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Peroxide production and apoptosis in cultured cells carrying mtDNA mutation causing encephalomyopathy
Author(s) -
Zhang Jin,
Yoneda Makoto,
Naruse Keiji,
Borgeld HarmJan W.,
Gong JianSheng,
Obata Shuichi,
Tanaka Masashi,
Yagi Kunio
Publication year - 1998
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216549800203572
Subject(s) - mitochondrial encephalomyopathy , mitochondrial dna , apoptosis , mutation , biology , genetics , microbiology and biotechnology , gene
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.