氧化锗对氯化镉致小鼠脑胆碱酯酶及单胺类神经递质变化的影响

Effects of Germanium Oxide on Cadmium Chloride-Induced Change of Acetylcholinesterase Activity and Catecholamine Neurotransmitters in Mice Brain

目的研究氧化锗(GeO2)对氯化镉(CdCl2)致小鼠脑胆碱酯酶(AchE)及单胺类神经递质变化的影响。方法将64只健康昆明种小鼠随机分为8组,雌雄各半,单纯镉染毒组分别隔日腹腔注射0.3、0.6、1.2mg/kgCdCl2(奇数天)和等体积生理盐水(偶数天),CdCl2+GeO2组分别为0.3mg/kgCdCl2+25mg/kgGeO2、0.6mg/kgCdCl2+25mg/kgGeO2、1.2mg/kgCdCl2+25mg/kgGeO2(奇数天注射CdCl2,偶数天注射GeO2),连续染毒20d,第21～30天每日注射等体积生理盐水。同时设单纯GeO2染毒组(奇数天注射生理盐水,偶数天按25mg/kg注射GeO2,连续30d)。生理盐水组小鼠每日腹腔注射生理盐水,10ml/kg,共30d。采用碱性羟胺法测定小鼠脑中AchE活力,荧光法测定小鼠脑中单胺类神经递质去甲肾上腺素(NE)、多巴胺(DA)、5-羟色胺含量(5-HT)。结果与生理盐水组比较,0.3、0.6、1.2mg/kg单纯CdCl2染毒组小鼠的脑组织AchE活力明显降低(P<0.05),同时给予25mg/kgGeO2可缓解此种变化。与生理盐水组比较,CdCl2染毒组脑组织NE、DA、5-HT含量明显下降(P<0.05或P<0.01),25mg/kgGeO2拮抗了这种变化。结论GeO2可保护CdCl2所致小鼠脑组织神经生化改变。

Objective To study the effects of germanium oxide on cadmium chloride-induced change of acetylcholinesterase （AchE） activity and contents of catecholamine neurotransmitters in the brains of adult mice. Methods Sixty-four Kunming mice were divided randomly into 8 groups, cadminum groups alternatively exposured to cadminum at 0.3, 0.6, 1.2 mg/kg and same volume of physiological saline through intraperitoneal injection once every two days, cadminum ＋ germanium groups were given germanium oxide at 25 mg/kg besides cadminum once every two days, the other two were germanium and physiological saline groups. All groups were injected for 20 d, then germanium oxide group mice were additional injected total 5 times once every two days .Alkaline hydroxylamine method was used in determining activity of AchE, flourimetric method was used in determining contents of NE, DA, 5-HT. Results The activities of AchE were significantly decreased in the cadmium-treated group, which could be antagonized by germanium oxide at 25 mg/kg. The levels of norepinephfine, dopamine, and serotonin were decreased significantly in the cadmium-treated mice, and this decreases were also antagonized by germanium oxide. Conclusion These data suggest that the germanium oxide antagonize the cadmium chloride-induced changes in neurobiochemical parameters.