Does strong hypertrophic condition induce fast mitochondrial DNA mutation of rabbit heart?

Homo- and heteroplasmic mitochondrial DNA (mtDNA) mutations were observed and identified in an isoproterenol-induced rabbit model of cardiac hypertrophy. Genes encoding proteins essential for catalyzing mitochondrial electron transfer and for generating the proton motive force, such as NADH dehydrog...

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Bibliographic Details
Published in:Mitochondrion 2008-06, Vol.8 (3), p.279-283
Main Authors: Kim, Taeho, Thu, Vu Thi, Han, Il-Yong, Youm, Jae Boum, Kim, Euiyong, Kang, Sun Woo, Kim, Yang Wook, Lee, Jae Hwa, Joo, Hyun
Format: Article
Language:English
Subjects:
Amino Acid Substitution
Animals
Cardiomegaly - chemically induced
Cardiomegaly - genetics
Cytochromes b - genetics
DNA, Mitochondrial - genetics
Electron Transport Complex I - genetics
Isoproterenol - toxicity
Male
Mitochondria, Heart - enzymology
Mitochondria, Heart - genetics
Mitochondrial Proton-Translocating ATPases - genetics
Multigene Family - genetics
Mutation - genetics
Myocardium - metabolism
Myocardium - pathology
NADH Dehydrogenase - classification
NADH Dehydrogenase - genetics
Point Mutation
Rabbits
Time Factors
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Summary:Homo- and heteroplasmic mitochondrial DNA (mtDNA) mutations were observed and identified in an isoproterenol-induced rabbit model of cardiac hypertrophy. Genes encoding proteins essential for catalyzing mitochondrial electron transfer and for generating the proton motive force, such as NADH dehydrogenases (ND2, ND3, ND4, and ND6), cytochrome b, and ATPase 8, showed increased susceptibility for mutation. Specifically, five mutations caused amino acid changes and were located in Complex I and Complex V gene clusters. To our knowledge, this is the first demonstration of a relationship between cardiac hypertrophy induced by a strong sympathetic load and rapid mtDNA mutations.
ISSN:1567-7249
DOI:10.1016/j.mito.2008.03.003