ArticleOccupational Health2026
Particulate Hexavalent Chromium Inhibits RAD51 Paralogs Necessary for RAD51 Filament Formation and Stabilization During Homologous Recombination Repair.
Article in Occupational Health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Hexavalent chromium [Cr(VI)] is a lung carcinogen. Central to its carcinogenic mechanism are Cr(VI)-induced DNA double strand breaks and chromosome instability. While breaks are usually repaired in healthy cells, Cr(VI) inhibits homologous recombination repair by targeting RAD51. RAD51 paralogs (RAD51B, RAD51C, RAD51D, XRCC2, and XRCC3) are responsible for RAD51 loading and the stabilization of nucleoprotein filaments necessary for DNA strand exchange and repair. This study aimed to investigate the effects of Cr(VI) exposure on RAD51 paralogs. WTHBF-6 cells, a human lung cell line, were exposed to various environmentally and occupationally relevant concentrations of zinc chromate for acute (24 h) and prolonged (120 h) exposure times. After exposure to Cr(VI), we collected RNA for sequencing and assessed the ability of DNA repair proteins to form foci using immunofluorescence. Protein levels were measured with western blotting, RNA-Seq was validated with RT-qPCR, and protein-protein interactions were assessed with the Proximity Ligation Assay (PLA) assay. Cr(VI) transcriptionally repressed all RAD51 paralogs. Further functional analyses showed that Cr(VI) inhibited the foci formation of RAD51D after acute and prolonged exposures and of XRCC2 and XRCC3 after prolonged exposure. Cr(VI) also inhibited overall RAD51D protein expression, as well as its interaction with RAD51. These findings suggest that Cr(VI) inhibits all RAD51 paralogs, but RAD51D might be an early target of Cr(VI), leading to the loss of RAD51 filament formation and function and the overall inhibition of homologous recombination repair.
Indexed as
Identifiers
What OpenQuestion holds
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.