Evaluation of KIM-1 as an early biomarker of snakebite-induced AKI in mice

dc.contributor.authorDantas, Rodrigo Tavares
dc.contributor.authorSampaio, Tiago Lima
dc.contributor.authorLima, Dânya Bandeira
dc.contributor.authorMenezes, Ramon Róseo Paula Pessoa Bezerra de
dc.contributor.authorCanuto, Jader Almeida
dc.contributor.authorToyama, Marcos Hikari [UNESP]
dc.contributor.authorEvangelista, Janaína Serra Azul Monteiro
dc.contributor.authorMartins, Alice Maria Costa
dc.contributor.institutionUniversidade Federal do Ceará
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Estadual do Ceará
dc.date.accessioned2018-12-11T17:21:02Z
dc.date.available2018-12-11T17:21:02Z
dc.date.issued2018-09-01
dc.description.abstractAcute kidney injury (AKI) is one of the most important complications of bothropic poisoning and its early identification remains challenging. The nephrotoxicity of Bothrops insularis venom (BinsV) was previously described by our research group. In this study, we continued to evaluate the effect of BinsV on kidney function in mice and LLC-MK2 proximal tubule cells, evaluating KIM-1 protein as an early AKI biomarker. Male Swiss mice were inoculated with BinsV intramuscularly and observed for 24 h in a metabolic cage model. Urine and blood were collected for biochemical analyses and the kidneys were examined for oxide-reducing balance and submitted to histological analysis. LLC-MK2 cells incubated with BinsV were assessed for cell viability and cell death mechanism by flow cytometry. Histological analysis of the kidneys indicated AKI and the oxide-reducing analyses demonstrated a decreasing in reduced glutathione (GSH) levels and an increasing on Malondialdehyde (MDA) levels. BinsV was cytotoxic to LLC-MK2 and the cytometry analyses suggested necrosis. Within 24 h after the envenomation, urinary creatinine did not increase, but the urinary levels of KIM-1 increased. In conclusion, we found AKI evidence in the kidney tissue and the increase in the KIM-1 levels suggest it can be used as an early AKI biomarker.en
dc.description.affiliationDepartamento de Fisiologia e Farmacologia Universidade Federal do Ceará
dc.description.affiliationDepartmento de Análises Clínicas e Toxicológicas Universidade Federal do Ceará
dc.description.affiliationUnidade de São Vicente Campus do litoral Paulista Universidade do Estado de São Paulo (UNESP)
dc.description.affiliationPrograma de Pós-Graduação em Ciências Veterinárias Faculdade de Veterinária Universidade Estadual do Ceará
dc.description.affiliationUnespUnidade de São Vicente Campus do litoral Paulista Universidade do Estado de São Paulo (UNESP)
dc.format.extent24-28
dc.identifierhttp://dx.doi.org/10.1016/j.toxicon.2018.06.074
dc.identifier.citationToxicon, v. 151, p. 24-28.
dc.identifier.doi10.1016/j.toxicon.2018.06.074
dc.identifier.file2-s2.0-85049061949.pdf
dc.identifier.issn1879-3150
dc.identifier.issn0041-0101
dc.identifier.lattes8573195327542061
dc.identifier.scopus2-s2.0-85049061949
dc.identifier.urihttp://hdl.handle.net/11449/176501
dc.language.isoeng
dc.relation.ispartofToxicon
dc.relation.ispartofsjr0,692
dc.rights.accessRightsAcesso aberto
dc.sourceScopus
dc.subjectAcute kidney injury
dc.subjectBothropic envenomation
dc.subjectBothrops insularis venom
dc.subjectKIM-1
dc.titleEvaluation of KIM-1 as an early biomarker of snakebite-induced AKI in miceen
dc.typeArtigo
unesp.advisor.lattes8573195327542061
unesp.author.orcid0000-0003-3109-9683[4]

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