ArticleWorld journal of biological chemistry2013
Effect of alcohol exposure on hepatic superoxide generation and hepcidin expression.
Article in World journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Excessive intake of fructose and alcohol aggravates high-fat diet-induced steatohepatitis and changes hepatic iron homeostasis.Histochemistry and cell biology · 2025Article
- Role of Ferroptosis in ALD: Focusing on Hepcidin and Besides Hepcidin.Current medicinal chemistry · 2025Review
- Alcohol- and Low-Iron Induced Changes in Antioxidant and Energy Metabolism Associated with Protein Lys Acetylation.International journal of molecular sciences · 2024Article
- Iron overload in alcoholic liver disease: underlying mechanisms, detrimental effects, and potential therapeutic targets.Cellular and molecular life sciences : CMLS · 2022Review
- Association of Habitual Dietary Intake with Liver Iron-A Population-Based Imaging Study.Nutrients · 2021Article
- Hepcidin-2 in mouse urine as a candidate radiation-responsive molecule.Journal of radiation research · 2016Article
- The effect of alcohol and hydrogen peroxide on liver hepcidin gene expression in mice lacking antioxidant enzymes, glutathione peroxidase-1 or catalase.Biomolecules · 2015Article
- Metallothionein-I/II Knockout Mice Aggravate Mitochondrial Superoxide Production and Peroxiredoxin 3 Expression in Thyroid after Excessive Iodide Exposure.Oxidative medicine and cellular longevity · 2015Article
- TLR4 signaling and the inhibition of liver hepcidin expression by alcohol.World journal of gastroenterology · 2014Article
- Apoptosis induced by Fas signaling does not alter hepatic hepcidin expression.World journal of biological chemistry · 2014Article
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5 authors.
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Abstract
aimTo understand the role of mitochondrial-produced superoxide (O2 (•-)) in the regulation of iron-regulatory hormone, hepcidin by alcohol in the liver.
methodsFor alcohol experiments, manganese superoxide dismutase knockout mice heterozygous for Sod2 gene expression (Sod2 (+/-)) and age-matched littermate control mice (LMC), expressing Sod2 gene on both alleles, were exposed to either 10% (w/v) ethanol in the drinking water or plain water (control) for 7 d. Total cellular O2 (•-) levels in hepatocytes isolated from the livers of mice were measured by electron paramagnetic resonance spectroscopy. The mitochondrial-targeted, O2 (•-)-sensitive fluorogenic probe, MitoSOX Red and flow cytometry were utilized to measure O2 (•-) in mitochondria. Gene and protein expression were determined by Taqman Real-time quantitative PCR and Western blotting, respectively.
resultsSod2 (+/-) mice expressed 40% less MnSOD protein (SOD2) in hepatocytes compared to LMC mice. The deletion of Sod2 allele did not alter the basal expression level of hepcidin in the liver. 10% ethanol exposure for 1 wk inhibited hepatic hepcidin mRNA expression three-fold both in Sod2 (+/-) and LMC mice. O2 (•-) levels in hepatocytes of untreated Sod2 (+/-) mice were three-fold higher than in untreated LMC mice, as observed by electron paramagnetic resonance spectroscopy. O2 (•-) levels in mitochondria of Sod2 (+/) mice were four-fold higher than in mitochondria of untreated LMC mice, as measured by MitoSOX Red fluorescence and flow cytometry. Alcohol induced a two-fold higher increase in O2 (•-) levels in hepatocytes of LMC mice than in Sod2 (+/-) mice compared to respective untreated counterparts. In contrast, 1 wk alcohol exposure did not alter mitochondrial O2 (•-) levels in both Sod2 (+/-) and control mice.
conclusionMitochondrial O2 (•-) is not involved in the inhibition of liver hepcidin transcription and thereby regulation of iron metabolism by alcohol. These findings also suggest that short-term alcohol consumption significantly elevates O2 (•-) levels in hepatocytes, which appears not to originate from mitochondria.
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