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Ethanol liver

There are no studies in humans directly demonstrating increased production of ROM in alcoholic liver disease. However, indirect evidence does support the hypothesis that ROM are involved in the pathogenesis of ethanolic liver injury (Arthur, 1988 Tsukamoto et al., 1990 Nordmann et /., 1992). Basal whole blood... [Pg.154]

What are the effects of the other metabolites of ethanol Liver mitochondria can convert acetate into acetyl CoA in a reaction requiring ATP. The enzyme is the thiokinase that normally activates short-chain fatty acids. [Pg.1272]

At low concentrations of ethanol, liver alcohol dehydrogenase is the major route of ethanol oxidation to acetaldehyde, a highly toxic chemical. Acetaldehyde not only damages the liver, it can enter the blood and potentially damage the heart and other tissues. At low ethanol intakes, much of the acetaldehyde produced is safely oxidized to acetate in the liver by acetaldehyde dehydrogenases. [Pg.134]

Many biological processes involve oxidation of alcohols to carbonyl compounds or the reverse process reduction of carbonyl compounds to alcohols Ethanol for example is metabolized m the liver to acetaldehyde Such processes are catalyzed by enzymes the enzyme that catalyzes the oxidation of ethanol is called alcohol dehydrogenase... [Pg.645]

As regards toxicity, pyrazole itself induced hyperplasia of the thyroid, hepatomegaly, atrophy of the testis, anemia and bone marrow depression in rats and mice (72E1198). The 4-methyl derivative is well tolerated and may be more useful than pyrazole for pharmacological and metabolic studies of inhibition of ethanol metabolism. It has been shown (79MI40404) that administration of pyrazole or ethanol to rats had only moderate effects on the liver, but combined treatment resulted in severe hepatotoxic effects with liver necrosis. The fact that pyrazole strongly intensified the toxic effects of ethanol is due to inhibition of the enzymes involved in alcohol oxidation (Section 4.04.4.1.1). [Pg.302]

Liver alcohol dehydrogenase (ADH) is relatively nonspecific and will oxidize ethanol or other alcohols, including methanol. Methanol oxidation yields formaldehyde, which is quite toxic, causing, among other things, blindness. Mistaking it for the cheap... [Pg.458]

FIGURE 16.13 Liver alcohol dehydrogenase catalyzes the transfer of a hydride ion (H ) from NADH to acetaldehyde (CH3CHO), forming ethanol (CH3CH9OH). [Pg.512]

Phosphatidylethanolamine synthesis begins with phosphorylation of ethanol-amine to form phosphoethanolamine (Figure 25.19). The next reaction involves transfer of a cytidylyl group from CTP to form CDP-ethanolamine and pyrophosphate. As always, PP, hydrolysis drives this reaction forward. A specific phosphoethanolamine transferase then links phosphoethanolamine to the diacylglycerol backbone. Biosynthesis of phosphatidylcholine is entirely analogous because animals synthesize it directly. All of the choline utilized in this pathway must be acquired from the diet. Yeast, certain bacteria, and animal livers, however, can convert phosphatidylethanolamine to phosphatidylcholine by methylation reactions involving S-adenosylmethionine (see Chapter 26). [Pg.821]

Ethanol metabolism occurs mainly in the liver and proceeds by oxidation in two steps, first to acetaldehyde (CHjCHO) and then to acetic add (CH3CO2H)- When continuously present in the body, ethanol and acetaldehyde are toxic, leading to the devastating physical and metabolic deterioration... [Pg.636]

Alcohol dehydrogenase is a cytoplasmic enzyme mainly found in the liver, but also in the stomach. The enzyme accomplishes the first step of ethanol metabolism, oxidation to acetaldehyde, which is further metabolized by aldehyde dehydrogenase. Quantitatively, the oxidation of ethanol is more or less independent of the blood concentration and constant with time, i.e. it follows zero-order kinetics (pharmacokinetics). On average, a 70-kg person oxidizes about 10 ml of ethanol per hour. [Pg.52]

Ethanol is almost entirely metabolized in the liver. The first step, oxidation by alcohol dehydrogenase, yields acetaldehyde, a reactive and toxic compound. Essentially all of the acetaldehyde is converted to acetate by the liver enzyme aldehyde dehydrogenase. Aldehyde dehydrogenase is inhibited by the drag disulfiram. Given alone, disulfiram is a nontoxic substance. However, ethanol consumption in the presence of... [Pg.52]

C2H5OH, ethanol is formed by bacteria in the gastrointestinal tract in low amounts. Most of the ethanol of bacterial source is metabolized during the first liver passage yielding acetaldehyde and subsequently acetic acid. [Pg.484]

Retinoids are alcohols and accordingly soluble in ethanol, isopropanol, and polyethylenglycol. Major sources of natural retinoids are animal fats, fish liver oil (retinylesters) and yellow and green vegetables (carotenoids). Ingested retinylesters (RE) are hydrolyzed to retinol by enteral hydrolases in the intestine. ROL and carotenoids are absorbed by intestinal mucosa cells. [Pg.1072]

Ethanol also inhibits ADH-catalyzed retinol oxidation in vitro, and ethanol treatment of mouse embtyos has been demonstrated to reduce endogenous RA levels. The inhibition of cytosolic RolDH activity and stimulation of microsomal RolDH activity could explain ethanol-mediated vitamin A depletion, separate from ADH isoenzymes. Although the exact mechanism of inhibition of retinoid metabolism by ethanol is unclear, these observations are consistent with the finding that patients with alcoholic liver disease have depletedhepatic vitamin A reserves [review see [2]. [Pg.1078]

By extraction of animal lymph glands, parotid glands, pancreas, liver, milt and blood serum with diluted acetic acid-ethanol-mixtures upon removal of fat and proteins. [Pg.134]

Alcoholism leads to fat accumulation in the liver, hyperlipidemia, and ultimately cirrhosis. The exact mechanism of action of ethanol in the long term is stiU uncertain. Ethanol consumption over a long period leads to the accumulation of fatty acids in the liver that are derived from endogenous synthesis rather than from increased mobilization from adipose tissue. There is no impairment of hepatic synthesis of protein after ethanol ingestion. Oxidation of ethanol by alcohol dehydrogenase leads to excess production of NADH. [Pg.212]

Nakajima T, Wang RS, Murayama N, et al. 1990b. Three forms of trichloroethylene-metabolizing enzymes in rat liver induced by ethanol, phenobarbital, and 3-methylcholanthrene. Toxicol Appl Pharmacol 102 546-552. [Pg.281]

Sato A, Nakajima T, Koyama Y. 1981. Dose-related effects of a single dose of ethanol on the metabolism in rat liver of some aromatic and chlorinated hydrocarbons. Toxicol Appl Pharmacol 60 8-15. [Pg.288]

NPYR Syrian golden hamster Liver microsomes enhanced a-hydroxylation and mutagenicity in ethanol-consuming hamsters 10... [Pg.56]

Allopurinol has been shown to attenuate lipid peroxidation in ethanol-fed rats (Kato etal., 1990). However, this was not correlated with any possible effect on histological damage and, as discussed previously, the significance of lipid peroxidation is unclear. Despite the evidence suggesting that oxidative stress and increased oxidative metabolism may play a role in the pathogenesis of human alcoholic liver disease, it remains to be shown that treatment with specific antioxidants will modify this process. [Pg.155]

Whilst there is some evidence that ethanol can induce increased production of ROM and that ischaemia may be involved in the pathogenesis of alcoholic liver disease, there is very little data to show that specific antioxidants can modify the disease process. [Pg.156]

Bautista, A.P. and Spitzer, J.J. (1992). Acute ethanol intoxication stimulates superoxide anion production by in situ perfused rat liver. Hepatology 15, 892-898. [Pg.161]

Bernstein, J., Videla, L. and Israel, Y. (1973). Metabolic alterations produced in the liver by chronic ethanol administration changes related to energy parameters of the cell. Biochem. J. 134, 515-521. [Pg.161]

Boveris, A., Fraga, C.G., Varsavsky, A.I. and Koch, O.I. (1983). Increased chemiluminescence and superoxide production in the liver of chronic ethanol-treated rats. Arch. Biochem. Biophys. 227, 534-541. [Pg.162]

D. (1991). The decrease of superoxide dismutase activity and depletion of sulfhydryl compounds in ethanol-induced liver injury. Drug Alcohol Depend. 28, 291-294. [Pg.163]

French, S.W., Benson, N.C. and Sun, P.S. (1984). Cen-trilobular liver necrosis induced by hypoxia in chronic ethanol-fed rats. Hepatology 4, 912-917. [Pg.163]

Inomata, T., Rao, G.A. and Tsukamoto, H. (1987). Lack of evidence for increased lipid peroxidation in ethanol-induced centrilobular necrosis of rat liver. Liver 7, 233-239. [Pg.165]

Iturriage, H., Ugarte, H. and Israel, Y, (1980). Hepatic vein oxygenation, liver blood flow and the rate of ethanol metabolism in recently abstinent alcoholic patients. Eur. J. Clin. Invest. 10, 211-218. [Pg.165]

Kawase, T., Kato, S. and Lieber, C.S. (1989). Lipid peroxidation and antioxidant defence systems in rat liver after chronic ethanol feeding. Hepatology 10, 815-820. [Pg.165]

Shaw, D.S. and Jayatilleke, E. (1992). The role of cellular oxidases and catalytic iron in the pathogenesis of ethanol-induced liver injury. Life Sci. 50, 2045-2052. [Pg.171]

Sinaceur, J., Ribiere, C., Sabourault, D. and Nordmann, R. (1985). Superoxide formation in liver mitochondria during ethanol intoxication possible role in alcohol toxicity. In Free Radicals in Liver Injury (eds. G. Poli, K.H. Cheeseman, M.U. Dianzani and T.F. Slater) pp. 175-177. IRL Press, Oxford. [Pg.171]


See other pages where Ethanol liver is mentioned: [Pg.13]    [Pg.13]    [Pg.106]    [Pg.212]    [Pg.212]    [Pg.235]    [Pg.78]    [Pg.119]    [Pg.172]    [Pg.174]    [Pg.200]    [Pg.154]    [Pg.154]    [Pg.154]    [Pg.155]    [Pg.155]    [Pg.155]    [Pg.233]   
See also in sourсe #XX -- [ Pg.423 , Pg.433 ]

See also in sourсe #XX -- [ Pg.21 , Pg.25 , Pg.26 ]




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