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Mitochondrial dysfunction may explain the cardiomyopathy of chronic iron overload
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Onkologi. Linköpings universitet, Hälsouniversitetet.
James Graham Brown Cancer Centre.
James Graham Brown Cancer Centre.
University of Louisville.
Vise andre og tillknytning
2010 (engelsk)Inngår i: Free Radical Biology & Medicine, ISSN 0891-5849, E-ISSN 1873-4596, Vol. 49, nr 3, s. 401-407Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

In patients with hemochromatosis, cardiac dysfunction may appear years after they have reached a state of iron overload. We hypothesized that cumulative iron-catalyzed oxidant damage to mitochondrial DNA (mtDNA) might explain the cardiomyopathy of chronic iron overload. Mice were given repetitive injections of iron dextran for a total of 4 weeks after which the iron-loaded mice had elevated cardiac iron, modest cardiac hypertrophy, and cardiac dysfunction. OCR amplification of near-full-length (similar to 16 kb) mtDNA revealed greater than50% loss of full-length product, whereas amounts of a OCR product of a nuclear gene (13 kb region of beta globin) were unaffected. Quantitative rtPCR analyses revealed 60-70% loss of mRNA for proteins encoded by mtDNA with no change in mRNA abundance for nuclear-encoded respiratory subunits. These changes coincided with proportionate reductions in complex I and IV activities and decreased respiration of isolated cardiac mitochondria. We conclude that chronic iron overload leads to cumulative iron-mediated damage to mtDNA and impaired synthesis of mitochondrial respiratory chain subunits. The resulting respiratory dysfunction may explain the slow development of cardiomyopathy in chronic iron overload and similar accumulation of damage to mtDNA may also explain the mitochondrial dysfunction observed in slowly progressing diseases such as neurodegenerative disorders.

sted, utgiver, år, opplag, sider
Elsevier Science B.V., Amsterdam. , 2010. Vol. 49, nr 3, s. 401-407
Emneord [en]
Mitochondrial DNA; Iron overload; Cardiomyopathy
HSV kategori
Identifikatorer
URN: urn:nbn:se:liu:diva-58233DOI: 10.1016/j.freeradbiomed.2010.04.033ISI: 000279645700011OAI: oai:DiVA.org:liu-58233DiVA, id: diva2:338040
Tilgjengelig fra: 2010-08-10 Laget: 2010-08-09 Sist oppdatert: 2017-12-12

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