携带mtDNA突变的培养细胞引起脑肌病的过氧化氢产生和细胞凋亡。

J Zhang, M Yoneda, K Naruse, H J Borgeld, J S Gong, S Obata, M Tanaka, K Yagi
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引用次数: 24

摘要

当具有mtDNA tRNALeu(UUR)基因点突变并导致线粒体脑肌病(MELAS综合征)的cy杂种暴露于高浓度氧(95%)时,过氧化氢产量在暴露6小时后显著增加,而在正常氧浓度下,过氧化氢产量在cy杂种之间相似。氧暴露增加了过氧化氢的产生,特别是在突变体mtDNA比例高和呼吸能力低的杂交体中。在呼吸功能受损的杂交体中,氧暴露导致细胞凋亡的发生率很高。抗氧化剂NAC成功地抑制了过氧化氢的产生和细胞凋亡。这些结果表明,过氧化氢的产生在诱导携带mtDNA突变引起脑肌病的细胞凋亡中起重要作用。
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Peroxide production and apoptosis in cultured cells carrying mtDNA mutation causing encephalomyopathy.

When cybrids with a point mutation, which locates in the tRNALeu(UUR) gene of mtDNA and causes a mitochondrial encephalomyopathy (MELAS syndrome), were exposed to a high concentration of oxygen (95%), the peroxide production markedly increased by 6 h of oxygen exposure, whereas the peroxide production was similar among the cybrids under a normal concentration of oxygen. The peroxide production by oxygen exposure was enhanced particularly in cybrids with high proportions of the mutant mtDNA and low respiratory capacities. The appearance of apoptotic cells by oxygen exposure was high in cybrids with the impaired respiratory function due to the mutation. An antioxidant NAC successfully suppressed both the peroxide production and apoptosis. These results imply that the peroxide production plays an important role in inducing apoptosis in cells carrying the mtDNA mutation causing encephalomyopathy.

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