ArticleThe Biochemical journal2009
Myocardial ischaemia inhibits mitochondrial metabolism of 4-hydroxy-trans-2-nonenal.
Article in The Biochemical journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 46 citations in OpenAlex.
- NAD metabolism and heart failure: Mechanisms and therapeutic potentials.Journal of molecular and cellular cardiology · 2024Review
- Mn(III) Porphyrin, MnTnBuOE-2-PyPInternational journal of molecular sciences · 2023Article
- The effects of nicotinamide adenine dinucleotide in cardiovascular diseases: Molecular mechanisms, roles and therapeutic potential.Genes & diseases · 2022Review
- Diabetic Aldehyde Dehydrogenase 2 Mutant (ALDH2*2) Mice Are More Susceptible to Cardiac Ischemic-Reperfusion Injury Due to 4-Hydroxy-2-Nonenal Induced Coronary Endothelial Cell Damage.Journal of the American Heart Association · 2021Article
- A Synthetic Epoxydocosapentaenoic Acid Analogue Ameliorates Cardiac Ischemia/Reperfusion Injury: The Involvement of the Sirtuin 3-NLRP3 Pathway.International journal of molecular sciences · 2020Article
- Mitochondria as a Source and a Target for Uremic Toxins.International journal of molecular sciences · 2019Review
- Cardiac-specific overexpression of aldehyde dehydrogenase 2 exacerbates cardiac remodeling in response to pressure overload.Redox biology · 2018Article
- Deficiency of aldose reductase exacerbates early pressure overload-induced cardiac dysfunction and autophagy in mice.Journal of molecular and cellular cardiology · 2018Article
- Regulation of Sirtuin 3-Mediated Deacetylation of Cyclophilin D Attenuated Cognitive Dysfunction Induced by Sepsis-Associated Encephalopathy in Mice.Cellular and molecular neurobiology · 2017Article
- Aldehyde dehydrogenase 2 activation in heart failure restores mitochondrial function and improves ventricular function and remodelling.Cardiovascular research · 2014Article
- Redox proteomic identification of HNE-bound mitochondrial proteins in cardiac tissues reveals a systemic effect on energy metabolism after doxorubicin treatment.Free radical biology & medicine · 2014Article
- Redox regulation of antioxidants, autophagy, and the response to stress: implications for electrophile therapeutics.Free radical biology & medicine · 2014Review
- Role of aldose reductase in the metabolism and detoxification of carnosine-acrolein conjugates.The Journal of biological chemistry · 2013Article
- Mitochondrial oxidative stress corrupts coronary collateral growth by activating adenosine monophosphate activated kinase-α signaling.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- 4-Hydroxy-2(E)-nonenal (HNE) catabolism and formation of HNE adducts are modulated by β oxidation of fatty acids in the isolated rat heart.Free radical biology & medicine · 2013Article
- Regional differences in prostaglandin E₂ metabolism in human colorectal cancer liver metastases.BMC cancer · 2013Article
- The lipid peroxidation product 4-hydroxy-2-nonenal: Advances in chemistry and analysis.Redox biology · 2013Review
- The G671V variant of MRP1/ABCC1 links doxorubicin-induced acute cardiac toxicity to disposition of the glutathione conjugate of 4-hydroxy-2-trans-nonenal.Pharmacogenetics and genomics · 2012Article
- Hemin causes mitochondrial dysfunction in endothelial cells through promoting lipid peroxidation: the protective role of autophagy.American journal of physiology. Heart and circulatory physiology · 2012Article
- Dietary regulation of catabolic disposal of 4-hydroxynonenal analogs in rat liver.Free radical biology & medicine · 2012Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Myocardial ischaemia is associated with the generation of lipid peroxidation products such as HNE (4-hydroxy-trans-2-nonenal); however, the processes that predispose the ischaemic heart to toxicity by HNE and related species are not well understood. In the present study, we examined HNE metabolism in isolated aerobic and ischaemic rat hearts. In aerobic hearts, the reagent [(3)H]HNE was glutathiolated, oxidized to [(3)H]4-hydroxynonenoic acid, and reduced to [(3)H]1,4-dihydroxynonene. In ischaemic hearts, [(3)H]4-hydroxynonenoic acid formation was inhibited and higher levels of [(3)H]1,4-dihydroxynonene and [(3)H]GS-HNE (glutathione conjugate of HNE) were generated. Metabolism of [(3)H]HNE to [(3)H]4-hydroxynonenoic acid was restored upon reperfusion. Reperfused hearts were more efficient at metabolizing HNE than non-ischaemic hearts. Ischaemia increased the myocardial levels of endogenous HNE and 1,4-dihydroxynonene, but not 4-hydroxynonenoic acid. Isolated cardiac mitochondria metabolized [(3)H]HNE primarily to [(3)H]4-hydroxynonenoic acid and minimally to [(3)H]1,4-dihydroxynonene and [(3)H]GS-HNE. Moreover, [(3)H]4-hydroxynonenoic acid was extruded from mitochondria, whereas other [(3)H]HNE metabolites were retained in the matrix. Mitochondria isolated from ischaemic hearts were found to contain 2-fold higher levels of protein-bound HNE than the cytosol, as well as increased [(3)H]GS-HNE and [(3)H]1,4-dihydroxynonene, but not [(3)H]4-hydroxynonenoic acid. Mitochondrial HNE oxidation was inhibited at an NAD(+)/NADH ratio of 0.4 (equivalent to the ischaemic heart) and restored at an NAD(+)/NADH ratio of 8.6 (equivalent to the reperfused heart). These results suggest that HNE metabolism is inhibited during myocardial ischaemia owing to NAD(+) depletion. This decrease in mitochondrial metabolism of lipid peroxidation products and the inability of the mitochondria to extrude HNE metabolites could contribute to myocardial ischaemia/reperfusion injury.
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