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目的采用氯化锰染毒建立锰毒性不同病程的动物模型并对其进行评价。方法 120只雄性SD大鼠按体重随机分为染锰30 d组、染锰90 d组与染锰90 d后再恢复30 d组及其相应的对照组,染锰组按6 mg(Mn)/kg·BW每日腹腔注射氯化锰溶液,对照组给予生理盐水。各组试验结束后进行体重、脏体比、食物利用率、血液学指标、血清生化指标、血清Mn、Fe、Mg等离子、黑质多巴胺能神经元活性的测定与分析以及肝脏、肾脏与睾丸等的病理组织学观察与分析。结果各染毒组大鼠的体重以及食物利用率与其相应对照组比较,差异均无统计学意义(P>0.05);各染毒组血清中Mn含量及Mn/Fe比值与相应对照组比较均升高,差异有统计学意义(P<0.05);以HE染色进行病理形态学观察,发现各染毒组与其相应对照组比较均出现不同程度的肝细胞核变性坏死以及睾丸曲细精管部分管腔内精子数减少,初级精母细胞空胞样变性等,且随染锰时间延长有加重的趋势,但脱离锰暴露后(90 d染毒+30 d恢复)病变有恢复迹象;酪氨酸羟化酶免疫组织化学染色观察发现各时间点染毒组与其相应对照组比较,脑组织中TH-阳性的多巴胺能神经元数量均减少,并且随着染锰时间的延长减少程度加重,脱离锰暴露后(90 d染毒+30 d恢复)损伤不可恢复。结论根据以上各指标综合判断,本次研究所建立的锰毒性不同病程的动物模型是成功的,为今后锰毒性机制的进一步研究提供了可靠的动物模型基础。
OBJECTIVE: To establish and evaluate the animal model of manganese toxicity in different course by using manganese chloride. Methods 120 male Sprague-Dawley rats were randomly divided into three groups according to body weight: 30 mg Mn-d for 30 d and 90 d Mn-d for 90 d, then resumed for 30 d and their corresponding control groups. / kg · BW daily intraperitoneal injection of manganese chloride solution, the control group given saline. The body weight, body mass ratio, food utilization rate, hematology index, serum biochemical index, plasma Mn, Fe, Mg and plasma nigrosine dopaminergic neuron activity were measured and analyzed, and liver, kidney and testis Histopathological observation and analysis. Results The body weight and food utilization rate of rats in each exposure group were not significantly different from those of the corresponding control groups (P> 0.05). The levels of Mn and Mn / Fe in serum of each exposure group were significantly lower than those of the corresponding control group (P <0.05). HE staining was used to observe the pathomorphology. It was found that there were different degrees of nuclear degeneration and necrosis in testis and testicular seminiferous tubules Intracavitary sperm count decreased, primary spermatocyte decellularization, etc., and with the trend of prolonging the duration of manganese exposure, there was a sign of recovery from the exposure to manganese (90 d recovery + 30 d recovery); tyrosine Hydroxylase immunohistochemical staining showed that the number of TH-positive dopaminergic neurons in brain tissue decreased compared with the corresponding control group at each time point, and the extent of TH-positive dopaminergic neurons decreased with the prolongation of manganese exposure, After (90 d exposure + 30 d recovery) Injury can not be recovered. Conclusion Based on the comprehensive judgment of the above indexes, the animal model of manganese toxicity established in this study is successful and provides a reliable animal model basis for further study of manganese toxicity mechanism in the future.