In vitro hemotoxic, α-neurotoxic and vasculotoxic effects of the Mexican black-tailed rattlesnake (Crotalus molossus nigrescens) venom
J Venom Res (2017), Vol 8, 1-8
Published online: 29 March 2017
David Meléndez-Martínez 1, Eduardo Macías-Rodríguez 1, Rodrigo Vázquez-Briones 1, Estuardo López-Vera 2, Martha Sandra Cruz-Pérez 3, Alejandra Vargas-Caraveo 1, Ana Gatica-Colima 1, Luis Fernando Plenge-Tellechea 1*
1 Laboratorio de Biología Molecular y Bioquímica, Departamento de Ciencias Químico Biológicas, Instituto de Ciencias Biomédicas, Universidad Autónoma de Ciudad Juárez, Chihuahua, México
2 Laboratorio de Toxinología Marina, Instituto de Ciencias del Mar y Limnología, Universidad Nacional Autónoma de México, Circuito Exterior s/n, Ciudad Universitaria, 04510 Coyoacán, Ciudad de México, México
3 Herpetario de la Universidad Autónoma de Querétaro, Facultad de Ciencias Naturales, Universidad Autónoma de Querétaro, Juriquilla, Querétaro, México
*Correspondence to: Luis Fernando Plenge-Tellechea, Email: email@example.com, Tel/Fax: +52 656 6881800 ext 1621
Received: 02 December 2016 | Revised: 03 March 2017 | Accepted: 09 March 2017
©Copyright The Author(s). First published by Library Publishing Media. This is an open access article, published under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0). This license permits non-commercial use, distribution and reproduction of this article, provided the original work is appropriately acknowledged, with correct citation details.
The Mexican black-tailed rattlesnake Crotalus molossus nigrescens is distributed in the Mexican plateau. Its venom is known to cause hemolysis and presents fibrinogen coagulase, collagenase and fibrinolytic activities. These activities may be associated with hemostatic alterations, such as platelet aggregation, hemolysis and fibrinolysis, often described in ophidic accidents. However, the mechanisms of action of the C. m. nigrescens venom remain unclear. In this study we investigated the in vitro hemotoxic, neurotoxic, and vasculotoxic effects of the venom. We found that this venom produces two types of hemolytic responses, Oxyhemoglobin release and Methemoglobin formation. As a result of the cytotoxicity to endothelial cells produces morphological biphasic toxicity. The first step in this process is characterized by morphological changes, as well as the loss of cellular adhesion and reduction in thickness. The second phase is characterized by massive cellular aggregation and death. It also induced laminin, type IV collagen, perlecan and nidogen degradation. However, the venom did not modulate the muscular fetal and neuronal nicotinic acetylcholine receptors activity. Thus, we concluded that the C. m. nigrescens venom produced hemolysis and hemorrhages via degradation of the basement membrane components and endothelial cell cytotoxicity, but not by neurotoxicity at the receptor level in nicotinic acetylcholine receptors.
KEYWORDS: Crotalus molossus nigrescens, hemolysis, hemorrhage, neurotoxicity, snake venom