ArticleToxicology2011
The intracellular redox stress caused by hexavalent chromium is selective for proteins that have key roles in cell survival and thiol redox control.
Article in Toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 44 citations in OpenAlex.
- The Protective Effects of Selenium Nanoparticles Against Metal Toxicity.Biological trace element research · 2026Review
- Protective effects of thymoquinone against hexavalent chromium-ınduced nephrotoxicity: a multiparametric evaluation of oxidative stress, ınflammation, ferroptosis- and apoptosis-related markers.Molecular and cellular biochemistry · 2026Article
- Trivalent chromium interacts directly with acetylated lysine.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025Article
- Chromate Affects Gene Expression and DNA Methylation in Long-Term In Vitro Experiments in A549 Cells.International journal of molecular sciences · 2024Article
- Corrosion Products from Metallic Implants Induce ROS and Cell Death in Human MotoneuronsJournal of functional biomaterials · 2023Article
- Impact of Nano- and Micro-Sized Chromium(III) Particles on Cytotoxicity and Gene Expression Profiles Related to Genomic Stability in Human Keratinocytes and Alveolar Epithelial Cells.Nanomaterials (Basel, Switzerland) · 2022Article
- Treatment of Cells and Tissues with Chromate Maximizes Mitochondrial 2Fe2S EPR Signals.International journal of molecular sciences · 2019Article
- Evaluation of hematological, biochemical parameters and thiol enzyme activity in chrome plating workers.Environmental science and pollution research international · 2019Article
- Effects of chromium picolinate on fat deposition, activity and genetic expression of lipid metabolism-related enzymes in 21 day old Ross broilers.Asian-Australasian journal of animal sciences · 2018Article
- Environmental Presence of Hexavalent but Not Trivalent Chromium Causes Neurotoxicity in Exposed Drosophila melanogaster.Molecular neurobiology · 2017Article
- CoQ10 Deficiency May Indicate Mitochondrial Dysfunction in Cr(VI) Toxicity.International journal of molecular sciences · 2017Article
- Hexavalent chromium induces expression of mesenchymal and stem cell markers in renal epithelial cells.Molecular carcinogenesis · 2016Article
- Role of direct reactivity with metals in chemoprotection by N-acetylcysteine against chromium(VI), cadmium(II), and cobalt(II).Free radical biology & medicine · 2013Article
- Thioredoxin reductase was nitrated in the aging heart after myocardial ischemia/reperfusion.Rejuvenation research · 2013Article
- The effects of chromium(VI) on the thioredoxin system: implications for redox regulation.Free radical biology & medicine · 2012Review
- Mammalian metallothionein in toxicology, cancer, and cancer chemotherapy.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2011Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hexavalent chromium [Cr(VI)] compounds (e.g. chromates) are strong oxidants that readily enter cells where they are reduced to reactive Cr intermediates that can directly oxidize some cell components and can promote the generation of reactive oxygen and nitrogen species. Inhalation is a major route of exposure which directly exposes the bronchial epithelium. Previous studies with non-cancerous human bronchial epithelial cells (BEAS-2B) demonstrated that Cr(VI) treatment results in the irreversible inhibition of thioredoxin reductase (TrxR) and the oxidation of thioredoxins (Trx) and peroxiredoxins (Prx). The mitochondrial Trx/Prx system is somewhat more sensitive to Cr(VI) than the cytosolic Trx/Prx system, and other redox-sensitive mitochondrial functions are subsequently affected including electron transport complexes I and II. Studies reported here show that Cr(VI) does not cause indiscriminant thiol oxidation, and that the Trx/Prx system is among the most sensitive of cellular protein thiols. Trx/Prx oxidation is not unique to BEAS-2B cells, as it was also observed in primary human bronchial epithelial cells. Increasing the intracellular levels of ascorbate, an endogenous Cr(VI) reductant, did not alter the effects on TrxR, Trx, or Prx. The peroxynitrite scavenger MnTBAP did not protect TrxR, Trx, Prx, or the electron transport chain from the effects of Cr(VI), implying that peroxynitrite is not required for these effects. Nitration of tyrosine residues of TrxR was not observed following Cr(VI) treatment, further ruling out peroxynitrite as a significant contributor to the irreversible inhibition of TrxR. Cr(VI) treatments that disrupt the TrxR/Trx/Prx system did not cause detectable mitochondrial DNA damage. Overall, the redox stress that results from Cr(VI) exposure shows selectivity for key proteins which are known to be important for redox signaling, antioxidant defense, and cell survival.
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