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Mitochondrial development in Trypanosoma brucei brucei transitional bloodstream forms.

E J Bienen1, M Saric, G Pollakis

  • 1Department of Medical and Molecular Parasitology, New York University Medical Center, NY 10010.

Molecular and Biochemical Parasitology
|April 11, 1991
PubMed
Summary

Mitochondria in transitional Trypanosoma brucei brucei bloodstream forms develop an electromotive force. This suggests these forms can produce ATP, challenging the long-held belief that bloodstream forms are incapable of this.

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Area of Science:

  • Mitochondrial biophysics
  • Parasitology
  • Cellular metabolism

Background:

  • Trypanosoma brucei brucei undergoes differentiation from mammal-infective long slender forms to tsetse vector procyclic forms.
  • Intermediate and short stumpy bloodstream forms represent transitional stages in this differentiation process.
  • Mitochondrial function and ATP production in bloodstream forms have been a subject of debate.

Purpose of the Study:

  • To investigate the development of mitochondrial electromotive force (EMF) in transitional Trypanosoma brucei brucei bloodstream forms.
  • To identify the components of the electron transport chain responsible for the observed mitochondrial EMF.
  • To determine the capacity for ATP production in the mitochondria of these transitional forms.

Main Methods:

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  • Rhodamine 123 accumulation was used to assess mitochondrial membrane potential.
  • Inhibition studies with 2,4-dinitrophenol, rotenone, salicylhydroxamic acid, antimycin A, and cyanide were performed.
  • Analysis of electron flow pathways involving NADH dehydrogenase and trypanosome alternative oxidase (TAO).

    • Main Results:

    • Mitochondria of transitional forms, unlike long slender forms, accumulate rhodamine 123, indicating a developed EMF.
    • The EMF is sensitive to inhibitors of Complex I (rotenone) and TAO (salicylhydroxamic acid), but not Complex III (antimycin A) or cyanide.
    • NADH dehydrogenase (Complex I) is identified as the source of the EMF, with TAO acting as the terminal oxidase.

    Conclusions:

    • The mitochondria of intermediate and short stumpy bloodstream forms of Trypanosoma brucei brucei possess a functional electron transport chain.
    • These mitochondria are likely capable of producing ATP through F1F0 ATPase activity or substrate-level phosphorylation, or both.
    • This finding challenges the established dogma that bloodstream form mitochondria are incapable of ATP production.