Phospholipase C from clostridium perfringens induces human platelet aggregation in plasma.
We studied the aggregating effect of different concentrations of phospholipase C (PLC) (extracted from Clostridium perfringens) on human platelet-rich plasma (PRP). PRP was preincubated with PLC for 3 min at 37 degrees C and the platelet aggregation was followed for 10 min. The threshold aggregating concentration (TAC) of PLC was 3-4 U/ml. We also studied the potentiation of PLC with other stimuli on platelet aggregation. Potentiating stimuli, such as arachidonic acid (AA), ADP. Platelet Activating Factor (PAF) and U-46619 (a stable analogue of cyclic endoperoxides) were all used at subthreshold concentrations. We also studied the possible inhibitory effect of aspirin, apyrase, TMQ, a prostaglandin endoperoxide/thromboxane receptor antagonist and BN-52021, a PAF receptor antagonist. Only aspirin and apyrase were able to reduce aggregation induced by PLC alone and PLC + AA and PLC + ADP respectively. TMQ and BN-52021 were inactive. In ex vivo experiments oral aspirin (500 mg) partially inhibited platelet aggregation induced by PLC alone, PLC + AA and PLC + ADP 2 and 24 h after administration. Aspirin 20 mg for 7 days also reduced aggregation induced by PLC + AA.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000328:Adult; D001081:Apyrase / Q000494:pharmacology; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology; D001241:Aspirin / Q000494:pharmacology; D003016:Clostridium perfringens / Q000201:enzymology; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects*; D010738:Type C Phospholipases / Q000302:isolation & purification / Q000494:pharmacology*
D001095:Arachidonic Acids; D016718:Arachidonic Acid; D000244:Adenosine Diphosphate; D010738:Type C Phospholipases; D001081:Apyrase; D001241:Aspirin