期刊
TOXICON
卷 181, 期 -, 页码 45-52出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.toxicon.2020.04.095
关键词
Coral snake; Acute kidney injury; Kidney perfusion; Cytotoxicity
资金
- Conselho Nacional de Desenvolvimento Cientifico e Tecnol.ogico (CNPq)
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
The Micrurus snake venoms mainly cause systemic complications, essentially neurotoxicity. Previous studies, however, have described that they are involved in the occurrence of acute kidney injury (AKI) in animal models. AKI pathogenesis in snakebites is multifactorial and involves immunological reactions, hemodynamic disturbances, and direct nephrotoxicity. The aim of this study was to compare the nephrotoxic effects of coral snake venoms from M. browni (MbV) and M. laticollaris (MIV) on the proximal tubular epithelial cell line (LLC-MK2) and isolated perfused kidney. Using an MTT assay, both venoms significantly reduced cell viability at higher concentrations (25-100 mu g/mL). MIV (10 mu g/mL) increased the perfusion pressure (PP) at 60, 90 and 120 min, while the MbV did it only at 90 and 120 min. Renal vascular resistance (RVR) decreased at 60 min and increased at 120 min with MbV, but decreased at 60, 90 and 120 min with MIV. Urinary flow (UF) alterations were not observed with MIV, but MbV elevated them at 90 and 120 min. Both venoms significantly decreased the glomerular filtration rate (GFR), %TNa+, %11X(+) and %TC1(-) levels as of 60 min of perfusion. Oxidative stress analysis revealed that both venoms behaved similarly, reducing glutathione and increasing malondialdehyde levels. Kidney injury is not usually described in clinical cases of Micrurus snakebites. However, the potential for nephrotoxicity should be considered in the overall picture of envenomation.
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