Search

PubMedID: 31736398 Acute exposure to mercury chloride (HgCl2) causes acute kidney injury (AKI). Some metals interfere with protein folding, leading to endoplasmic reticulum stress (ERS), and the activation of cell death mechanisms, but in the case of mercury, there is no knowledge about whether the ERS mediates tubular damage. This study aimed to determinate if HgCl2 causes an AKI course with temporary activation of ERS and if this mechanism is involved in kidney cell death. Male mice were intoxicated with 5 mg/kg HgCl2 and sacrificed after 24, 48, 72, and 96 h of mercury administration. The kidneys of euthanized mice were used to assess the renal function, oxidative stress, redox environment, antioxidant enzymatic system, cell death, and reticulum stress markers (PERK, ATF-6, and IRE1? pathways). The results indicate temporary-dependent renal dysfunction, oxidative stress, and an increase of glutathione-dependent enzymes involved in the bioaccumulation process of mercury, as well as the enhancement of caspase 3 activity along with IRE1a, GADD-153, and caspase 12 expressions. Mercury activates the PERK/eIF2? branch during the first 48 h. Meanwhile, the activation of PERK/ATF-4 branch allowed for ATF-4, ATF-6, and IRE1? pathways to enhance GADD-153. It led to the activation of caspases 12 and 3, which mediated the deaths of the tubular and glomerular cells. This study revealed temporary-dependent ERS present during AKI caused by HgCl2, as well as how it plays a pivotal role in kidney cell damage. © 2019, © 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. Secretaría de Investigación y Posgrado, Instituto Politécnico Nacional Consejo Nacional de Ciencia y Tecnología Edgar Cano-Europa thanks COTEBAL-IPN for the support given this year for the realization of this project. The authors thank INSTITUTO POLITÉCNICO NACIONAL, SECRETARÍA DE INVESTIGACIÓN Y POSGRADO-IPN, and CONACyT for financial support. The researchers are fellows of EDI, COFAA, and SNI. more...