ArticleAmerican journal of physiology. Cell physiology2012
Ethanol stimulates epithelial sodium channels by elevating reactive oxygen species.
Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Emerging roles of mechanosensitive ion channels in acute lung injury/acute respiratory distress syndrome.Respiratory research · 2022Review
- Tempol Alters Urinary Extracellular Vesicle Lipid Content and Release While Reducing Blood Pressure during the Development of Salt-Sensitive Hypertension.Biomolecules · 2021Article
- Alcohol inhibits alveolar fluid clearance through the epithelial sodium channel via the A2 adenosine receptor in acute lung injury.Molecular medicine reports · 2021Article
- Alcohol Consumption Can be a "Double-Edged Sword" for Chronic Kidney Disease Patients.Medical science monitor : international medical journal of experimental and clinical research · 2019Review
- Effects of reactive oxygen species on renal tubular transport.American journal of physiology. Renal physiology · 2019Review
- Acetate Mediates Alcohol Excitotoxicity in Dopaminergic-like PC12 Cells.ACS chemical neuroscience · 2019Article
- The role of stretch-activated ion channels in acute respiratory distress syndrome: finally a new target?American journal of physiology. Lung cellular and molecular physiology · 2016Review
- The Polarized Effect of Intracellular Calcium on the Renal Epithelial Sodium Channel Occurs as a Result of Subcellular Calcium Signaling Domains Maintained by Mitochondria.The Journal of biological chemistry · 2015Article
- Hydrogen Sulfide Prevents Advanced Glycation End-Products Induced Activation of the Epithelial Sodium Channel.Oxidative medicine and cellular longevity · 2015Article
- ENaC activity and expression is decreased in the lungs of protein kinase C-α knockout mice.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Chronic ethanol exposure alters the lung proteome and leads to mitochondrial dysfunction in alveolar type 2 cells.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Chronic alcohol feeding inhibits physiological and molecular parameters of intestinal and renal riboflavin transport.American journal of physiology. Cell physiology · 2013Article
- Ethanol alters alveolar fluid balance via Nadph oxidase (NOX) signaling to epithelial sodium channels (ENaC) in the lung.PloS one · 2013Article
- ROS production as a common mechanism of ENaC regulation by EGF, insulin, and IGF-1.American journal of physiology. Cell physiology · 2013Article
- Intoxicated Na(+) channels. Focus on "ethanol stimulates epithelial sodium channels by elevating reactive oxygen species".American journal of physiology. Cell physiology · 2012Article
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6 authors at 1 institution in 1 country.
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Abstract
Alcohol affects total body sodium balance, but the molecular mechanism of its effect remains unclear. We used single-channel methods to examine how ethanol affects epithelial sodium channels (ENaC) in A6 distal nephron cells. The data showed that ethanol significantly increased both ENaC open probability (P(o)) and the number of active ENaC in patches (N). 1-Propanol and 1-butanol also increased ENaC activity, but iso-alcohols did not. The effects of ethanol were mimicked by acetaldehyde, the first metabolic product of ethanol, but not by acetone, the metabolic product of 2-propanol. Besides increasing open probability and apparent density of active channels, confocal microscopy and surface biotinylation showed that ethanol significantly increased α-ENaC protein in the apical membrane. The effects of ethanol on ENaC P(o) and N were abolished by a superoxide scavenger, 4-hydroxy-2,2,6,6-tetramethylpiperidinyloxy (TEMPOL) and blocked by the phosphatidylinositol 3-kinase inhibitor LY294002. Consistent with an effect of ethanol-induced reactive oxygen species (ROS) on ENaC, primary alcohols and acetaldehyde elevated intracellular ROS, but secondary alcohols did not. Taken together with our previous finding that ROS stimulate ENaC, the current results suggest that ethanol stimulates ENaC by elevating intracellular ROS probably via its metabolic product acetaldehyde.
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