Kininogenase activity of Thalassophryne nattereri fish venom

Kininogenase activity of Thalassophryne nattereri fish venom

Autor Lopes-Ferreira, M. Google Scholar
Emim, JADS Google Scholar
Oliveira, V Google Scholar
Puzer, L. Google Scholar
Cezari, M. H. Google Scholar
Araujo, MDS Google Scholar
Juliano, L. Google Scholar
Lapa, A. J. Google Scholar
Souccar, C. Google Scholar
Silva, AMMA Google Scholar
Instituição Inst Butantan
Universidade Federal de São Paulo (UNIFESP)
Resumo Accidents caused by the venomous fish Thalassophryne nattereri are characterized by edema, intense pain and necrosis at the site of the sting. This study assessed the nociceptive and edematogenic activities of T nattereri venom after injection into the mouse hindpaw and determination of the paw licking duration and weight. Subplantar injections of the venom (0.1-6 mug) induced a dose-related increase of the paw licking time and paw swelling with maximal values at 3 mug (209.5+/-57.5 s and 135.0+/-6.8 mg, respectively). Pretreatment of mice with either indomethacin (10 mg/kg, i.p.), a cyclooxygenase inhibitor, dexamethasone (1 mg/kg, s.c.), a steroid anti-inflammatory agent, cyproheptadine (1 mg/kg, i.p.), antagonist of serotonin receptors or L-NAME (100 mg/kg, s.c.), inhibitor of nitric oxide syntase, did not affect the venom-induced nociceptive and edematogenic responses. Injection of the opioid analgesic fentanyl (0.1 mg/kg, s.c.) reduced the paw licking time induced by 1 mug venom by 84% of control, without affecting the paw swelling. Both nociceptive and edematogenic responses were reduced after treatment with a specific tissue kallikrein inhibitor (TKI, 100 mg/kg, i.p.) by 78% and 24% from control values, respectively. Administration of a specific plasma kallikrein inhibitor (PKSI527, 100 mg/kg, s.c.) did not affect the venom-induced nociceptive response, but it decreased the paw edema by 15% from control. After injection of the angiotensin-converting enzyme inhibitor captopril (100 mg/kg, i.p.) the venom-induced nociceptive end edematogenic responses were increased by two-fold. the role of kallikreins possibly present in the venom was further assessed by hydrolysis of human kininogen and kininogen-derived synthetic peptides, showing the release of kallidin (Lys-bradykinin). the hydrolysis was inhibited by metal chelating agents but not by serino-, aspartyl- or cysteino-proteinase inhibitors. the data suggest that a protease with tissue-kallikrein-like activity plays a major role in nociception and edema induced by T. nattereri venom and this should be considered to achieve efficient treatments for human accidents with this venom. (C) 2004 Elsevier Inc. All rights reserved.
Palavra-chave Thalassophryne nattereri
edema
Nociception
specific tissue kallikrein inhibitor
Lys-bradykinin
Idioma Inglês
Data de publicação 2004-12-01
Publicado em Biochemical Pharmacology. Oxford: Pergamon-Elsevier B.V., v. 68, n. 11, p. 2151-2157, 2004.
ISSN 0006-2952 (Sherpa/Romeo, fator de impacto)
Publicador Elsevier B.V.
Extensão 2151-2157
Fonte http://dx.doi.org/10.1016/j.bcp.2004.07.037
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000224952200006
Endereço permanente http://repositorio.unifesp.br/handle/11600/28035

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