PAF-like activity of O-acetylated sphingomyelin.
O-acetylated sphingomyelin (Ac-SM) was found to cause aggregation of rabbit platelets in vitro. The Ac-SM-induced aggregation was accompanied by subsequent desensitisation of platelets to platelet-activating factor (PAF). The activity of Ac-SM exceeded that of acyl-PAF by about fourfold. BN 52021, a specific PAF-receptor antagonist, was found to inhibit the Ac-SM-induced aggregation. These results, together with earlier reports that sphingomyelin can inhibit the effects of PAF, suggest a new physiological function for sphingomyelin as a regulator of PAF-receptor binding. A search for enzymes to catalyse specifically the acetylation and deacetylation of sphingomyelin is required to confirm the physiological existence of sphingomyelin derivatives.
Berdyshev
E V
EV
Laboratory of Comparative Biochemistry, Russian Academy of Sciences, Vladivostok.
Getmanova
O E
OE
D000107:Acetylation / Q000187:drug effects; D000818:Animals; D004224:Diterpenes; D046934:Ginkgolides; D007783:Lactones / Q000494:pharmacology; D010972:Platelet Activating Factor / Q000037:antagonists & inhibitors; D010974:Platelet Aggregation / Q000187:drug effects*; D011817:Rabbits; D013109:Sphingomyelins / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000494:pharmacology*; D013215:Starfish; D013552:Swine
D004224:Diterpenes; D046934:Ginkgolides; D007783:Lactones; D010972:Platelet Activating Factor; D013109:Sphingomyelins; C045856:ginkgolide B