity of PAG in corpora striatum,which led to disrupt glutamate metabolism.
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