双酚A对成年雄性小鼠的生殖毒性及其作用机制

发布时间：2018-04-11 13:37

本文选题：双酚A + Fas蛋白　；参考：《吉林大学学报(医学版)》2016年02期

【摘要】：目的:探讨双酚A(BPA)对成年小鼠睾丸组织的损伤作用,阐明BPA对动物机体的生殖毒性及其作用机制。方法:8周龄昆明小鼠40只随机分为对照组(玉米油)和低(100 mg·kg~(-1) BPA)、中(200mg·kg~(-1)BPA)、高(400mg·kg~(-1)BPA)剂量BPA组。灌胃染毒4周后,取小鼠睾丸组织,采用流式细胞术检测小鼠睾丸组织中细胞凋亡率;免疫组织化学法检测Fas和FADD蛋白表达情况。结果:与对照组比较,低剂量BPA组小鼠睾丸组织中细胞凋亡率、Fas和FADD阳性细胞表达率无明显变化(P0.05);中和高剂量BPA组小鼠睾丸组织中细胞凋亡率、Fas和FADD阳性细胞表达率明显升高(P0.05)。与低剂量BPA组比较,中和高剂量BPA组小鼠睾丸组织中细胞凋亡率、FAS和FADD阳性细胞表达率明显升高(P0.05);与中剂量BPA组比较,高剂量BPA组小鼠睾丸组织中细胞凋亡率、FAS和FADD阳性细胞表达率明显升高(P0.05)。中剂量BPA组细胞凋亡率与FAS、FADD阳性细胞表达率呈正相关关系(r=0.430,P0.05;r=0.238,P0.01),高剂量组细胞凋亡率与Fas、FADD阳性细胞表达率呈正相关关系(r=0.637,P0.01;r=0.359,P0.01)。结论:一定剂量BPA会导致小鼠睾丸组织中细胞凋亡率升高,凋亡调控基因Fas和FADD表达上调;BPA对小鼠睾丸组织有损伤作用,其生殖毒性与激活Fas死亡受体信号通路从而导致细胞过度凋亡有关。
[Abstract]:Aim: to investigate the damage effect of bisphenol A (BPA) on testis of adult mice and to elucidate the reproductive toxicity of BPA and its mechanism.Methods Forty 8 week-old Kunming mice were randomly divided into two groups: control group (corn oil) and low dose (100mg / kg) BPA group.After 4 weeks of gastric administration, the mouse testis were collected and the apoptosis rate was detected by flow cytometry, and the expression of Fas and FADD protein was detected by immunohistochemistry.Results: compared with the control group, the apoptotic rate and the expression rate of FAS and FADD positive cells in testis of mice in low dose BPA group were not significantly changed, while those in middle and high dose BPA group were significantly higher than those in middle and high dose BPA group, and the expression rate of FAS and FADD positive cells in testicular tissue was significantly higher than that in high dose BPA group.Apoptosis rate in testis of high dose BPA group and the expression rate of FAS and FADD positive cells were significantly increased in high dose BPA group.Conclusion: the apoptosis rate of mouse testis can be increased by certain dose of BPA, and the expression of Fas and FADD is up-regulated.Its reproductive toxicity is related to the activation of Fas death receptor signaling pathway, which leads to excessive apoptosis.
【作者单位】：内蒙古医科大学形态学实验中心;内蒙古医科大学心身医学实验室;内蒙古医科大学遗传学教研室;内蒙古医科大学;
【基金】：国家自然科学基金资助课题(81260111) 内蒙古自治区教育厅高等学校研究项目资助课题(NJZC13439) 内蒙古医科大学“英才培育”项目资助课题(2014YCPY002)
【分类号】：R114

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