ArticleBiology2025
Inhibition of Thioredoxin Reductase Activity and Oxidation of Cellular Thiols by Antimicrobial Agent, 2-Bromo-2-nitro-1,3-propanediol, Causes Oxidative Stress and Cell Death in Cultured Noncancer and Cancer Cells.
Article in Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Exploring the protease inhibitory potential of 2-bromo-2-nitro-1,3- propanediol (Bronopol): Initial findings.Biochemistry and biophysics reports · 2026Article
- Involvement of the thioredoxin system in multiple diseases: A focus on mechanisms of action in autophagy and ferroptosis (Review).Molecular medicine reports · 2026Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe thioredoxin system (TrxS) is crucial for maintaining redox balance by regulating cellular thiol levels and is involved in various biological processes, including cancer progression. Thioredoxin reductase (TrxR), a key component of TrxS, reduces oxidized thioredoxin (Trx) using NADPH. This study investigates the inhibitory effects of 2-bromo-2-nitro-1,3-propanediol (Bronopol, BP), a preservative, on TrxR activity and its impact on cellular thiols and cell viability.
methodsPurified recombinant TrxR and noncancer and cancer cells were treated with different concentrations of BP and TrxR activity measured. BP-treated cells were examined for effects of BP on total cellular thiol level and GSH/GSSG ratio.
resultsBP effectively inhibited TrxR in a dose-dependent manner, an effect that was reversible with dithiothreitol (DTT). BP treatment significantly reduced total thiol levels, decreased the GSH/GSSG ratio, and increased reactive oxygen species (ROS) in cells. Additionally, BP decreased cell viability and induced apoptosis, as indicated by morphological changes and increased c-fos mRNA expression.
conclusionsThese findings highlight BP's potential as a TrxR inhibitor and its cytotoxicity toward both noncancer and cancer cells. The observed effects-TrxR inhibition, thiol oxidation, GSH/GSSG imbalance, and ROS accumulation-may underlie BP's cytotoxicity. Further research is needed to explore the precise molecular mechanisms by which BP exerts these effects.
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