Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Alcohol and the Liver

It is noteworthy, here, that one conunercial source of purified alcohol dehydrogenase is horse liver. There is a considerable quantity of this enzyme in horse liver. It is likely that alcohol arises from fermentation in the caecum of the high content of fibre present in the food of the horse. Hence its liver will be exposed chronically to high concentrations of alcohol, and the liver adapts by synthesising large quantities of the enzyme. [Pg.327]

Psychological Effects Alcohol and Behavior Effects of Chronic Heavy Drinking Alcohol and Brain Functioning Alcohol and the Liver Alcohol and Reproductive Functioning Fetal Alcohol Syndrome Moderate Drinking and Health The Development of Alcohol Abuse and Dependence Traditional Approaches to Etiology "Biopsychosocial" Approaches to Etiology Summary... [Pg.199]

Brunt PW (1984) Alcohol and the liver. In Weath-erall DJ, Ledingham JGG, Warrell DA, eds. Oxford Textbook of Medicine, pp. 12.209- 12.13. Oxford University Press, Oxford. [Pg.746]

Prescott LF Paracetamol, alcohol and the liver. BrJ Clin Pharmacol (2000) 49,291-301. [Pg.74]

Non-cancer toxicity inciudes effects that injure specific or multiple organs or systems (e.g., alcohol and the liver, lead and the nervous system). The mechanisms are almost as numerous as the number of chemicals. Specific effects and examples of chemicals that cause them are discussed in chapter 4. The mciin point to mcike here is that, for non-cancer effects, a threshold level is assumed. Below this threshold level, no toxic effects are expected because there is not enough chemical present to overcome the defense mechanisms of the cell, organ, or system. Above this threshold level, toxic effects may occur because the defense mechanisms are overwhelmed. [Pg.34]

In the past, dissociation of the nucleoprotein complex has been brought about by salt solutions or by heat denaturation,129 but, more recently, decomposition has been effected by hydrolysis with trypsin,126 or by the use of dodecyl sodium sulfate130 or strontium nitrate.131 Some virus nucleoproteins are decomposed by ethyl alcohol.132 This effect may be similar to that of alcohol on the ribonucleoproteins of mammalian tissues. If minced liver is denatured with alcohol, and the dried tissue powder is extracted with 10% sodium chloride, the ribonucleoproteins are decomposed to give a soluble sodium ribonucleate while the deoxyribonucleoproteins are unaffected.133 On the other hand, extraction with 10 % sodium chloride is not satisfactory unless the proteins have first been denatured with alcohol. Denaturation also serves to inactivate enzymes of the tissues which might otherwise bring about degradation of the nucleic acid during extraction. [Pg.309]

Ueno, S., Hidaka, T., and Okamoto, T. (1955). The occurrence of highly unsaturated, triethe-noid, and diethenoid alcohols in the liver oil of Laemonema morosum, a preliminary report. J. Jpn. Oil Chemists Soc. 4, 26-27. [Pg.51]

Avoid alcohol (ethanol), because alcohol is processed into poisonous acetaldehyde, a substance more poisonous and harmful than alcohol itself. The liver must subsequently break down this harmful substance, which is an extra burden upon the liver of a MCS patient, especially when this patient also has a defective cytochrome P450 liver enzyme (see entry 27) ... [Pg.36]

This occurs typically in alcoholic steatosis. Macrovesicular steatosis has less effect on the function of the hepatocyte and liver function tests are usually only minimally abnormal. The accumulation of fat within the hepatocyte may trigger an inflammatory response this inflammation within the hepatocyte, or hepatitis related to steatosis, is termed steatohepatitis. Continued inflammatory responses further damage hepatocytes, and the liver disease may then progress to fibrosis and cirrhosis. [Pg.51]

The physiological consequence of if jy[ is illustrated by the sensitivity of some individuals to ethanol. Such persons exhibit facial flushing and rapid heart rate (tachycardia) after ingesting even small amounts of alcohol. In the liver, alcohol dehydrogenase converts ethanol into acetaldehyde. [Pg.320]

Tht fatty liver condition can be described as follows. With alcohol consumption, the liver s main source of energy (fatly acids) is replaced by alcohol. This results in accumulation of unused fatty acids, in the form of triglycerides, with the consequent deposition of these TGs as fat. This mechanism is different from the fatty liver provoked by kwashiorkor, where a fatty liver results from the failure to synthesize the apoHpopioteins needed for exporting TGs from the liver. The fatty liver of kwashiorkor is not associated with cirrhosis, but that of alcoholism is associated with conversion of stellate cells to cells resembling those of connective tissue, i-c-, fibroblasts, Stellate cells are fat-storing cells that occur In the interstitial space between the capillaries and hcpalocytcs, called the space of Disse. [Pg.251]

Table 9.6 lists the major effects of chronic heavy drinking on body systems. As you can. see, alcohol can be highly toxic to the human body and cause extensive damage to it in a variety of ways. Two prominent body systems that alcohol harms are the brain and the liver. We will look at alcohol s chronic effects on these systems in more detail. Alcohol s chronic effects also extend to human reproductive fimetioning, which has to do with alcohol s altering the fimetioning of the hypothalamic-pituitary-gonadal endocrine axis and with fetal alcohol syndrome (FAS). [Pg.228]

Depending upon the size and time of the dose, ethanol may have two opposing effect on the biotransformation of VOCs. Intake of ethanol (short-term) in moderate amounts has a marked inhibitory effect on the biotransformation of several VOCs such as toluene, TCE, styrene, and w-xylene. However, chronic ingestion of alcohol induces the liver P450s. [Pg.2846]

A wide range of toxins has now been investigated including the kidney cortical toxins mercury chloride, - p-aminophenol, " ifosfamide, the kidney medullary toxins propyleneimine and 2-bromoethanamine hydrochloride and the liver toxins hydrazine, allyl alcohol, thioacetamide and carbon tetrachloride. The testicular toxin cadmium chloride has also been investigated in detail. The aldose reductase inhibitor HOE-843 has also been studied. ... [Pg.56]

Figure 9.3. A schematic of the active site of horse liver alcohol dehydrogenase. The bound substrate (In this case benzyl alcohol) and the cofactor NAD are sho A/n together A/ith several residues in the active site. Figure 9.3. A schematic of the active site of horse liver alcohol dehydrogenase. The bound substrate (In this case benzyl alcohol) and the cofactor NAD are sho A/n together A/ith several residues in the active site.
The mechanism of hepatocellular damage by alcohol and the reasons why there are marked interindividual variations in the susceptibility to alcohol-related liver damage are poorly understood. Ethanol may be metabolized to acetaldehyde by cytosolic alcohol dehydrogenase or it can be oxidized by the microsomal ethanol oxidase system. The metabolites from ethanol metabolism can have direct toxic effects on the cell or they may lead to a reduction in membrane fluidity or increased free radical damage potentiated by a reduction in hepatic glutathione (L9, LIO, R12). [Pg.336]

Liver Extract Kyer89 prepared a concentrated liver extract by precipitating the proteins with lead acetate and then adsorbing the active principle on carbon. The use of the lead salt had certain disadvantages in a later method, calcium chloride and sodium carbonate were added to form a precipitate of calcium carbonate which removed the protein as did lead acetate. The filtrate adjusted to pH 5 is treated with activated carbon, and the filtrate from this is treated with an additional quantity of carbon. The carbon cakes are extracted with hot 50% alcohol and the eluate is concentrated in vacuo. Tyrosine also is adsorbed and eluted with the active substance, although, with some carbons, the adsorption of tyrosine is incomplete. [Pg.292]

In conclusion, it seems very probable that the three-dimensional structures of the subunits of the yeast and liver alcohol dehydrogenases, including the presence of two zinc atoms, are similar. There must be differences in the subunit contacts since the yeast enzyme is tetrameric and the liver enzyme dimeric. There are also differences in the size of the active site pocket of the subunit and at the carboxyl terminal region of the chain since the yeast enzyme is about 40 residues shorter. [Pg.140]


See other pages where Alcohol and the Liver is mentioned: [Pg.40]    [Pg.208]    [Pg.559]    [Pg.230]    [Pg.79]    [Pg.68]    [Pg.626]    [Pg.40]    [Pg.208]    [Pg.559]    [Pg.230]    [Pg.79]    [Pg.68]    [Pg.626]    [Pg.19]    [Pg.293]    [Pg.417]    [Pg.78]    [Pg.253]    [Pg.94]    [Pg.452]    [Pg.637]    [Pg.400]    [Pg.117]    [Pg.205]    [Pg.289]    [Pg.128]    [Pg.522]    [Pg.540]    [Pg.1043]    [Pg.1119]    [Pg.230]    [Pg.543]    [Pg.9]    [Pg.70]    [Pg.60]    [Pg.396]   


SEARCH



Alcohol liver

Liver alcoholics

Liver alcoholism and

The Alcohols

The Liver

© 2024 chempedia.info