ArticleProceedings of the National Academy of Sciences of the United States of America2004
Chronic exposure to nitric oxide alters the free iron pool in endothelial cells: role of mitochondrial respiratory complexes and heat shock proteins.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 65 citations in OpenAlex.
- Ferroptotic neurodegeneration and diet: a narrative review.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Nitric oxide-releasing PHEMA/polysilsesquioxane photocrosslinked hybrids.RSC advances · 2025Article
- The effects of two gold-N-heterocyclic carbene (NHC) complexes in ovarian cancer cells: a redox proteomic study.Cancer chemotherapy and pharmacology · 2022Article
- Iron supplementation inhibits hypoxia-induced mitochondrial damage and protects zebrafish liver cells from death.Frontiers in physiology · 2022Article
- Acetaminophen hepatotoxicity: A mitochondrial perspective.Advances in pharmacology (San Diego, Calif.) · 2019Review
- iNOS-derived nitric oxide promotes glycolysis by inducing pyruvate kinase M2 nuclear translocation in ovarian cancer.Oncotarget · 2017Article
- Protection by Nitric Oxide Donors of Isolated Rat Hearts Is Associated with Activation of Redox Metabolism and Ferritin Accumulation.PloS one · 2016Article
- Cancer cell metabolism and the modulating effects of nitric oxide.Free radical biology & medicine · 2015Review
- Deficits in bioenergetics and impaired immune response in granulocytes from children with autism.Pediatrics · 2014Review
- Integration of cellular bioenergetics with mitochondrial quality control and autophagy.Biological chemistry · 2012Review
- Bicarbonate plays a critical role in the generation of cytotoxicity during SIN-1 decomposition in culture medium.Oxidative medicine and cellular longevity · 2012Article
- Excess no predisposes mitochondrial succinate-cytochrome c reductase to produce hydroxyl radical.Biochimica et biophysica acta · 2011Article
- Prevention of diabetic nephropathy in Ins2(+/)⁻(AkitaJ) mice by the mitochondria-targeted therapy MitoQ.The Biochemical journal · 2010Article
- Mitochondrial reserve capacity in endothelial cells: The impact of nitric oxide and reactive oxygen species.Free radical biology & medicine · 2010Article
- Nitration of the mitochondrial complex I subunit NDUFB8 elicits RIP1- and RIP3-mediated necrosis.Free radical biology & medicine · 2010Article
- Regulation of oxygen utilization by angiotensin II in chronic kidney disease.Kidney international · 2009Article
- Mitochondrial respiratory complex I regulates neutrophil activation and severity of lung injury.American journal of respiratory and critical care medicine · 2008Article
- The role of tobacco smoke induced mitochondrial damage in vascular dysfunction and atherosclerosis.Mutation research · 2007Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The mechanisms of nitric oxide (NO) signaling include binding to the iron centers in soluble guanylate cyclase and cytochrome c oxidase and posttranslational modification of proteins by S-nitrosation. Low levels of NO control mitochondrial number in cells, but little is known of the impact of chronic exposure to high levels of NO on mitochondrial function in endothelial cells. The focus of this study is the interaction of NO with mitochondrial respiratory complexes in cell culture and the effect this has on iron homeostasis. We demonstrate that chronic exposure of endothelial cells to NO decreased activity and protein levels of complexes I, II, and IV, whereas citrate synthase and ATP synthase were unaffected. Inhibition of these respiratory complexes was accompanied by an increase in cellular S-nitrosothiol levels, modification of cysteines residues, and an increase in the labile iron pool. The NO-dependent increase in the free iron pool and inhibition of complex II was prevented by inhibition of mitochondrial protein synthesis, consistent with a major contribution of the organelle to iron homeostasis. In addition, inhibition of mitochondrial protein synthesis was associated with an increase in heat shock protein 60 levels, which may be an additional mechanism leading to preservation of complex II activity.
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