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Cell death in trichomonads: new insights
Rafael M Mariante1, Ricardo G Vancini, Marlene Benchimol
1Programa de Ciências Morfológicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.
Histochemistry and Cell Biology
|November 8, 2005
Summary
Tritrichomonas foetus treated with griseofulvin shows significant morphological changes and phosphatidylserine exposure, suggesting alternative cell death pathways beyond caspase-3 activation. This parasite
Area of Science:
- Parasitology
- Cell Biology
- Biochemistry
Background:
- Tritrichomonas foetus is an amitochondriate parasite lacking typical mitochondrial cell death pathways.
- Understanding cell demise mechanisms in T. foetus is crucial due to its unique organelles (hydrogenosomes).
- Previous studies suggested a caspase-like pathway in trichomonads.
Purpose of the Study:
- To investigate the effects of the fungicide griseofulvin on T. foetus cell death.
- To explore potential alternative cell death mechanisms in T. foetus.
- To characterize morphological and molecular alterations induced by griseofulvin.
Main Methods:
- Treatment of T. foetus cultures with griseofulvin.
- Morphological analysis using microscopy (observing plasma membrane, nuclear envelope, vacuoles).
- Detection of phosphatidylserine (PS) exposure and assessment of caspase-3 activity.
Main Results:
- Griseofulvin induced dramatic morphological changes: plasma membrane and nuclear envelope blebbing, nucleus fragmentation, and enlarged vacuoles.
- Phosphatidylserine exposure on the outer plasma membrane leaflet was observed.
- Misshapen flagella and tubulin precipitates within vacuoles suggest autophagy; activated caspase-3 was notably absent.
- Absence of caspase-3 activation during griseofulvin treatment contrasts with H2O2 treatment.
Conclusions:
- Griseofulvin triggers distinct cell death processes in T. foetus, differing from hydrogen peroxide-induced death.
- The findings support the existence of multiple, potentially non-caspase-dependent, cell death pathways in T. foetus.
- Autophagy may play a role in clearing abnormal cellular components during griseofulvin-induced cell demise.