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哺乳期暴露于双酚A对雄性小鼠后代睾丸线粒体的影响

[Effects of bisphenol A exposure during lactation on testicular mitochondria in male mouse offspring].

作者信息

Xie Meina, Li Fengjie

机构信息

Medicine Experiment Center, Weifang Medical University, Weifang 261053, China.

出版信息

Wei Sheng Yan Jiu. 2014 Nov;43(6):962-6.

PMID:25603607
Abstract

OBJECTIVE

To study whether maternal bisphenol A (BPA) exposure during lactation stage will induce oxidative stress and apoptosis in male offspring's testis by mitochondrial pathway.

METHODS

After delivery, maternal mice were randomly divided into four groups, including high dose group (50 mg/kg), medium dose group (5 mg/kg), low dose group (0.01 mg/kg) and solvent control group. BPA were given daily by gavage to maternal mice during lactation stage. The pups were raised and sacrificed at PND 75. The effect of BPA exposure on the activity of testicular mitochondrial succinate dehydrogenase (SDH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in male offspring were detected. The expressions of cytochrome C (Cyt C), caspase 3 and apoptosis-inducing factor (AIF) in testes of male offspring were detected by Western blot. Changes of mitochondrial substructure in testicular cells were observed by transmission electron microscopy.

RESULTS

The exposed mice had a significant decrease in the activities of testicular mitochondrial SDH (P < 0.05) in all groups and with notable decrease in the activities of GSH-Px and SOD in the high and medium-dose groups (P < 0.05). BPA also caused testicular mitochondrial MDA increased markedly (P < 0.05). Western blot showed that the expression levels of Cyt C, caspase 3 and AIF increased significantly in the testes of BPA-treated groups (P < 0.05). Under transmission electron microscopy, mitochondria swell, crests obscure and disappear were founded in the high and medium-dose groups.

CONCLUSION

During lactation stage, maternal exposed to BPA induce oxidative stress and apoptosis of testicular cells by possible mechanisms of mitochondrial pathway,which would cause adverse effects on the early development of testis.

摘要

目的

研究哺乳期母体双酚A(BPA)暴露是否会通过线粒体途径诱导雄性子代睾丸氧化应激和细胞凋亡。

方法

分娩后,将母鼠随机分为四组,包括高剂量组(50 mg/kg)、中剂量组(5 mg/kg)、低剂量组(0.01 mg/kg)和溶剂对照组。在哺乳期,每天通过灌胃给予母鼠BPA。幼崽饲养至出生后第75天处死。检测BPA暴露对雄性子代睾丸线粒体琥珀酸脱氢酶(SDH)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性和丙二醛(MDA)含量的影响。采用蛋白质免疫印迹法检测雄性子代睾丸中细胞色素C(Cyt C)、半胱天冬酶3(caspase 3)和凋亡诱导因子(AIF)的表达。通过透射电子显微镜观察睾丸细胞线粒体亚结构的变化。

结果

各暴露组小鼠睾丸线粒体SDH活性均显著降低(P<0.05),高、中剂量组GSH-Px和SOD活性显著降低(P<0.05)。BPA还导致睾丸线粒体MDA含量显著增加(P<0.05)。蛋白质免疫印迹法显示,BPA处理组睾丸中Cyt C、caspase 3和AIF的表达水平显著升高(P<0.05)。透射电子显微镜下观察到,高、中剂量组线粒体肿胀,嵴模糊、消失。

结论

哺乳期母体暴露于BPA可通过线粒体途径诱导睾丸细胞氧化应激和凋亡,对睾丸早期发育产生不良影响。

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