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The role of endoplasmic reticulum stress in renal damage caused by acute mercury chloride poisoning.

Abstract
Acute mercury chloride (HgCl2) poisoning may lead to kidney injury, but the underlying mechanism remains largely unknown. Endoplasmic reticulum (ER) stress plays a role in some heavy metal poisoning. Whether it mediates kidney injury in acute HgCl2 poisoning remains unknown. In this study, we examined the kidney injury and the corresponding ER stress in the mouse model of different doses of acute HgCl2 poisoning. To further confirm the role of ER stress, we tested the effects of its chemical chaperone [4-phenylbutyric acid (4-PBA)]. The results revealed that acute HgCl2 poisoning caused more severe kidney injury with dose on and activated ER stress, as indicated by increased expression of GRP78 and CHOP. Inhibition of ER stress restored the functional and morphological changes of kidneys, and partly attenuated renal tubular epithelial cell apoptosis. In summary, ER stress contributes to the acute kidney injury following HgCl2 poisoning, and inhibition of ER stress may alleviate the kidney injury via reducing apoptosis.
AuthorsYuxin Zhong, Baoqiang Wang, Shan Hu, Tingting Wang, Yumiao Zhang, Jinling Wang, Yuqing Liu, Hongxia Zhang
JournalThe Journal of toxicological sciences (J Toxicol Sci) Vol. 45 Issue 9 Pg. 589-598 ( 2020) ISSN: 1880-3989 [Electronic] Japan
PMID32879258 (Publication Type: Journal Article)
Chemical References
  • 4-phenylbutylamine
  • Butylamines
  • Ddit3 protein, mouse
  • Endoplasmic Reticulum Chaperone BiP
  • HSPA5 protein, human
  • Heat-Shock Proteins
  • Hspa5 protein, mouse
  • Transcription Factor CHOP
  • Mercuric Chloride
Topics
  • Acute Kidney Injury (etiology)
  • Animals
  • Butylamines
  • Disease Models, Animal
  • Endoplasmic Reticulum Chaperone BiP
  • Endoplasmic Reticulum Stress (genetics, physiology)
  • Gene Expression
  • Heat-Shock Proteins (genetics, metabolism)
  • Humans
  • Male
  • Mercuric Chloride (poisoning)
  • Mice, Inbred C57BL
  • Transcription Factor CHOP (genetics, metabolism)

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