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Action of heparin and acetylcholine modulators on the neurotoxicity of the toad Rhinella schneideri (Anura: Bufonidae) in Brazil / Acción de la heparina y moduladores de acetilcolina en la neurotoxicidad del sapo Rhinella schneideri (Anura: Bufonidae) en Brasil
Rostelato-Ferreira, Sandro; Vettorazzo, Orlando-B; Tribuiani, Natália; Leal, Allan-P; Dal-Belo, Cháriston-A; Rodrigues-Simioni, Léa; Floriano, Rafael-S; Oshima-Franco, Yoko.
Afiliação
  • Rostelato-Ferreira, Sandro; Institute of Health Sciences. Paulista University. BR
  • Vettorazzo, Orlando-B; Graduate Program in Pharmaceutical Sciences. University of Sorocaba. BR
  • Tribuiani, Natália; Graduate Program in Pharmaceutical Sciences. University of Sorocaba. BR
  • Leal, Allan-P; Graduate Program in Toxicological Biochemistry. Federal University of Santa Maria. BR
  • Dal-Belo, Cháriston-A; Graduate Program in Toxicological Biochemistry. Federal University of Santa Maria. BR
  • Rodrigues-Simioni, Léa; Department of Pharmacology. Faculty of Medical Sciences. State University of Campinas. BR
  • Floriano, Rafael-S; Graduate Program in Health Sciences. University of Western São Paulo. BR
  • Oshima-Franco, Yoko; Graduate Program in Pharmaceutical Sciences. University of Sorocaba. BR
Rev. biol. trop ; 69(2)jun. 2021.
Artigo em Inglês | LILACS, SaludCR | ID: biblio-1387647
Biblioteca responsável: CR1.1
ABSTRACT
Abstract

Introduction:

Rhinella schneideri is a toad widely distributed in South America and its poison is characterized by inducing cardiotoxicity and neurotoxicity.

Objective:

In this work, we investigated pharmacological strategies to attenuate the peripheral neurotoxicity induced by R. schneideri poison in avian neuromuscular preparation.

Methods:

The experiments were carried out using isolated chick biventer cervicis preparation subjected to field stimulation for muscle twitches recordings or exposed to acetylcholine and potassium chloride for contracture responses.

Results:

Poison (10 μg/ml) produced complete neuromuscular blockade in chick biventer cervicis preparation within approximately 70 min incubation (times for 50 and 90 % blockade 15 ± 3 min and 40 ± 2 min, respectively; P < 0.05, N= 5); contracture responses to exogenous acetylcholine and KCl were unaffected by poison indicating no specificity with postsynaptic receptors or myotoxicity, respectively. Poison (10 μg/ml)-induced neuromuscular blockade was not prevented by heparin (5 and 150 IU/ml) under pre- or post-treatment conditions. Incubation at low temperature (23-25 °C) abolished the neuromuscular blockade; after raising the temperature to 37 °C, the complete neuromuscular blockade was slightly slower than that seen in preparations directly incubated at 37 °C (times for 50 and 90 % blockade 23 ± 2 min and 60 ± 2.5 min, respectively; P < 0.05, N= 4). Neostigmine (3.3 μM) did not reverse the neuromuscular blockade in BC preparation whereas 3,4-diaminopyridine (91.6 μM) produced a partial and sustained reversal of the twitch responses (29 ± 7.8 % of maximal reversal reached in approximately 40 min incubation; P < 0.05, N= 4).

Conclusions:

R. schneideri poison induces potent peripheral neurotoxicity in vitro which can be partially reversible by 3,4-diaminopyridine.
RESUMEN
Resumen

Introducción:

Rhinella schneideri está ampliamente distribuida en Suramérica y su veneno es caracterizado por inducir cardiotoxicidad y neurotoxicidad.

Objetivo:

En este trabajo, investigamos estrategias farmacológicas para atenuar la neurotoxicidad periférica inducida por el veneno de R. schneideri en preparaciones neuromusculares de aves.

Métodos:

Los experimentos fueron realizados usando preparaciones de biventer cervicis de pollos sometidas a estimulación de campo para el registro de las contracciones musculares o expuestas a la acetilcolina y al cloruro de potasio para la respuesta contractural.

Resultados:

El veneno (10 µg/ml) provocó un bloqueo neuromuscular completo en las preparaciones después de aproximadamente 70 min de incubación (tiempos para 50 y 90 % de bloqueo 15 ± 3 min y 40 ± 2 min, respectivamente; P < 0.05, N = 5); las contracturas en respuesta a la acetilcolina y el KCl exógenos no fueron afectadas por el veneno, indicando que no hay una interacción especifica con receptores postsinápticos o miotoxicidad respectivamente. El bloqueo neuromuscular causado por el veneno (10 µg/ml) no fue prevenido por la heparina (5 y 150 UI/ml) bajo condiciones pre y post-tratamiento. La incubación a bajas temperaturas (23-25 ºC) abolió el bloqueo neuromuscular; después de aumentar la temperatura a 37 ºC, el bloqueo neuromuscular total fue levemente más lento que el visto en preparaciones directamente incubadas a 37 ºC (tiempos para 50 y 90 % de bloqueo 23 ± 2 min y 60 ± 2.5 min, respectivamente; P < 0.05, N= 4). Neostigmina (3.3 µM) no revirtió el bloqueo neuromuscular, mientras que 3.4-diaminopiridina (91.6 µM) produjo una reversión parcial y sostenida de las respuestas neuromusculares (29 ± 7.8 % de la reversión máxima alcanzada en aproximadamente 40 min de incubación; P < 0.05, N = 4).

Conclusiones:

El veneno de R. schneideri indujo neurotoxicidad periférica potente in vitro, el cual puede ser revertido por 3.4-diaminopiridina.
Assuntos

Texto completo: Disponível Base de dados: LILACS / SaludCR Assunto principal: Bufo marinus / Bloqueio Neuromuscular Tipo de estudo: Estudo observacional Idioma: Inglês Revista: Rev. biol. trop Ano de publicação: 2021 Tipo de documento: Artigo Instituição/País de afiliação: Department of Pharmacology/BR / Graduate Program in Health Sciences/BR / Graduate Program in Pharmaceutical Sciences/BR / Graduate Program in Toxicological Biochemistry/BR / Institute of Health Sciences/BR
Texto completo: Disponível Base de dados: LILACS / SaludCR Assunto principal: Bufo marinus / Bloqueio Neuromuscular Tipo de estudo: Estudo observacional Idioma: Inglês Revista: Rev. biol. trop Ano de publicação: 2021 Tipo de documento: Artigo Instituição/País de afiliação: Department of Pharmacology/BR / Graduate Program in Health Sciences/BR / Graduate Program in Pharmaceutical Sciences/BR / Graduate Program in Toxicological Biochemistry/BR / Institute of Health Sciences/BR
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