| Literature DB >> 31145051 |
Yurisbeth Zanotty1,2, Marco Álvarez2, Lourdes Perdomo2, Elda E Sánchez3, María E Giron1, Juan C Jimenez4, Montamas Suntravat3, Belsy Guerrero5, Carlos Ibarra5, Yuyibeth Montero1, Rafael Medina1, Luis F Navarrete1, Alexis Rodríguez-Acosta1.
Abstract
Envenomation by the Venezuelan bushmaster snake (Lachesis muta muta) (Serpentes: Viperidae) is characterized by local and cardiac alterations. This study investigates the in vivo cardiac dysfunction, tissue destruction, and cellular processes triggered by Lachesis muta muta snake crude venom and a C-type lectin (CTL)-like toxin named Mutacytin-1 (MC-1). The 28 kDa MC-1 was obtained by molecular exclusion, ion exchange, and C-18 (checking pureness) reverse-phase chromatographies. N-terminal sequencing of the first eight amino acids (NNCPQ LLM) revealed 100% identity with Mutina (CTL-like) isolated from Lachesis stenophrys, which is a Ca2+-dependent-type galactoside-binding lectin from Bothrops jararaca and CTL BpLec from Bothrops pauloensis. The cardiotoxicity in zebrafish of MC-1 was evaluated by means of specific phenotypic expressions and larvae behavior at 5, 15, 30, 40 and 60 min post-treatment. The L. muta muta venom and MC-1 also produced heart rate/rhythm alterations, circulation modifications, and the presence of thrombus and apoptotic phenomenon with pericardial damages. Acridine orange (100 μg/mL) was used to visualize apoptosis cellular process in control and treated whole embryos. The cardiotoxic alterations happened in more than 90% of all larvae under the action of L. muta muta venom and MC-1. The findings have demonstrated the potential cardiotoxicity by L. muta muta venom, suggesting the possibility of cardiovascular damages to patients after bushmaster envenoming.Entities:
Keywords: cardiotoxicity; larvae; venom; zebrafish
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Year: 2019 PMID: 31145051 PMCID: PMC6685195 DOI: 10.1089/zeb.2019.1731
Source DB: PubMed Journal: Zebrafish ISSN: 1545-8547 Impact factor: 1.985