PRELIMINARY CHARACTERIZATION OF HEPATOTOXICTY OF CROTALIC VENOM

Teixeira, G.N.(1), Vilela-Goulart M.G.(2), Iakimoff; A.(1), Bastos, W.P.(3), Mattos Filho T. R.(2), Pacheco, C.S.(1), Lopes-Martins, R.A.(1), Cogo, J.C.(1), Ribeiro, W.(1)

(1)Universidade do Vale do Paraíba, IP&D- Serpentário do CEN, São José dos Campos, (2)Universidade de Campinas, Faculdade Odontologia de Piracicaba, (3)Universidade Estadual de São Paulo, Faculdade de Odontologia de São José dos Campos, SP, Brazil.

The purpose of this study was to investigate the hepatoprotective effect of calcium channel blocker verapamil against the of Crotalus durissus terrificus (C.d.t.) venom. 48 Wistar male rats (250 ±50g) were divided in 4 groups of 12 rats each. The groups were divided in 4 sub-groups (n=3) sacrificed at the time 1 h, 2h, 3h, and 12h, after saline, verapamil, venom and verapamil + venom administration. The samples were processed and centrifuged to posterior analyze of the enzymes: alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma glutamiltransferase(Gamma GT), acetyl cholinesterase (AchE) and total protein (TP). Control group (G1): Inoculated only with saline, Venom group (G2): Inoculated with C.d.t. venom (100 mg of venom to each Kg of rat weight), Verapamil group (G3): Inoculated i.p. with verapamil(26,7 mg/Kg), Venom + Verapamil(G4): Pre-treated with verapamil (26,7 mg/Kg) before 2 hour of the venom administration. The group G2 showed elevations of enzymes derived from liver tissue when compared with all groups. Already G4 showed reduced liver tissue enzymes levels when compared with G2. The values of hepatic tissue enzymes at the time of 1 hour to G4 vsG2 were respectively: ALP : 6,67 ±1,98 vs 12,52 ±3,22 (U/L), ALT: 71,33 ±3,77 vs 127,13 ±6,06 (U/L), AST: 102,56 ±41,36 vs149,27 ±5,15 (U/L), GGT: 124,64 ±27,53 vs  295,95 ±102,80 (U/L),  AchE: 6,84 ±1,73 vs 9,87 ±0,85 (U/ml), TP: 1,93 ±0,21 vs 3,51 ±0,95 (g/DL). In conclusion, we suggest that calcium channel blockers may have a role to play in limiting hepatocellular damage, especially the increase of liver dysfunction mechanism due the cytoplasmatic and mithocondrial lesions, resulting, in the elevation of enzymes derived from liver tissue.

CORRESPONDENCE TO:

Gustavo Neves Teixeira, Universidade do Vale do Paraíba, UNIVAP - Serpentário do CEN - Avenida Shishima Hifumi, 2911, São José dos Campos, SP, CEP: 12244-000, Brasil, Email: gustavo_teixeira@bol.com.br