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Calcium mobilization by arachidonic acid in trypanosomatids
R Catisti1, S A Uyemura, R Docampo
1Department of Pathobiology, University of Illinois at Urbana-Champaign, Urbana 61802, USA.
Molecular and Biochemical Parasitology
|February 29, 2000
Summary
Calcium entry in trypanosomatids like Trypanosoma brucei is regulated by phospholipase A2 and arachidonic acid. Melittin and arachidonic acid stimulate calcium influx, potentially mobilizing intracellular stores and affecting cell membranes.
Area of Science:
- Parasitology
- Cell Biology
- Biochemistry
Background:
- Calcium influx in Trypanosoma brucei bloodstream trypomastigotes is linked to phospholipase A2 and arachidonic acid.
- This pathway involves arachidonic acid generation and calcium channel stimulation.
Purpose of the Study:
- To investigate calcium (Ca2+) influx regulation in various trypanosomatids.
- To explore the roles of melittin and arachidonic acid in Ca2+ signaling across different life stages and species.
Main Methods:
- Studied Ca2+ influx in T. brucei procyclic trypomastigotes, Leishmania donovani promastigotes, and T. cruzi amastigotes.
- Utilized melittin, arachidonic acid, a phospholipase A2 inhibitor, and LaCl3.
- Assessed intracellular Ca2+ ([Ca2+]i) changes, mitochondrial membrane potential, and acridine orange release.
Main Results:
- Melittin stimulated Ca2+ influx in a dose-dependent manner across all tested trypanosomatids.
- Arachidonic acid also induced Ca2+ entry, sensitive to LaCl3.
- Both agents increased [Ca2+]i in Ca2+-free medium, indicating intracellular Ca2+ mobilization.
- Arachidonic acid promoted Ca2+ release from acidocalcisomes.
Conclusions:
- Melittin and arachidonic acid stimulate Ca2+ entry in trypanosomatids, involving both plasma membrane channels and intracellular stores.
- Arachidonic acid can mobilize Ca2+ from acidocalcisomes.
- High concentrations of arachidonic acid may exert non-specific effects on trypanosomatid membranes.