ReviewEnvironmental health perspectives2005
Ascorbate depletion: a critical step in nickel carcinogenesis?
Review in Environmental health perspectives, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
17 citing papers in PubMed, 71 citations in OpenAlex.
- iHyd-LysSite (EPSV): Identifying Hydroxylysine Sites in Protein Using Statistical Formulation by Extracting Enhanced Position and Sequence Variant Feature Technique.Current genomics · 2020Article
- Deletion of hemojuvelin, an iron-regulatory protein, in mice results in abnormal angiogenesis and vasculogenesis in retina along with reactive gliosis.Investigative ophthalmology & visual science · 2014Article
- Plasma Anti-Glycan Antibody Profiles Associated with Nickel level in Urine.Journal of proteomics & bioinformatics · 2013Article
- Inhibitory effect of a mixture containing vitamin C, lysine, proline, epigallocatechin gallate, zinc and alpha-1-antitrypsin on lung carcinogenesis induced by benzo(a) pyrene in mice.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2013Article
- Effects of ascorbic acid on carcinogenicity and acute toxicity of nickel subsulfide, and on tumor transplants growth in gulonolactone oxidase knock-out mice and wild-type C57BL mice.Toxicology and applied pharmacology · 2011Article
- Vitamin-C as anti-Helicobacter pylori agent: More prophylactic than curative- Critical review.Indian journal of pharmacology · 2011Article
- Article
- Selective macrophage ascorbate deficiency suppresses early atherosclerosis.Free radical biology & medicine · 2011Article
- Article
- Vitamin C: update on physiology and pharmacology.British journal of pharmacology · 2009Review
- Ferric reducing antioxidant power and square wave voltammetry for assay of low molecular weight antioxidants in blood plasma: performance and comparison of methods.Sensors (Basel, Switzerland) · 2009Article
- Truncation of histone H2A's C-terminal tail, as is typical for Ni(II)-assisted specific peptide bond hydrolysis, has gene expression altering effects.Annals of clinical and laboratory science · 2009Article
- Development of ascorbate transporters in brain cortical capillary endothelial cells in culture.Brain research · 2008Article
- Genetic and epigenetic mechanisms in metal carcinogenesis and cocarcinogenesis: nickel, arsenic, and chromium.Chemical research in toxicology · 2008Review
- The role of ascorbate in the modulation of HIF-1alpha protein and HIF-dependent transcription by chromium(VI) and nickel(II).Free radical biology & medicine · 2007Article
- Cobalt-induced oxidant stress in cultured endothelial cells: prevention by ascorbate in relation to HIF-1alpha.BioFactors (Oxford, England)Article
- Safety of nanotechnology in food industries.Electronic physicianArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Nickel compounds are known to cause respiratory cancer in humans and induce tumors in experimental animals. The underlying molecular mechanisms may involve genotoxic effects; however, the data from different research groups are not easy to reconcile. Here, we challenge the common premise that direct genotoxic effects are central to nickel carcinogenesis and probably to that of other metals. Instead, we propose that it is formation of metal complexes with proteins and other molecules that changes cellular homeostasis and provides conditions for selection of cells with transformed phenotype. This is concordant with the major requirement for nickel carcinogenicity, which is prolonged action on the target tissue. If DNA is not the main nickel target, is there another unique molecule that can be attacked with carcinogenic consequences? Our recent observations indicate that ascorbate may be such a molecule. Nickel depletes intracellular ascorbate, which leads to the inhibition of cellular hydroxylases, manifested by the loss of hypoxia-inducible factor (HIF)-1alpha and -2alpha hydroxylation and hypoxia-like stress. Proline hydroxylation is crucial for collagen and extracellular matrix assembly as well as for assembly of other protein molecules that have collagen-like domains, including surfactants and complement. Thus, the depletion of ascorbate by chronic exposure to nickel could be deleterious for lung cells and may lead to lung cancer. Key words: ascorbate, carcinogenesis, collagens, extracellular matrix, hypoxia-inducible transcription factor, metals, nickel, protein hydroxylation.
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.