ArticleJournal of cellular physiology2006
Chromium (VI) inhibits heme oxygenase-1 expression in vivo and in arsenic-exposed human airway epithelial cells.
Article in Journal of cellular physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Cr(VI) and DON co-exposure triggers intestinal epithelial cells ferroptosis and pyroptosis through Nrf2/NF-κB/NLRP3 to impair intestinal barrier function.Redox report : communications in free radical research · 2026Article
- Two- and Three-Dimensional Culture Systems: Respiratory In Vitro Tissue Models for Chemical Screening and Risk-Based Decision Making.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Mixture toxicity of the combinations of silver nanoparticles and environmental pollutants.Environmental science and pollution research international · 2020Article
- Uranium-induced rat kidney cell cytotoxicity is mediated by decreased endogenous hydrogen sulfide (HToxicology research · 2016Article
- Oxidative stress-related lung dysfunction by chromium(VI): alleviation by Citrus aurantium L.Journal of physiology and biochemistry · 2013Article
- Long-term exposure to hexavalent chromium inhibits expression of tumor suppressor genes in cultured cells and in mice.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2012Article
- The effects of chromium(VI) on the thioredoxin system: implications for redox regulation.Free radical biology & medicine · 2012Review
- Application of the U.S. EPA mode of action Framework for purposes of guiding future research: a case study involving the oral carcinogenicity of hexavalent chromium.Toxicological sciences : an official journal of the Society of Toxicology · 2011Review
- Chromium genotoxicity: A double-edged sword.Chemico-biological interactions · 2010Review
- Mechanism of DNA-protein cross-linking by chromium.Chemical research in toxicology · 2010Article
- Signal transducer and activator of transcription 1 (STAT1) is essential for chromium silencing of gene induction in human airway epithelial cells.Toxicological sciences : an official journal of the Society of Toxicology · 2009Article
- Nickel mobilizes intracellular zinc to induce metallothionein in human airway epithelial cells.American journal of respiratory cell and molecular biology · 2009Article
- Lung injury, inflammation and Akt signaling following inhalation of particulate hexavalent chromium.Toxicology and applied pharmacology · 2009Article
- Chromium cross-links histone deacetylase 1-DNA methyltransferase 1 complexes to chromatin, inhibiting histone-remodeling marks critical for transcriptional activation.Molecular and cellular biology · 2007Article
- Mechanisms of action of inhaled fibers, particles and nanoparticles in lung and cardiovascular diseases.Particle and fibre toxicology · 2007Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Inhaled hexavalent chromium (Cr(VI)) promotes lung injury and pulmonary diseases through poorly defined mechanisms. One hypothesis for this lung pathogenesis is that Cr(VI) silences induction of cytoprotective genes, such as heme oxygenase-1 (HO-1), whose total lung mRNA levels were reduced 21 days after nasal instillation of potassium dichromate in C57BL/6 mice. To investigate the mechanisms for this inhibition, Cr(VI) effects on basal and arsenic (As(III))-induced HO-1 expression were examined in cultured human bronchial epithelial (BEAS-2B) cells. An effect of Cr(VI) on the low basal HO-1 mRNA and protein levels in BEAS-2B cells was not detectible. In contrast, Cr(VI) added to the cells before As(III), but not simultaneously with As(III), attenuated As(III)-induced HO-1 expression. Transient transfection with luciferase reporter gene constructs controlled by the full length ho-1 promoter or deletion mutants demonstrated that this inhibition occurred in the E1 enhancer region containing critical antioxidant response elements (ARE). Cr(VI) pretreatment inhibited As(III)-induced activity of a transiently expressed reporter construct regulated by three ARE tandem repeats. The mechanism for this Cr(VI)-attenuated transactivation appeared to be Cr(VI) reduction of the nuclear levels of the transcription factor Nrf2 and As(III)-stimulated Nrf2 transcriptional complex binding to the ARE cis element. Finally, exposing cells to Cr(VI) prior to co-exposure with As(III) synergized for apoptosis and loss of membrane integrity. These data suggest that Cr(VI) silences induction of ARE-driven genes required for protection from secondary insults. The data also have important implications for understanding the toxic mechanisms of low level, mixed metal exposures in the lung.
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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.