ArticleScientific reports2016
Differential protein expression in metallothionein protection from depleted uranium-induced nephrotoxicity.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 32 citations in OpenAlex.
- Study on the mechanism of vitamin E alleviating non-alcoholic fatty liver function based on non-targeted metabolomics analysis in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Gallic acid rescues uranyl acetate induced-hepatic dysfunction in rats by its antioxidant and cytoprotective potentials.BMC complementary medicine and therapies · 2023Article
- Article
- Review of Knowledge of Uranium-Induced Kidney Toxicity for the Development of an Adverse Outcome Pathway to Renal Impairment.International journal of molecular sciences · 2022Review
- Use of omics analysis for low-dose radiotoxicology and health risk assessment: the case of uranium.Environmental epigenetics · 2022Review
- The association of blood lead levels and renal effects may be modified by genetic combinations of Metallothionein 1A 2A polymorphisms.Scientific reports · 2020Article
- Nephrotoxicity: Role and significance of renal biomarkers in the early detection of acute renal injury.Journal of advanced pharmaceutical technology & researchReview
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The purpose of this study was to investigate the underlying mechanism of metallothionein (MT) protection from depleted uranium (DU) using a proteomics approach to search for a DU toxicity-differential protein. MT-/- and MT+/+ mice were administrated with a single dose of DU (10 mg/kg, i.p.) or equal volume of saline. After 4 days, protein changes in kidney tissues were evaluated using a proteomics approach. A total of 13 differentially expressed proteins were identified using two-dimensional electrophoresis and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. The validating results showed that the expression of aminoacylase-3 (ACY-3) and the mitochondrial ethylmalonic encephalopathy 1 (ETHE1) decreased significantly after DU exposure; in addition, the reduction in MT-/- mice was more significant than that in MT+/+ mice. The results also showed that exogenous ETHE1 or ACY-3 could increase the survival rate of human embryonic kidney 293 (HEK293) cells after DU exposure. A specific siRNA of ETHE1 significantly increased cell apoptosis rates after DU exposure, whereas exogenous ETHE1 significantly decreased cell apoptosis rates. In summary, ACY-3 and ETHE1 might involve in protection roles of MT. ETHE1 could be a new sensitive molecular target of DU-induced cell apoptosis.
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