EFFECTS OF A GARLIC-DERIVED PRINCIPLE (AJOENE) ON AGGREGATION AND ARACHIDONIC-ACID METABOLISM IN HUMAN BLOOD-PLATELETS

Citation
Kc. Srivastava et Od. Tyagi, EFFECTS OF A GARLIC-DERIVED PRINCIPLE (AJOENE) ON AGGREGATION AND ARACHIDONIC-ACID METABOLISM IN HUMAN BLOOD-PLATELETS, Prostaglandins, leukotrienes and essential fatty acids, 49(2), 1993, pp. 587-595
Citations number
30
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
09523278
Volume
49
Issue
2
Year of publication
1993
Pages
587 - 595
Database
ISI
SICI code
0952-3278(1993)49:2<587:EOAGP(>2.0.ZU;2-C
Abstract
When garlic cloves are chopped or crushed several dialkyl thiosulfinat es are rapidly formed by the action of the enzyme alliin lyase or alli inase (EC 4.4.1.4) on S(+)-alkyl-L-cysteine sulfoxides. Allicin (diall yl thiosulfinate or allyl 2-propene thiosulfinate) is the dominant thi osulfinate released. A variety of sulfur containing compounds are form ed from allicin and other thiosulfinates depending on the way in which garlic is handled. One such compound identified recently is ajoene wh ich has been reported to possess antithrombotic properties. We present here data on the antiplatelet properties of ajoene together with its effects on the metabolism of arachidonic acid (AA) in intact platelets . Thus, ajoene was found to inhibit platelet aggregation induced by AA , adrenaline, collagen, adenosine diphosphate (ADP) and calcium ionoph ore A23187; the nature of the inhibition was irreversible. In washed p latelets stimulated by labelled arachidonate, ajoene inhibited the for mation of thromboxane A2; 12-lipoxygenase product(s) were reduced at h igher ajoene concentrations. This garlic-derived substance inhibited t he incorporation of labelled AA into platelet phospholipids at higher concentration. In labelled platelets, on stimulation with either calci um ionophore A23187 or collagen, reduced amounts of thromboxane and 12 -HETE (12-hydroxyeicosatetraenoic acid) were produced in ajoene-treate d platelets compared to control platelets. This substance had no effec t on the deacylation of platelet phospholipids. The results suggest th at at least one of the mechanisms by which ajoene shows antiplatelet e ffects could be related to altered metabolism of AA.