Cardiac cytochrome c and cardiolipin depletion during anthracycline-induced chronic depression of mitochondrial function

It is still unclear why anthracycline treatment results in a cardiac-specific myopathy. We investigated whether selective doxorubicin (DOX) cardiotoxicity involving mitochondrial degeneration is explained by different respiratory complexes reserves between tissues by comparing and contrasting treatm...

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Detalhes bibliográficos
Autor principal: Pereira, Gonçalo C. (author)
Outros Autores: Pereira, Susana P. (author), Tavares, Ludgero C. (author), Carvalho, Filipa S. (author), Magalhães-Novais, Sílvia (author), Barbosa, Inês A. (author), Santos, Maria S. (author), Bjork, James (author), Moreno, António J. (author), Wallace, Kendall B. (author), Oliveira, Paulo J. (author)
Formato: article
Idioma:eng
Publicado em: 2016
Assuntos:
Animals
Antibiotics, Antineoplastic
Cardiolipins
Cytochromes c
Doxorubicin
Kidney
Liver
Male
Mitochondria
Mitochondrial Myopathies
Myocardium
Rats, Wistar
Texto completo:http://hdl.handle.net/10316/47559
País:Portugal
Oai:oai:estudogeral.sib.uc.pt:10316/47559
Descrição
Resumo:It is still unclear why anthracycline treatment results in a cardiac-specific myopathy. We investigated whether selective doxorubicin (DOX) cardiotoxicity involving mitochondrial degeneration is explained by different respiratory complexes reserves between tissues by comparing and contrasting treatment effects in heart vs liver and kidney. Alternatively, we have also explored if the degeneration is due to alterations of mitochondrial thresholds to incompatible states.

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