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首页> 外文期刊>Archives of Toxicology >The influence of chronic fluorosis on mitochondrial dynamics morphology and distribution in cortical neurons of the rat brain.
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The influence of chronic fluorosis on mitochondrial dynamics morphology and distribution in cortical neurons of the rat brain.

机译：慢性氟中毒对大鼠皮质神经元线粒体动力学形态和分布的影响。

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The present study was designed to evaluate the effects of chronic fluorosis on the dynamics (including fusion and fission proteins), fragmentation, and distribution of mitochondria in the cortical neurons of the rat brain in an attempt to elucidate molecular mechanisms underlying the brain damage associated with excess accumulation of fluoride. Sixty Sprague-Dawley rats were divided randomly into three groups of 20 each, that is, the untreated control group (drinking water naturally containing <0.5?mg fluoride/l, NaF), the low-fluoride group (whose drinking water was supplemented with 10?mg fluoride/l) and the high-fluoride group (50?mg fluoride/l). After 6?months of exposure, the expression of mitofusin-1 (Mfn1), fission-1 (Fis1), and dynamin-related protein-1 (Drp1) at both the protein and mRNA levels were detected by Western blotting, immunohistochemistry, and real-time PCR, respectively. Moreover, mitochondrial morphology and distribution in neurons were observed by transmission electron or fluorescence microscopy. In the cortices of the brains of rats with chronic fluorosis, the level of Mfn1 protein was clearly reduced, whereas the levels of Fis1 and Drp1 were elevated. The alternations of expression of the mRNAs encoding all three of these proteins were almost the same as the corresponding changes at the protein levels. The mitochondria were fragmented and the redistributed away from the axons of the cortical neurons. These findings indicate that chronic fluorosis induces abnormal mitochondrial dynamics, which might in turn result in a high level of oxidative stress.
机译：本研究旨在评估慢性氟中毒对大鼠脑皮质神经元的动力学（包括融合蛋白），断裂和分布的慢性氟中毒的影响，以阐明与之相关的脑损伤的分子机制氟化物的过量积聚。将六十Sprague-Dawley大鼠随机分成三组，即未处理对照组（天然含有<0.5？Mg氟化物/ L，NAF），低氟化物组（补充其饮用水氟化物/ L）和高氟化物基团（50毫克氟化物/ L）。在6个？几个月的暴露后，通过Western印迹，免疫组化和蛋白质和mRNA水平的MITOFUSIN-1（MFN1），裂变-1（FIS1）和发电机相关蛋白-1（DRP1）的表达。实时PCR分别。此外，通过透射电子或荧光显微镜观察神经元的线粒体形态和分布。在慢性氟中毒大鼠大脑的皮质中，MFN1蛋白的水平显然降低，而FIS1和DRP1的水平升高。编码所有三种这些蛋白质的MRNA的表达的交替与蛋白质水平的相应变化几乎相同。线粒体分散，并从皮质神经元的轴突中重新分配。这些发现表明，慢性氟中毒诱导异常线粒体动力学，其又导致高水平的氧化应激。

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