ArticleAlcoholism, clinical and experimental research2017
Combined Catalase and ADH Inhibition Ameliorates Ethanol-Induced Myocardial Dysfunction Despite Causing Oxidative Stress in Conscious Female Rats.
Article in Alcoholism, clinical and experimental research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Steamed daylily flower (Hemerocallis fulva L.) protected cardiac and hepatic cells against ethanol induced apoptotic and oxidative damage.Journal of food and drug analysis · 2023Article
- Ethanol Metabolism in the Liver, the Induction of Oxidant Stress, and the Antioxidant Defense System.Antioxidants (Basel, Switzerland) · 2022Review
- Tetrahydrobiopterin paradoxically mediates cardiac oxidative stress and mitigates ethanol-evoked cardiac dysfunction in conscious female rats.European journal of pharmacology · 2021Article
- Alcohol Use Disorders and Their Harmful Effects on the Contractility of Skeletal, Cardiac and Smooth Muscles.Advances in drug and alcohol research · 2021Article
- Alcohol suppresses cardiovascular diurnal variations in male normotensive rats: Role of reduced PER2 expression and CYP2E1 hyperactivity in the heart.Alcohol (Fayetteville, N.Y.) · 2020Article
- Aldehyde Dehydrogenase Inhibition Ameliorates Cardiac Dysfunction and Exacerbates Hypotension Caused by Alcohol in Female Rats.Alcoholism, clinical and experimental research · 2020Article
- Role of Alcohol Oxidative Metabolism in Its Cardiovascular and Autonomic Effects.Advances in experimental medicine and biology · 2019Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEthanol (EtOH)-evoked oxidative stress, which contributes to myocardial dysfunction in proestrus rats, is mediated by increases in NADPH oxidase (Nox) activity, malondialdehyde (MDA), and ERK1/2 phosphorylation. Whether these biochemical responses, which are triggered by alcohol-derived acetaldehyde in noncardiac tissues, occur in proestrus rats' hearts remains unknown. Therefore, we elucidated the roles of alcohol dehydrogenase (ADH), cytochrome P4502E1 (CYP2E1), and catalase, which catalyze alcohol oxidation to acetaldehyde, in these alcohol-evoked biochemical and hemodynamic responses in proestrus rats.
methodsConscious proestrus rats prepared for measurements of left ventricular (LV) function and blood pressure (BP) received EtOH (1.5 g/kg, intravenous [i.v.] infusion over 30 minutes) or saline 30 minutes after an ADH and CYP2E1 inhibitor, 4-methylpyrazole (4-MP) (82 mg/kg, intraperitoneal), a catalase inhibitor, 3-AT (0.5 g/kg, i.v.), their combination, or vehicle. LV function and BP were monitored for additional 60 minutes after EtOH or saline infusion before collecting the hearts for ex vivo measurements of LV reactive oxygen species (ROS), Nox activity, MDA, and ERK1/2 phosphorylation.
resultsEtOH reduced LV function (dP/dt
conclusionsEtOH oxidative metabolism plays a pivotal role in the EtOH-evoked LV oxidative stress and dysfunction in proestrus rats. Notably, catalase inhibition (3-AT) caused cardiac oxidative stress and hypotension.
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