Hemostatic interference of Indian king cobra (Ophiophagus hannah) venom. Comparison with three other snake venoms of the subcontinent

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• 作者：Yashonandana J. Gowtham (1)
  M. S. Kumar (12)
  K. S. Girish (1)
  K. Kemparaju (1) kemparaj@rediffmail.com
• 关键词：Key words O. hannah – ; D. russellii – ; E. carinatus – ; N. naja – ; fibri(noge)nolytic – ; defibrinogenation – ; platelet aggregation
• 刊名：Biochemistry (Moscow)
• 出版年：2012
• 出版时间：June 2012
• 年：2012
• 卷：77
• 期：6
• 页码：639-647
• 全文大小：240.7 KB
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• 作者单位：1. Department of Studies in Biochemistry, University of Mysore, Manasagangothri, Mysore, 570006 Karnataka, India2. Department of Biochemistry, Government College for Women, Mandya, Karnataka, India
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Life Sciences
  Biochemistry
  Bioorganic Chemistry
  Microbiology
  Biomedicine
  Russian Library of Science
  
• 出版者：MAIK Nauka/Interperiodica distributed exclusively by Springer Science+Business Media LLC.
• ISSN：1608-3040

文摘

Unlike Naja naja, Bungarus caeruleus, Echis carinatus, and Daboia/Vipera russellii venoms, Ophiophagus hannah venom is medically ignored in the Indian subcontinent. Being the biggest poisonous snake, O. hannah has been presumed to inject several lethal doses of venom in a single bite. Lack of therapeutic antivenom to O. hannah bite in India makes any attempt to save the victim a difficult exercise. This study was initiated to compare O. hannah venom with the above said venoms for possible interference in hemostasis. Ophiophagus hannah venom was found to actively interfere in hemostatic stages such as fibrin clot formation, platelet activation/aggregation, and fibrin clot dissolution. It decreased partial thromboplastin time (aPTT), prothrombin time (PT), and thrombin clotting time (TCT). These activities are similar to that shown by E. carinatus and D. russellii venoms, and thus O. hannah venom was found to exert procoagulant activity through the common pathway of blood coagulation, while N. naja venom increased aPTT and TCT but not PT, and hence it was found to exert anticoagulant activity through the intrinsic pathway. Venoms of O. hannah, E. carinatus, and D. russellii lack plasminogen activation property as they do not hydrolyze azocasein, while they all show plasmin-like activity by degrading the fibrin clot. Although N. naja venom did not degrade azocasein, unlike other venoms, it showed feeble plasmin-like activity on fibrin clot. Venom of E. carinatus induced clotting of human platelet rich plasma (PRP), while the other three venoms interfered in agonist-induced platelet aggregation in PRP. Venom of O. hannah least inhibited the ADP induced platelet aggregation as compared to D. russellii and N. naja venoms. All these three venoms showed complete inhibition of epinephrine-induced aggregation at varied doses. However, O. hannah venom was unique in inhibiting thrombin induced aggregation.