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KMID : 0811719990030020199
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Korean Journal of Physiology & Pharmacology
1999 Volume.3 No. 2 p.199 ~ p.205
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Increase of Intracellular Ca2+ Concentration by Vibrio Vulnificus Cytolysin in Rat Platelets; Triggering Mechanism of Platelet Cytolysis
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Jin Bong Park
Soo Wan Chae
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Abstract
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Vibrio vulnificus cytolysin caused platelet cytolysis and increased intracellular calcium concentration ([Ca2+]i) of rat platelets in a concentration-dependent manner. In the presence of V. vulnificus cytolysin (3 HU/ml), lactate dehydrogenase (LDH) activity was increased from 1.3±0.4 of control to 64.3±3.4 in platelet suspension buffer. In Ca2+?free platelet suspension buffer, however, V. vulnificus cytolysin did not induce [Ca2+]i increase and LDH release. Addition of EGTA (2 mM) to suspension buffer after the initial Ca2+ influx reversed [Ca2+]i to the control level. However, a Ca2+ channel blocker verapamil (20μM) or mefenamic acid (20μM) did not inhibit V. vulnificus cytolysin-induced [Ca2+]i increase and LDH release. Divalent cations such as Co2+,Cd2+orMn2+ (2 mM each) also did not alter V. vulnificus cytolysin-induced [Ca2+]i increase and LDH release. V. vulnificus cytolysin (3 HU/ml)-induced calcium influx was completely blocked by lanthanum (2 mM). Lanthanum (2 mM) also completely blocked V. vulnificus cytolysin (3 HU/ml)-induced LDH release. Osmotic protectants such as, raffinose, sucrose or PEG600 (50 mM each) did not inhibit the lytic activity of V. vulnificus cytolysin. In conclusion, lanthanum sensitive Ca2+ influx plays a significant role in Vibrio vulnificus cytolysin-induced platelet cytolysis and thrombocytopenia in V. vulnificus infection.
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