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Association of a missense nucleotide polymorphism in the MT‐ND2 gene with mitochondrial reactive oxygen species production in the T ibet chicken embryo incubated in normoxia or simulated hypoxia
Author(s) -
Wang X. Y.,
He Y.,
Li J. Y.,
Bao H. G.,
Wu Ch.
Publication year - 2013
Publication title -
animal genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.756
H-Index - 81
eISSN - 1365-2052
pISSN - 0268-9146
DOI - 10.1111/age.12020
Subject(s) - missense mutation , biology , reactive oxygen species , mitochondrion , oxygen , microbiology and biotechnology , nadh dehydrogenase , mitochondrial dna , genotype , biochemistry , genetics , gene , mutation , chemistry , organic chemistry
Summary NADH dehydrogenase (complex I) catalyzes the transfer of electrons from NADH to ubiquinone with pumping protons across the mitochondrial inner membrane and produces reactive oxygen species as a major source in mitochondria. A missense mutation in the mitochondrially encoded NADH dehydrogenase 2 ( MT‐ND2 ) gene, which could produce a change in the protein's secondary structure, has been found in the T ibet chicken breed. In this study, breeding eggs of the Tibet chicken breed with the two genotypes were divided into two groups. One group was incubated in normoxia (20.9% oxygen concentration) and the other in simulated hypoxia (14.5% oxygen concentration). On the 16th day of incubation, complex I activity and mitochondrial reactive oxygen species production in the T ibet chicken embryonic liver with different genotypes in each group were measured. Results showed that: (1) hypoxia reduced complex I activity standardized and mitochondrial reactive oxygen species production significantly compared with normoxia and (2) the missense mutation in the MT‐ND2 gene was significantly associated with the production of reactive oxygen species in mitochondria while not associated with the standardized or unstandardized activity of complex I.