A drug resistance determinant in Trypanosoma brucei

Resistance to antimicrobial agents is undermining the treatment of infectious diseases. Elucidation of the mechanisms determining this resistance would help us understand how drugs can be selectively toxic and also give insight into methods of circumvention. African trypanosomiasis (sleeping sicknes...

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Bibliographic Details
Published in:Trends in microbiology (Regular ed.) 1999-12, Vol.7 (12), p.469-471
Main Authors: Carter, Nicola S, Barrett, Michael P, de Koning, Harry P
Format: Article
Language:English
Subjects:
Animals
Arsenical-diamidine cross resistance
Carrier Proteins - genetics
Carrier Proteins - metabolism
diminazene aceturate
Drug Resistance
Genes, Protozoan - genetics
Membrane Proteins - genetics
Membrane Proteins - metabolism
Nucleoside Transport Proteins
P2 membrane transporter
sodium melarsen
Trypanocidal Agents - pharmacology
Trypanosoma brucei
Trypanosoma brucei brucei - drug effects
Trypanosoma brucei brucei - genetics
Trypanosoma equiperdum
Trypanosomiasis, African - drug therapy
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Summary:Resistance to antimicrobial agents is undermining the treatment of infectious diseases. Elucidation of the mechanisms determining this resistance would help us understand how drugs can be selectively toxic and also give insight into methods of circumvention. African trypanosomiasis (sleeping sickness), which is caused by a subspecies of the parasitic protozoan Trypanosoma brucei, is resurgent in Africa. A T. brucei clone selected for resistance to an arsenical, sodium melarsen, had no detectable P2 transport activity, whereas a Trypanosoma equiperdum cell line selected for resistance to berenil retained P2 transport activity, although its affinity for the substrate was markedly reduced. T. brucei possess a plethora of purine transporters and salvage enzymes and, therefore, loss of P2 transport has no detectable impact on parasite viability.
ISSN:0966-842X
1878-4380
DOI:10.1016/S0966-842X(99)01643-1