RENAL ALTERATIONS PROMOTED BY Thalassophryne nattereri VENOM

Facó, P.E.G., Havt, A., Bezerra, G.P., Barbosa, P.S.F., Bezerra, I.S.A.M., Martins, A.M.C., Nobre, A.C.L., Fonteles, M.C., Lopes-Ferreira, M., Monteiro, H.S.A.

Butantan Institute and Federal University of Ceará, Brazil. 

The accidents with the Brazilian venomous fish, Thalassophryne nattereri (niquim), causes severe local damages including pain and necrosis. However its renal effects were never investigated. Our goal is to identify the possible renal alterations promoted by this fish using the isolated perfused rat kidney method. Wistar rats were anesthetized with sodium pentobarbitone (50mg/mL), and their kidneys were surgically removed following Fonteles and coworkers (Am. J. Physiol. 244, 235-346, 1983) technique. We used a Krebs-Henseleit perfusion solution (KHPS) modified by serum bovine albumin (6g%). Each experiment (n=6) lasted 120 minutes. We tested the effects of three doses (0.3, 1 and 3 mg/mL) named T1, T2 and T3, respectively. The venom was always administered 30 minutes after the beginning of each perfusion. The treated groups were compared to an external control group (CG) where we perfused the kidneys with only KHPS (ANOVA with *p<0,05). Thalassophryne nattereri venom altered intensely the renal parameters especially in the last 30 minutes of each experiment (120 min.). We noticed an increase after administration of all three doses in the perfusion pressure (CG₁₂₀ =111.5 ± 0.34, T1₁₂₀ = 147.8 ± 3.28*, T2₁₂₀ = 134.2 ± 0.94*, T3₁₂₀ = 130.2 ± 2.68* mmHg) and renal vascular resistance (CG₁₂₀ = 4.53 ± 0.07, T1₁₂₀ = 6.72 ± 0.15*, T2₁₂₀ = 5.13 ± 0.04*, T3₁₂₀ = 5.76 ± 0.13* mmHg/mL/g/min). The sodium and potassium tubular transport were reduced only with the dose of 3mg/mL (CG₁₂₀ = 81.15 ± 0.2, T3₁₂₀ = 73.10 ± 1.07* %), (CG₁₂₀ = 72.90 ± 0.84, T3₁₂₀ = 67.22 ± 1.63* %), respectively. The urinary flow and glomerular filtration rate were increased after 0,3 and 1 mg/mL, but decreased after 3 mg/mL. We concluded that the Thalassophryne nattereri venom was nephrotoxic and altered intensely the vascular and glomerular renal parameters, but tubular transport was only affected by the largest dose.

Supported by FUNCAP/FAPESP

CORRESPONDENCE TO:

Patrícia Emília Gomes Faço, Rua Síria nº 23, Fortaleza, CE, CEP: 60740840, Brasil, Email: patyfaco@uol.com.br