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

Abstract
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.
AuthorsTaeho Kim, Vu Thi Thu, Il-Yong Han, Jae Boum Youm, Euiyong Kim, Sun Woo Kang, Yang Wook Kim, Jae Hwa Lee, Hyun Joo
JournalMitochondrion (Mitochondrion) Vol. 8 Issue 3 Pg. 279-83 (Jun 2008) ISSN: 1567-7249 [Print] Netherlands
PMID18467192 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • DNA, Mitochondrial
  • Cytochromes b
  • NADH Dehydrogenase
  • Mitochondrial Proton-Translocating ATPases
  • Electron Transport Complex I
  • Isoproterenol
Topics
  • Amino Acid Substitution
  • Animals
  • Cardiomegaly (chemically induced, genetics)
  • Cytochromes b (genetics)
  • DNA, Mitochondrial (genetics)
  • Electron Transport Complex I (genetics)
  • Isoproterenol (toxicity)
  • Male
  • Mitochondria, Heart (enzymology, genetics)
  • Mitochondrial Proton-Translocating ATPases (genetics)
  • Multigene Family (genetics)
  • Mutation (genetics)
  • Myocardium (metabolism, pathology)
  • NADH Dehydrogenase (classification, genetics)
  • Point Mutation
  • Rabbits
  • Time Factors

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