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Effect of bovine adenovirus 3 on mitochondria

机译:牛腺病毒3对线粒体的影响

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摘要

Viruses alter the structure and the function of mitochondria for survival. Electron microscopy analysis of the cells infected with bovine adenovirus 3 revealed extensive damage to the inner mitochondrial membrane characterized by dissolution of the cristae and amorphous appearance of mitochondrial matrix with little or no damage to the outer mitochondrial membrane. There were fewer cristae with altered morphology. Potential patches of protein synthesis machinary around mitochondria could be observed at 12 hours post infection (hpi). At 24 hpi, the multi vascular bodies were evident throughout the infected cell. ATP production, mitochondrial Ca2+ and mitochondrial membrane potential (MMP) peaked at 18 hpi but decreased significantly at 24 hpi. This decrease coincided with the increased production of superoxide (SO) and reactive oxygen species (ROS), at 24 hpi indicating acute oxidative stress in the cells and suggesting a complete failure of the cellular homeostatic machinary. The results reveal an intericate relationship between Ca2+ homeostasis, the ATP generation ability of cells, SO and ROS production, and regulation of MMP following infection by bovine adenovirus 3.
机译:病毒会改变线粒体的结构和功能以维持生存。对被牛腺病毒3感染的细胞进行的电子显微镜分析表明,线粒体内膜受到了广泛破坏,其特征是线粒体的the裂和无定形出现,线粒体外膜几乎没有或没有损坏。形态改变的cr骨较少。在感染(hpi)后12小时,可以观察到线粒体周围机械合成蛋白质的潜在斑点。在感染后24 h,在整个感染细胞中都可见到多血管。 ATP产生,线粒体Ca 2 + 和线粒体膜电位(MMP)在18 hpi达到峰值,但在24 hpi时显着下降。这种降低与24 hpi时超氧化物(SO)和活性氧(ROS)产量的增加相吻合,表明细胞中存在急性氧化应激,表明细胞稳态机械完全失效。结果揭示了牛腺病毒感染后Ca 2 + 稳态,细胞ATP生成能力,SO和ROS生成以及MMP调节之间的复杂关系。

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