TY  - JOUR
PY  - 2013//
TI  - Histological and ultrastructural analyses of muscle damage induced by a myotoxin isolated from Bothrops alternatus snake venom
JO  - Protein and peptide letters
A1  - Mamedea, Carla Cristine Neves
A1  - de Queiroz, Mayara Ribeiro
A1  - Fonseca, Kelly Cortes
A1  - de Morais, Nadia Cristina Gomes
A1  - Filho, Saulo Antônio Gomes
A1  - Beletti, Marcelo Emílio
A1  - Stanziola, Leonilda
A1  - de Oliveira, Fábio
SP  - 192
EP  - 199
VL  - 20
IS  - 2
N2  - Muscular necrosis is a serious consequence of Bothrops snake bites that may lead to permanent loss of tissue or function. Myonecrosis may be due to injury to blood vessels, destabilization and/or rupture of plasma membrane, and inflammatory mechanisms triggered by different proteins from the snake venom. In this work we describe the isolation and partial functional characterization of a myotoxin from B. alternatus snake venom. The myotoxin was isolated by a combination of ion exchange and gel filtration chromatography and displayed a molecular weight of approximately 15,000, as estimated by SDS-PAGE under reducing conditions. In non-reducing conditions a protein band of approximately 25,000 was also observed, suggesting that its native form is a homodimer. The myotoxin induced myonecrosis, but had no proteolytic and phospholipase A2 activities. The myotoxic activity was assessed on the basis of the histological and ultrastructural alterations induced by the toxin in the gastrocnemius skeletal muscle of Swiss mice. The toxin led to a series of drastic degenerative events characterized by extensive cellular destruction, loss of the arrangements of skeletal fibers, intense infiltration of inflammatory cells, fatty degeneration and hemorrhage. Electron microscopy analyses revealed that the myotoxin caused cell swelling, mitochondrial alterations and dilation of the sarcoplasmic reticulum, but did not affect the integrity of the muscle cell membranes. The myonecrosis caused by this toxin was related to the perturbation in the membrane permeability, intracellular alterations and inflammatory reaction.<p />  <p>Language: en</p>
LA  - en
SN  - 0929-8665
UR  - http://dx.doi.org/
ID  - ref1
ER  -