ArticleFree radical biology & medicine2009
The effects of hexavalent chromium on thioredoxin reductase and peroxiredoxins in human bronchial epithelial cells.
Article in Free radical biology & medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 71 citations in OpenAlex.
- Crosstalk of thioredoxin system and programmed cell death: from pathophysiology to novel therapy.Redox biology · 2026Review
- An Overview of Hexavalent Chromium-Induced Necroptosis, Pyroptosis, and Ferroptosis.Biological trace element research · 2025Review
- Inhibition of Thioredoxin-Reductase by Auranofin as a Pro-Oxidant Anticancer Strategy for Glioblastoma: In Vitro and In Vivo Studies.International journal of molecular sciences · 2025Review
- ATR activation by Cr-DNA damage is a major survival response establishing late S and G2 checkpoints after Cr(VI) exposure.Toxicology and applied pharmacology · 2023Article
- Magnolia extract is effective for the chemoprevention of oral cancer through its ability to inhibit mitochondrial respiration at complex I.Cell communication and signaling : CCS · 2020Article
- Mitochondria-targeted magnolol inhibits OXPHOS, proliferation, and tumor growth via modulation of energetics and autophagy in melanoma cells.Cancer treatment and research communications · 2020Article
- Molecular and epigenetic mechanisms of Cr(VI)-induced carcinogenesis.Toxicology and applied pharmacology · 2019Review
- Treatment of Cells and Tissues with Chromate Maximizes Mitochondrial 2Fe2S EPR Signals.International journal of molecular sciences · 2019Article
- Detection of mitochondria-generated reactive oxygen species in cells using multiple probes and methods: Potentials, pitfalls, and the future.The Journal of biological chemistry · 2018Article
- Selenium Concentrations for Maximisation of Thioredoxin Reductase 2 Activity and Upregulation of Its Gene Transcripts in Senescent Human Fibroblasts.Antioxidants (Basel, Switzerland) · 2017Article
- Impact of 5'-amp-activated Protein Kinase on Male Gonad and Spermatozoa Functions.Frontiers in cell and developmental biology · 2017Review
- Predicting the Cytotoxic Potency of Cigarette Smoke by Assessing the Thioredoxin Reductase Inhibitory Capacity of Cigarette Smoke Extract.International journal of environmental research and public health · 2016Article
- The cysteine proteome.Free radical biology & medicine · 2015Review
- Cross-linking of thioredoxin reductase by the sulfur mustard analogue mechlorethamine (methylbis(2-chloroethyl)amine) in human lung epithelial cells and rat lung: selective inhibition of disulfide reduction but not redox cycling.Chemical research in toxicology · 2014Article
- Short-term exposure of nontumorigenic human bronchial epithelial cells to carcinogenic chromium(VI) compromises their respiratory capacity and alters their bioenergetic signature.FEBS open bio · 2014Article
- Thioredoxin reductase was nitrated in the aging heart after myocardial ischemia/reperfusion.Rejuvenation research · 2013Article
- Redox activation of Fe(III)-thiosemicarbazones and Fe(III)-bleomycin by thioredoxin reductase: specificity of enzymatic redox centers and analysis of reactive species formation by ESR spin trapping.Free radical biology & medicine · 2013Article
- Article
- Glutathione and glutaredoxin act as a backup of human thioredoxin reductase 1 to reduce thioredoxin 1 preventing cell death by aurothioglucose.The Journal of biological chemistry · 2012Article
- The effects of chromium(VI) on the thioredoxin system: implications for redox regulation.Free radical biology & medicine · 2012Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Inhalational exposure to hexavalent chromium (Cr(VI)) compounds (e.g., chromates) is of concern in many Cr-related industries and their surrounding environments. The bronchial epithelium is directly exposed to inhaled Cr(VI). Cr(VI) species gain easy access inside cells, where they are reduced to reactive Cr species, which may also contribute to the generation of reactive oxygen species. The thioredoxin (Trx) system promotes cell survival and has a major role in maintaining intracellular thiol redox balance. Previous studies with normal human bronchial epithelial cells (BEAS-2B) demonstrated that chromates cause dose- and time-dependent oxidation of Trx1 and Trx2. The Trx's keep many intracellular proteins reduced, including the peroxiredoxins (Prx's). Prx1 (cytosolic) and Prx3 (mitochondrial) were oxidized by Cr(VI) treatments that oxidized all, or nearly all, of the respective Trx's. Prx oxidation is therefore probably the result of a lack of reducing equivalents from Trx. Trx reductases (TrxR's) keep the Trx's largely in the reduced state. Cr(VI) caused pronounced inhibition of TrxR, but the levels of TrxR protein remained unchanged. The inhibition of TrxR was not reversed by removal of residual Cr(VI) or by NADPH, the endogenous electron donor for TrxR. In contrast, the oxidation of Trx1, Trx2, and Prx3 was reversible by disulfide reductants. Prolonged inhibition of TrxR in Cr(VI)-treated cells might contribute to the sustained oxidation of Trx's and Prx's. Reduced Trx binds to an N-terminal domain of apoptosis signaling kinase (ASK1), keeping ASK1 inactive. Cr(VI) treatments that significantly oxidized Trx1 resulted in pronounced dissociation of Trx1 from ASK1. Overall, the effects of Cr(VI) on the redox state and function of the Trx's, Prx's, and TrxR in the bronchial epithelium could have important implications for redox-sensitive cell signaling and tolerance of oxidant insults.
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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.