ArticleToxicology research2017
Inhibitory effect of uranyl nitrate on DNA double-strand break repair by depression of a set of proteins in the homologous recombination pathway.
Article in Toxicology research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 16 citations in OpenAlex.
- Experimental assessment of radioprotective efficiency of Rhizoplaca chrysoleuca (Sm.) Zopf extract against uranyl nitrate hexahydrate.Scientific reports · 2026Article
- 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
- Differential response of human T-lymphocytes to arsenic and uranium.Toxicology letters · 2020Article
- BECN1 promotes radiation-induced G2/M arrest through regulation CDK1 activity: a potential role for autophagy in G2/M checkpoint.Cell death discovery · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Occupational and environmental exposure to uranium has been confirmed to cause tissue injury and carcinogenesis. As a heavy metal from actinide series, the chemical and radiological toxicities of uranium jointly induce the detrimental effects. However, the mutual action and mechanism of both forms of toxicities still need to be further elucidated. DNA double-strand break (DSB) is a fundamental cause of cell death or genomic instability induced by ionizing radiation. Herein, we investigate the effect of uranyl nitrate on the cellular function of DNA damage response and intrinsic DSB repair on the aspect of chemical toxicity. The results indicated that uranyl ion increased the accumulation of nuclear DNA DSBs in a dose-dependent manner. Both homologous recombination (HR) and non-homologous end joining (NHEJ) pathways of DSB repair were affected by the uranyl ion. The inhibition of DSB repair efficiency is attributed to the depression of a set of critical repair proteins, particularly those for the HR pathway such as ATM, BRCA1, RPA80 and EXO1. The available data enable us to imagine that the chemical toxicity of uranium leads to inhibition of cellular DNA repair capability, which can further aggravate its radiological toxicity.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.