Journal
JOURNAL OF TOXICOLOGICAL SCIENCES
Volume 45, Issue 9, Pages 589-598Publisher
JAPANESE SOC TOXICOLOGICAL SCIENCES
DOI: 10.2131/jts.45.589
Keywords
Acute mercury chloride poisoning; Acute kidney injury; endoplasmic reticulum stress; Poisoning
Categories
Funding
- National Nature Science Foundation of China [NFSC: 81802474]
- Nature Science Foundation of Shandong Province, China [ZR2018MH040, ZR2018MC012]
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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.
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