ArticleFree radical biology & medicine2013
Bicarbonate modulates oxidative and functional damage in ischemia-reperfusion.
Article in Free radical biology & medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Bicarbonate signalling via G protein-coupled receptor regulates ischaemia-reperfusion injury.Nature communications · 2024Article
- Mitochondrial ATP Synthase and Mild Uncoupling by Butyl Ester of Rhodamine 19, C4R1.Antioxidants (Basel, Switzerland) · 2023Article
- Early acid/base and electrolyte changes in permanent middle cerebral artery occlusion: Aged male and female rats.Journal of neuroscience research · 2020Article
- Acid-Base and Electrolyte Changes Drive Early Pathology in Ischemic Stroke.Neuromolecular medicine · 2019Review
- Article
- The Mitochondrial Unfolded Protein Response Protects against Anoxia in Caenorhabditis elegans.PloS one · 2016Article
- An anoxia-starvation model for ischemia/reperfusion in C. elegans.Journal of visualized experiments : JoVE · 2014Article
- Topiramate ameliorates abdominal aorta cross-clamping induced liver injury in rats.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology AssociationArticle
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Authors and funding
7 authors.
Funding
Abstract
The carbon dioxide/bicarbonate (CO(2)/HCO(3)(-)) pair is the main biological pH buffer. However, its influence on biological processes, and in particular redox processes, is still poorly explored. Here we study the effect of CO(2)/HCO(3)(-) on ischemic injury in three distinct models (cardiac HL-1 cells, perfused rat heart, and Caenorhabditis elegans). We found that, although various concentrations of CO(2)/HCO(3)(-) do not affect function under basal conditions, ischemia-reperfusion or similar insults in the presence of higher CO(2)/HCO(3)(-) resulted in greater functional loss associated with higher oxidative damage in all models. Because the effect of CO(2)/HCO(3)(-) was observed in all models tested, we believe this buffer is an important determinant of oxidative damage after ischemia-reperfusion.
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Registered trials
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