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作 者:陈亮[1] 石年[1] 董杰[1] 李涛[1] 陈丹[1]
机构地区:[1]华中科技大学同济医学院卫生毒理学系,湖北武汉430030
出 处:《卫生毒理学杂志》2004年第3期145-147,共3页Journal of Health Toxicology
基 金:国家自然科学基金资助 (30 371 2 2 5)
摘 要:目的 以去卵巢大鼠皮层脑片为研究对象 ,观察内分泌激素 17 β 雌二醇对溴氰菊酯 (Deltamethrin ,DM )染毒脑片兴奋性氨基酸递质释放、ATPase活力的影响。方法 高效液相色谱 (HPLC)检测不同水平雌二醇 (10 - 5、10 - 8和10 - 1 1 mol/L)对DM染毒大鼠皮层脑片氨基酸释放的影响 ,化学比色法检测雌二醇对DM染毒大鼠皮层脑片Na+ K+ ATPase、Mg2 + ATPase、Ca2 + ATPase和Ca2 + Mg2 + ATPase活力的影响 ,并观察雌激素受体拮抗剂Tamoxifen对雌二醇作用的影响。结果 2× 10 - 5mol/L的DM处理可增加高钾去极化状态下皮层脑片天冬氨酸 (ASP)和谷氨酸 (GLU)释放 ,3个剂量的 17 β 雌二醇均可抑制DM所致GLU的释放 ,10 - 1 1 mol/L的 17 β 雌二醇可抑制DM所致ASP的释放 ,Tamoxifen可拮抗10 - 8mol/L 17 β 雌二醇对DM染毒脑片EAAs释放的作用 ;2× 10 - 4mol/L的DM可抑制脑片 4种ATPase活力 ,10 - 5和 10 - 8mol/L雌二醇可拮抗DM对Mg2 + ATPase、Ca2 + Mg2 + ATPase活力的抑制 ,Tamoxifen对雌二醇的作用未见明显影响。结论 在大鼠皮层脑片中 17 β 雌二醇对DM的神经毒性有一定的保护作用 ,该作用可能部分通过雌激素受体介导产生。Objective Using rat cortical brain slices as study models to investigate the effects of estradiol on the neurotoxicity of deltamethrin.Methods Using HPLC to detect the excitatory amino acids (EAAs) release and employing colorimeter method to measure the activities of ATPase of different 17-β estradiol dose level (10 -5 ,10 -8 ,10 -11 mol/L)on the cortical brain slices treated with deltamethrin. The estrogen receptor(ER) antagonist tamoxifen was used to investigate the possible mechanisms of estradiol.Results The ASP and GLU release was increased significantly by 2×10 -5 mol/L deltamethrin at the depolarizing state,and 10 -5 ,10 -8 ,10 -11 mol/L 17-β-estradiol could partly block the release of GLU,10 -11 mol/L 17-β-estradiol could partly block the release of ASP.The effect of 10 -8 mol/L 17-β-estradiol on the GLU release can be antagonisted by 10 -6 mol/L tamoxifen.The activities of ATPase were inhibited by 2×10 -4 mol/L deltamethrin,and 10 -5 ,10 -8 mol/L estradiol could block this effects in some aspects,whereas tamoxifen had not any effects on the function of estradiol on the activities of ATPase. Conclusion Estradiol has showed a neuroprotective effect on the release of EAAs or inhibition of ATPase by deltamethrin,and this effect on GLU release may be partly attributed to the genomic mechanism of estradiol.
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