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KMID : 0359319960360040873
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Korean Journal of Veterinary Research
1996 Volume.36 No. 4 p.873 ~ p.886
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Effects of cyclopiazonic acid and aflatxin B1 on arachidonic acid metabolism , calcium mobilization and ultrastructure in rabbit platelet aggregation
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장동덕/Jang, Dong Deuk
조명행/홍충만/Cho, Myung Haing/Hong, Choong Man
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Abstract
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For better understanding the interrelationship of hemorrhage and aggregation mechanism, cyclopiazonic acid(CPA) known as promoting the aggregation of platelet, aflatoxin B₁(AFB₁) inhibiting platelet aggregation were used as toxic mycotoxins in these studies. In order to investigate the potential role of prostaglandin metabolism on the platelet aggregation, a variety of prostaglandin metabolites such as PGF_(2α), PGE₂and TXB₂were measured in homogenized rabbit platelets by TLC and LSC. And the role of Ca^(++) on the platelet aggregation was investigated by flow cytometer. Finally, the morphological effects of mycotoxins on platelet were determined by transmission electron microscope. The results and conclusions obtained from these studies are: 1) CPA induced no changes but AFB₁increased PGE₂and TXB₂. 2) CPA promoted ADP, collagen, thrombin, A.A., and PAF-induced Ca^(++) release. AFB₁, however, decreased Ca^(++) level except collagen-induced Ca^(++) release. When the calcium blocker, verapamil, was used, CPA decreased thrombin-induced Ca^(++) release and increased collagen, ADP, PAF and A.A.-induced Ca^(++) release. AFB₁in contrast decreased the all factors induced Ca^(++) release. 3) AFB₁did not induce any ultrastructural changes except large vacuole formation in a few platelets. And CPA also did not induce any changes except moderate shape change, indicator of platelet activation. In conclusion, CPA promoted platelet aggregation by the increases of Ca^(++) release but had no changes in A.A. metabolites. Antiaggregating effects of AFB₁may be due to decreases of Ca^(++) release and increases of PGE₂and PGF_(2α) formation.
These data provide the basis for the future study of mobilization and function of Ca^(++) in platelet aggregation.
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KEYWORD
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