Advances in research on the nephrotoxicity of uranium and its molecular mechanism
10.20001/j.issn.2095-2619.20241018
- VernacularTitle:铀的肾毒性及其分子机制研究进展
- Author:
Jiamei BAI
1
;
Xuhong DANG
;
Yayi YUAN
;
Ruifeng ZHANG
Author Information
1. China Institute of Radiation Protection, Taiyuan, Shanxi 030006, China
- Publication Type:Review
- Keywords:
Uranium;
Nephrotoxicity;
Molecular mechanism;
Research progress
- From:
China Occupational Medicine
2024;51(5):581-585
- CountryChina
- Language:Chinese
-
Abstract:
With the extensive application of uranium in military, industrial and civil fields, the possibility of human exposure to uranium has become increasingly likely. When uranium is accidentally released into the environment, it can enter the human body by various pathways and accumulate in the kidneys, leading to proximal tubule epithelial cell damage or even death, and in severe cases, nephrotoxicity. Uranium exerts both chemical and radiological toxicity, with its kidney-damaging effects primarily attributed to chemical toxicity. Low-level uranium exposure causes mild kidney damage, while prolonged or high-level exposure alters kidney structure and biomarker level of uranium-induced nephrotoxicity (such as creatinine, urea nitrogen and kidney injury molecule-1, etc.). Uranium exposure also induces DNA damage and mutations, kidney inflammation, and renal cell autophagy. Current research on uranium nephrotoxicity primarily focuses on uranium-induced mitochondrial dysfunction, which leads to oxidative stress and apoptosis (mainly by mitochondrial and endoplasmic reticulum pathway), ultimately causing renal tissue damage. However, the molecular mechanisms underlying uranium-induced kidney toxicity remain incomplete. Future research on mechanism of uranium-induced cell damage, especially metabolism, intracellular distribution, and additional mechanisms, remains a long-term and challenging endeavor.
