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首页> 外文会议>Asian Society for Mitochondrial Research and Medicine >Bcl-2 Gene Family Expression in the Brain of Rat Offspring after Gestational and Lactational Dioxin Exposure
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Bcl-2 Gene Family Expression in the Brain of Rat Offspring after Gestational and Lactational Dioxin Exposure

机译：Bcl-2基因家族在妊娠期和泌乳二恶英暴露后大鼠后代的脑中表达

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Recent epidemiological studies have shown that dioxin, a persistent organic pollutant, is related to cognitive and behavioral abnormalities in the offspring of exposed cohort. In order to investigate the possible impact of dioxin in survival gene expression during brain development, we established an animal model of gestational and lactational dioxin-exposed rat offspring. The expressions of dioxin-responsive gene cytochrome P450 1A1 (CYP1A1), apoptotic gene Bax, and anti-apoptotic genes Bcl-2 and Bcl-x_L were examined in rat liver and brains using Western blot analysis and RT-PCR. The results showed that treatment of pregnant rats with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (2 μg/kg body weight through oral delivery) at gestation day 15 resulted in an increase of Bcl-x_L in offspring male liver and cerebral cortex, but a decrease in female offspring. In contrast, the expression of Bcl-x_L in the cerebellum was decreased in male, but increased in female. Bcl-2, another anti-apoptotic gene, was also downregulated in P0 female liver, cerebral cortex, but was not observed in male. In the 4-month-old offspring, however, the Bcl-2 protein levels in the liver and cerebellum of both male and female pups were higher in the TCDD group as compared with the control group. However, the Bcl-2 level in the cerebral cortex of TCDD-treated groups was higher than the control group only in female but not male offspring at 4 months old. The expression of Bax showed no significant changes upon TCDD exposure at P0 stage, but was significantly reduced in the 4-month-old male cortex. These results indicate that early exposure of dioxin could affect the development of certain brain regions with gender difference, in terms of its differential effect on expressions of Bcl-x_L, Bcl-2, and Bax.
机译：最近的流行病学研究表明，Dioxin是一种持久的有机污染物，与暴露的队列的后代中的认知和行为异常有关。为了探讨二恶英在脑发育期间存活基因表达中的可能影响，我们建立了一种妊娠和泌乳二恶英暴露大鼠后代的动物模型。使用Western印迹分析和RT-PCR在大鼠肝脏和大脑中检查二恶英响应基因细胞色素P4501A1（CYP1A1），凋亡基因Bax和抗凋亡基因Bcl-2和Bcl-X11的表达。结果表明，在妊娠第15天（通过口服递送2μg/ kg体重通过口服递送2μg/ kg体重）治疗孕腺大鼠导致后代Bcl-X1增加雄性肝脏和脑皮质，但是女性后代减少。相反，在雄性中，小脑中Bcl-X11的表达减少，但在雌性中增加。 Bcl-2，另一种抗凋亡基因，也在P0雌性肝脏，脑皮层中下调，但在雄性中未观察到。然而，在4个月历史的后代，与对照组相比，TCDD组肝脏和雌性幼虫的肝脏和小脑中的Bcl-2蛋白水平较高。然而，TCDD处理基团的脑皮层中的BCL-2水平高于对照组仅在女性，而不是在4个月内的男性后代。 BAX的表达显示在P0阶段的TCDD暴露时没有显着变化，但在4个月大的雄性皮质中显着降低。这些结果表明，在其对Bcl-X11，Bcl-2和Bax表达的差异效应方面，二恶英早期暴露可能影响某些脑区的发展。

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