ArticleBioFactors (Oxford, England)
Cobalt-induced oxidant stress in cultured endothelial cells: prevention by ascorbate in relation to HIF-1alpha.
Article in BioFactors (Oxford, England). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Exploring the Ascorbate Requirement of the 2-Oxoglutarate-Dependent Dioxygenases.Journal of medicinal chemistry · 2025Review
- Melatonin counteracts cobalt nanoparticle‑induced cytotoxicity and genotoxicity by deactivating reactive oxygen species‑dependent mechanisms in the NRK cell line.Molecular medicine reports · 2017Article
- Aged garlic extract and S-allylcysteine prevent apoptotic cell death in a chemical hypoxia model.Biological research · 2016Article
- Increased Tumor Ascorbate is Associated with Extended Disease-Free Survival and Decreased Hypoxia-Inducible Factor-1 Activation in Human Colorectal Cancer.Frontiers in oncology · 2014Article
- Ascorbate as a co-factor for fe- and 2-oxoglutarate dependent dioxygenases: physiological activity in tumor growth and progression.Frontiers in oncology · 2014Review
- Role of vitamin C in the function of the vascular endothelium.Antioxidants & redox signaling · 2013Review
- Article
- Oxidized LDL up-regulates the ascorbic acid transporter SVCT2 in endothelial cells.Molecular and cellular biochemistry · 2010Article
- Low vitamin C and increased oxidative stress and cell death in mice that lack the sodium-dependent vitamin C transporter SVCT2.Free radical biology & medicine · 2010Article
- Chelation of intracellular iron enhances endothelial barrier function: a role for vitamin C?Archives of biochemistry and biophysics · 2010Article
- Hepatocyte nuclear factor 1 is essential for transcription of sodium-dependent vitamin C transporter protein 1.American journal of physiology. Cell physiology · 2009Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Endothelial cells respond to hypoxia by decreased degradation of hypoxia-inducible factor 1alpha (HIF-1alpha), accumulation of which leads to increased transcription of numerous proteins involved in cell growth and survival. Ascorbic acid prevents HIF-1alpha stabilization in many cell types, but the physiologic relevance of such effects is uncertain. Given their relevance for angiogenesis, endothelial cells in culture were used to evaluate the effects of ascorbate on HIF-1alpha expression induced by hypoxia and the hypoxia mimic cobalt. Although EA.hy926 cells in culture under oxygenated conditions did not contain ascorbate, HIF-1alpha expression was very low, showing that the vitamin is not necessary to suppress HIF-1alpha. On the other hand, hypoxia- or cobalt-induced HIF-1alpha expression/stabilization was almost completely suppressed by what are likely physiologic intracellular ascorbate concentrations. Increased HIF-1alpha expression was not associated with significant changes in expression of the SVCT2, the major transporter for ascorbate in these cells. Cobalt at concentrations sufficient to stabilize HIF-1alpha both oxidized intracellular ascorbate and induced an oxidant stress in the cells that was prevented by ascorbate. Whereas the interaction of ascorbate and cobalt is complex, the presence of physiologic low millimolar concentrations of ascorbate in endothelial cells effectively decreases HIF-1alpha expression and protects against cobalt-induced oxidant stress.
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