Defibrinogenation by batroxobin and acylated batroxobin in rats.
The thrombin-like snake venom enzyme, batroxobin, was acylated by 4-amidinophenyl benzoate at the active site serine hydroxyl. From the enzymatically inactive benzoyl-batroxobin, batroxobin is generated with a half-life of deacylation of about 1 hour. The clotting activity of benzoyl-batroxobin in plasma is recovered with deacylation. The effect of batroxobin and benzoyl-batroxobin were studied following intravenous injection in rats. Compared to defibrinogenation with batroxobin, that obtained with benzoyl-batroxobin was much retarded. Batroxobin caused microthrombosis initially, which did not develop upon injection of benzoyl-batroxobin in equivalent doses.
Richter
M
M
Institute of Pharmacology and Toxicology, Medical Academy, Erfurt, GDR.
Paintz
M
M
Stürzebecher
J
J
D000215:Acylation; D000818:Animals; D012103:Batroxobin / Q000494:pharmacology*; D001550:Benzamidines; D001565:Benzoates; D005260:Female; D005340:Fibrinogen / Q000378:metabolism*; D005342:Fibrinolysis / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012697:Serine Endopeptidases / Q000494:pharmacology*; D013927:Thrombosis / Q000097:blood / Q000139:chemically induced
D001550:Benzamidines; D001565:Benzoates; C006491:4-amidinophenylbenzoate; D005340:Fibrinogen; D012103:Batroxobin; D012697:Serine Endopeptidases