Abstract
Inositol 1,4,5-trisphosphate (InsP3) and cyclic ADP-ribose (cADPR) released Ca2+ from microsome fraction prepared from Euglena gracilis in dose-dependent manners. Caffeine, which also induced Ca2+ release from the microsomes, caused desensitization of the Ca2+ response to cADPR, although the Ca2+ response to InsP3 was not affected by caffeine. Further, ruthenium red inhibited the Ca2+ release induced by cADPR, but not by InsP3. These results suggest that cADPR functions as an endogenous messenger to activate a caffeine-sensitive, Ca(2+)-release mechanism, whereas InsP3 induces Ca2+ release by a distinct mechanism in E. gracilis.
MeSH terms
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Adenosine Diphosphate Ribose / analogs & derivatives*
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Adenosine Diphosphate Ribose / antagonists & inhibitors
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Adenosine Diphosphate Ribose / pharmacology
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Animals
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Caffeine / pharmacology
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Calcium / metabolism*
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Cell Cycle / drug effects
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Cyclic ADP-Ribose
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Dose-Response Relationship, Drug
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Drug Interactions
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Euglena gracilis
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Inositol 1,4,5-Trisphosphate / pharmacology*
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Microsomes / drug effects
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Microsomes / metabolism
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Phosphodiesterase Inhibitors / pharmacology
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Ruthenium Red / pharmacology
Substances
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Phosphodiesterase Inhibitors
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Ruthenium Red
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Cyclic ADP-Ribose
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Adenosine Diphosphate Ribose
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Caffeine
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Inositol 1,4,5-Trisphosphate
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Calcium