缺血缺氧与线粒体DNA损伤

Anoxia and hypoxia and mitocondril DNA damage

线粒体DNA(mtDNA)编码细胞色素氧化酶 Ⅰ、Ⅱ、Ⅲ (COX Ⅰ、COX Ⅱ、COX Ⅲ )及ATP酶亚单位 6、8(ATPase 6 .8)等蛋白质及多肽 ,控制着氧化磷酸化和ATP合成。缺血缺氧时氧化磷酸化障碍 ,ATP合成减少 ,COX Ⅰ mRNA、NADH辅酶Q氧化还原酶 mRNA (NDmRNA)转录水平升高 ,基因上调。缺血缺氧引起线粒体DNA突变率升高 ,mtDNA4977、mtDNA743 6、mtDNA1 0 42 3 缺失 ,ATPase6～ 8亚单位基因突变。葡萄糖糖酵解酶、热休克蛋白 (HSP)、磷酶甘油还原酶B(PGM B)及基因疗法可提高机体对缺氧的耐受性和适应性。

Cytochrome coxidase subunit Ⅰ to Ⅲ,ATPase subunit 6 and 8 et al proteins are encoded by mitocondrial genes.It controlled oxidative phosphorylation(OXPHOS) and synthesis of ATP.Anoxia and hypoxia may iduduce OXPHOS deficiency and ATP synthesis damage,increase of COX ⅠmRNA,NDmRNA transcription,up regulation of gene expression of mitocondrial genes.Anoxia or ischemia increases mtDNA mutation and initiates mtDNA 4977 mtDNA 7436 mtDNA 10423 deletion,promotes ATPase subunite 6 and 8 genes mutation .Glucose glycolysis enzyme,HSP,PGM B and gene treatment may increase the tolerance and adaptability of mitochondria to anoxia.