Počet záznamů: 1  

Trypanocidal action of bisphosphonium salts through a mitochondrial target in bloodstream form Trypanosoma brucei

  1. 1.
    SYSNO ASEP0461180
    Druh ASEPJ - Článek v odborném periodiku
    Zařazení RIVJ - Článek v odborném periodiku
    Poddruh JČlánek ve WOS
    NázevTrypanocidal action of bisphosphonium salts through a mitochondrial target in bloodstream form Trypanosoma brucei
    Tvůrce(i) Alkhaldi, A.A.M. (GB)
    Martínek, Jan (BC-A)
    Panicucci, Brian (BC-A)
    Dardonville, C. (ES)
    Zíková, Alena (BC-A) RID, ORCID
    de Koning, H.P. (GB)
    Zdroj.dok.International Journal for Parasitology-Drugs and Drug Resistance . - : Elsevier - ISSN 2211-3207
    Roč. 6, č. 1 (2016), s. 23-34
    Poč.str.12 s.
    Forma vydáníTištěná - P
    Jazyk dok.eng - angličtina
    Země vyd.GB - Velká Británie
    Klíč. slovaTrypanosoma brucei ; mitochondrion ; FoF1 ATPase ; succinate dehydrogenase ; phosphonium salt ; SDH complex
    Vědní obor RIVEB - Genetika a molekulární biologie
    CEPLL1205 GA MŠMT - Ministerstvo školství, mládeže a tělovýchovy
    Institucionální podporaBC-A - RVO:60077344
    UT WOS000372717200003
    EID SCOPUS84953438596
    DOI10.1016/j.ijpddr.2015.12.002
    AnotaceLipophilic bisphosphonium salts are among the most promising antiprotozoal leads currently under investigation. As part of their preclinical evaluation we here report on their mode of action against African trypanosomes, the etiological agents of sleeping sickness. The bisphosphonium compounds CD38 and AHI-9 exhibited rapid inhibition of Trypanosoma brucei growth, apparently the result of cell cycle arrest that blocked the replication of mitochondrial DNA, contained in the kinetoplast, thereby preventing the initiation of S-phase. Incubation with either compound led to a rapid reduction in mitochondrial membrane potential, and ATP levels decreased by approximately 50% within 1 h. Between 4 and 8 h, cellular calcium levels increased, consistent with release from the depolarized mitochondria. Within the mitochondria, the Succinate Dehydrogenase complex (SDH) was investigated as a target for bisphosphonium salts, but while its subunit 1 (SDH1) was present at low levels in the bloodstream form trypanosomes, the assembled complex was hardly detectable. RNAi knockdown of the SDH1 subunit produced no growth phenotype, either in bloodstream or in the procyclic (insect) forms and we conclude that in trypanosomes SDH is not the target for bisphosphonium salts. Instead, the compounds inhibited ATP production in intact mitochondria, as well as the purified F-1 ATPase, to a level that was similar to 1 mM azide. Co-incubation with azide and bisphosphonium compounds did not inhibit ATPase activity more than either product alone. The results show that, in T. brucei, bisphosphonium compounds do not principally act on succinate dehydrogenase but on the mitochondrial FoF1 ATPase.
    PracovištěBiologické centrum (od r. 2006)
    KontaktDana Hypšová, eje@eje.cz, Tel.: 387 775 214
    Rok sběru2017
Počet záznamů: 1  

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