• presence of ethanol
  • Results: Cultures maintained in the presence of ethanol demonstrated a G2/M cell cycle arrest that was associated with a reduction in DNA content and increased levels of p-Cdc2 and p21, compared with cells cultured in its absence. (mdpi.com)
  • Studies demonstrate that the removal of this accumulated ethanol does not immediately restore fermentative activity, and they provide evidence that the decline in metabolic rate is due to physiological changes (including possible ethanol damage) rather than to the presence of ethanol. (wikipedia.org)
  • glucose
  • While the causes of a hangover are still poorly understood, several factors are known to be involved including acetaldehyde accumulation, changes in the immune system and glucose metabolism, dehydration, metabolic acidosis, disturbed prostaglandin synthesis, increased cardiac output, vasodilation, sleep deprivation and malnutrition. (wikipedia.org)
  • Inhibits
  • Data show that the administration of N-acetyl cysteine (NAC) a strong antioxidant inhibits chronic ethanol maintenance by 60%-70%, without inhibiting its initial intake. (frontiersin.org)
  • consumption
  • We also show a meta-analytical correlational approach that proposes how differences in the activity of brain catalase across ontogeny, could be modulating patterns of ethanol consumption. (frontiersin.org)
  • The role of β-endorphin and µ-opioid receptors (OR) have been suggested to be of particular importance in mediating some of the behavioral effects of ethanol, including psychomotor stimulation and sensitization, consumption and conditioned place preference (CPP). (frontiersin.org)
  • A hangover is the experience of various unpleasant physiological and psychological effects following the consumption of ethanol, as found in wine, beer and distilled spirits. (wikipedia.org)
  • pyruvate
  • Finally, pyruvate is converted to ethanol and CO2 in two steps, regenerating oxidized NAD+ needed for glycolysis: 1. (wikipedia.org)
  • intake
  • Ethanol intake usually begins during adolescence, with a decrease in the average age of initiation in the United States from 17.8 years in 1987 to 15.9 years in 1996 ( Windle, 2003 ). (frontiersin.org)
  • Oral intake of slow-release L-cysteine 200 mg before challenge with ethanol. (clinicaltrials.gov)
  • Inhibition of brain acetaldehyde synthesis does not influence the maintenance of chronic ethanol intake. (frontiersin.org)
  • and (iv) the intra-cerebroventricular administration of anti-inflammatory and antioxidant MSCs inhibit both the maintenance of chronic ethanol intake and relapse-like drinking . (frontiersin.org)
  • ALDH2
  • Since ALDH2 assembles and functions as a tetramer and requires all four of its components to be active in order to metabolize acetaldehyde, heterozygotes have very little ALDH2 activity. (wikipedia.org)
  • toxic
  • Cholesterol Enhances the Toxic Effect of Ethanol and Acetaldehyde in Primary Mouse Hepatocytes," Oxidative Medicine and Cellular Longevity , vol. 2016, Article ID 9209825, 9 pages, 2016. (hindawi.com)
  • exposure
  • Why Should we Study Early Ethanol Exposure Effects? (frontiersin.org)
  • Yet, ethanol exposure can occur involuntarily earlier in ontogeny ( Spear and Molina, 2005 ). (frontiersin.org)
  • Ethanol drinking during breastfeeding is still highly prevalent and implies an alternative mode of early exposure to the drug (e.g. (frontiersin.org)
  • These epidemiological studies highlight the need for developing experimental animal models for understanding the above mentioned effects of early ethanol exposure. (frontiersin.org)
  • Expected results show mitigated exposure of the gastric mucosa to acetaldehyde. (clinicaltrials.gov)
  • The initial symptoms of methanol exposure are usually less severe than the symptoms from the ingestion of a similar quantity of ethanol. (wikipedia.org)
  • The increased exposure to acetaldehyde in individuals with the catalytically inactive form may also confer greater susceptibility to many types of cancer. (wikipedia.org)
  • Exposure to oxygen can exacerbate the fault due to the oxidation of ethanol to acetaldehyde, which leaves the wine with a sharp vinegar-like taste. (wikipedia.org)
  • reactive
  • Although reactive oxygen species are thought to have a significant role in ethanol-induced hepatocellular damage, they may have a less important role in the inability of hepatocytes to replace dead or damaged cells. (mdpi.com)
  • metabolize
  • Background: Hepatocytes metabolize the vast majority of ingested ethanol. (mdpi.com)
  • The increase in rest energy expenditure has, according to some studies, been explained by indicating that the MEOS "expends" nine calories per gram of ethanol to metabolize versus 7 calories per gram of ethanol ingested. (wikipedia.org)
  • dopamine
  • Ethanol increases the release of β-endorphin from the hypothalamic arcuate nucleus (NArc), which can modulate activity of other neurotransmitter systems such as mesolimbic dopamine (DA). (frontiersin.org)
  • formate
  • In 1822, Georges-Simon Serullas added potassium metal to a solution of iodine in ethanol and water to form potassium formate and iodoform, called in the language of that time hydroiodide of carbon. (wikipedia.org)
  • catalyst
  • Byproducts of the dehydrogenation include diethyl ether, which is thought to arise primarily due to aluminum sites in the catalyst, acetaldehyde and its aldol products, higher esters, and ketones. (wikipedia.org)
  • ingestion
  • Buccal cells were collected before ethanol ingestion. (separationsnow.com)
  • First, methanol (whether it enters the body by ingestion, inhalation, or absorption through the skin) can be fatal due to its CNS depressant properties in the same manner as ethanol poisoning. (wikipedia.org)
  • intermediate
  • By using static headspace-gas chromatography for liquid phase analysis, we identify acetaldehyde as a minor product and key intermediate in the electroreduction of CO to ethanol on OD-Cu electrodes. (osti.gov)
  • levels
  • Additionally, culturing the cells in the presence of acetaldehyde alone resulted in increased levels of p-Cdc2 and p21. (mdpi.com)
  • Individuals with the ADH1B GG genotype had median ethanol levels of 5.0mM (IQR 3.4-7.2), and those with the ADH1B GT/TT genotype had 4.7mM (IQR 4.2-4.8). (separationsnow.com)
  • Corresponding acetaldehyde levels were 1.5μM (IQR 0.7-2.6) for ADH1B GG genotype and 1.6μM (IQR 1.5-1.7) for ADH1B CG/GG genotype. (separationsnow.com)
  • Individuals with the ADH7 CC genotype had median ethanol levels of 5.0mM (IQR 3.3-7.2), while 5.0mM (IQR 4.7-5.6) was in those with the ADH7 CG/GG genotype. (separationsnow.com)
  • Ethanol modulates opioidergic signaling and function at different levels, including biosynthesis, release, and degradation of opioid peptides, as well as binding of endogenous ligands to opioid receptors. (frontiersin.org)
  • consume
  • This is supported by research that determined the kinetic behavior of the ancestral ADH protein, which was found to be optimized to make ethanol, rather than consume it. (wikipedia.org)
  • effects
  • Acetaldehyde (ACD), the first oxidation product of ethanol, has been found to share many neurobehavioral effects with the drug. (frontiersin.org)
  • Nevertheless very few studies have been conducted to analyze the role of ACD in ethanol postabsorptive effects, in newborns or infant rats. (frontiersin.org)
  • What do we Know About Ethanol Pharmacological Effects in Early Ontogeny? (frontiersin.org)
  • Significant evidence implicates the endogenous opioid system (EOS) (opioid peptides and receptors) in the mechanisms underlying the psychopharmacological effects of ethanol. (frontiersin.org)
  • Evidence indicates that ethanol modulates the activity of different components of the endogenous opioid system (EOS), with a large body of data supporting the implication of opioid ligands and receptors in the mediation of some of the psychopharmacological effects of ethanol. (frontiersin.org)
  • In addition, certain genetic factors can amplify the negative effects of acetaldehyde. (wikipedia.org)