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Systemic vascular leakage induced in mice by Russell’s viper venom from Pakistan
Envenomings by some populations of the Russell’s viper (Daboia russelii) are characterized by a systemic capillary leak syndrome (CLS) which causes hemoconcentration, and is associated with the severity of envenoming. We adapted a model of CLS in mice by assessing hemoconcentration. The venom of D....
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6208380/ https://www.ncbi.nlm.nih.gov/pubmed/30382131 http://dx.doi.org/10.1038/s41598-018-34363-1 |
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author | Rucavado, Alexandra Escalante, Teresa Camacho, Erika Gutiérrez, José María Fox, Jay W. |
author_facet | Rucavado, Alexandra Escalante, Teresa Camacho, Erika Gutiérrez, José María Fox, Jay W. |
author_sort | Rucavado, Alexandra |
collection | PubMed |
description | Envenomings by some populations of the Russell’s viper (Daboia russelii) are characterized by a systemic capillary leak syndrome (CLS) which causes hemoconcentration, and is associated with the severity of envenoming. We adapted a model of CLS in mice by assessing hemoconcentration. The venom of D. russelii from Pakistan, but not that of another viperid, Bothrops asper, induced hemoconcentration and an increment in vascular permeability, being devoid of hemorrhagic activity at the doses tested. These findings reveal a dichotomous pattern of vasculotoxicity in viperid snake venoms. This difference might depend on variations in venom composition, especially regarding metalloproteinases (SVMPs), which are low in Pakistani D. russelii and high in B. asper. Inhibition of SVMPs and phospholipases A(2) in D. russelii venom did not abrogate hemoconcentration. An hemoconcentration-inducing fraction was obtained by chromatography, which contains vascular endothelial growth factor (VEGF), a known potent inducer of increment in vascular permeability. Exudates collected from tissue injected with venom also induced hemoconcentration, and the effect was inhibited by antivenom. However, the amount of venom in exudate required to induce the effect is low, as compared with venom dissolved in saline solution, hence suggesting that endogenous proteins present in the exudate, probably inflammatory mediators, potentiate the effect. |
format | Online Article Text |
id | pubmed-6208380 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-62083802018-11-01 Systemic vascular leakage induced in mice by Russell’s viper venom from Pakistan Rucavado, Alexandra Escalante, Teresa Camacho, Erika Gutiérrez, José María Fox, Jay W. Sci Rep Article Envenomings by some populations of the Russell’s viper (Daboia russelii) are characterized by a systemic capillary leak syndrome (CLS) which causes hemoconcentration, and is associated with the severity of envenoming. We adapted a model of CLS in mice by assessing hemoconcentration. The venom of D. russelii from Pakistan, but not that of another viperid, Bothrops asper, induced hemoconcentration and an increment in vascular permeability, being devoid of hemorrhagic activity at the doses tested. These findings reveal a dichotomous pattern of vasculotoxicity in viperid snake venoms. This difference might depend on variations in venom composition, especially regarding metalloproteinases (SVMPs), which are low in Pakistani D. russelii and high in B. asper. Inhibition of SVMPs and phospholipases A(2) in D. russelii venom did not abrogate hemoconcentration. An hemoconcentration-inducing fraction was obtained by chromatography, which contains vascular endothelial growth factor (VEGF), a known potent inducer of increment in vascular permeability. Exudates collected from tissue injected with venom also induced hemoconcentration, and the effect was inhibited by antivenom. However, the amount of venom in exudate required to induce the effect is low, as compared with venom dissolved in saline solution, hence suggesting that endogenous proteins present in the exudate, probably inflammatory mediators, potentiate the effect. Nature Publishing Group UK 2018-10-31 /pmc/articles/PMC6208380/ /pubmed/30382131 http://dx.doi.org/10.1038/s41598-018-34363-1 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Rucavado, Alexandra Escalante, Teresa Camacho, Erika Gutiérrez, José María Fox, Jay W. Systemic vascular leakage induced in mice by Russell’s viper venom from Pakistan |
title | Systemic vascular leakage induced in mice by Russell’s viper venom from Pakistan |
title_full | Systemic vascular leakage induced in mice by Russell’s viper venom from Pakistan |
title_fullStr | Systemic vascular leakage induced in mice by Russell’s viper venom from Pakistan |
title_full_unstemmed | Systemic vascular leakage induced in mice by Russell’s viper venom from Pakistan |
title_short | Systemic vascular leakage induced in mice by Russell’s viper venom from Pakistan |
title_sort | systemic vascular leakage induced in mice by russell’s viper venom from pakistan |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6208380/ https://www.ncbi.nlm.nih.gov/pubmed/30382131 http://dx.doi.org/10.1038/s41598-018-34363-1 |
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