A drug-selected Plasmodium falciparum lacking the need for conventional electron transport.
Mol Biochem Parasitol
; 159(1): 64-8, 2008 May.
Article
em En
| MEDLINE
| ID: mdl-18308406
ABSTRACT
Mitochondrial electron transport is essential for survival in Plasmodium falciparum, making the cytochrome (cyt) bc(1) complex an attractive target for antimalarial drug development. Here we report that P. falciparum cultivated in the presence of a novel cyt bc(1) inhibitor underwent a fundamental transformation in biochemistry to a phenotype lacking a requirement for electron transport through the cyt bc(1) complex. Growth of the drug-selected parasite clone (SB1-A6) is robust in the presence of diverse cyt bc(1) inhibitors, although electron transport is fully inhibited by these same agents. This transformation defies expected molecular-based concepts of drug resistance, has important implications for the study of cyt bc(1) as an antimalarial drug target, and may offer a glimpse into the evolutionary future of Plasmodium.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Plasmodium falciparum
/
Acridinas
/
Resistência a Medicamentos
/
Complexo III da Cadeia de Transporte de Elétrons
/
Transporte de Elétrons
/
Antimaláricos
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Mol Biochem Parasitol
Ano de publicação:
2008
Tipo de documento:
Article
País de afiliação:
Estados Unidos