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• W176273816 abstract "Alcohol abuse is a major health problem in the developed world. Excessive alcohol intake is associated with the development of characteristic pathology, primarily of the liver. Hence, there is much interest in the link between alcohol ingestion and the development of these diseases. There is much interest in the development of measurable markers of excessive alcohol intake as well as markers to identify those individuals at risk of alcohol-related disease. This thesis examines two metabolites of ethanol: acetaldehyde and fatty acid ethyl esters, focussing on the mechanisms whereby they may be implicated in alcohol-related disease and also how they may be used as markers of alcohol intake. Acetaldehyde is the primary oxidative metabolite of ethanol and reacts with proteins to form covalent adducts, Malondialdehyde is a bifunctional aldehyde which has been shown to be increased in the plasma of alcoholics. As with acetaldehyde, malondialdehyde is capable of covalently modifying proteins. Malondialdehyde and acetaldehyde may also combine to produce a mixed adduct that may be significant in vivo. One of the initial aims of these experiments was to develop a sandwich ELISA to measure acetaldehyde-modified proteins in the plasma of human alcoholics as a marker of alcohol use. An assay was developed that reliably measured proteins modified with reactive aldehydes in vitro, but none of the plasma samples tested showed any reactivity in this assay suggesting that the concentration of modified proteins was below the sensitivity of the assay. After a considerable number of experiments aimed at increasing the sensitivity of the sandwich ELISA were unsuccessful, it was decided that other ELISA assays for the detection of alcohol related adducts be developed. These included mixed sandwich ELISAs for the measurement of acetaldehyde-modified and acetaldehyde/malondialdehyde-modified albumin, and direct ELISAs for the measurement of antibodies reactive with acetaldehyde-modified, malondialdehyde-modified and acetaldehyde-malondialdehyde- modified proteins. These assays were trialled in a small pilot study of drinkers (patients drawn from the Drug and Alcohol Rehabilitation Clinic at the Royal Brisbane Hospital) and non-drinkers drawn from students and staff of the University of Queensland, In none of the assays did the drinking groups (known alcoholics and patients admitted with a high blood alcohol level but unknown drinking history) show a statistically significant increase compared with the nondrinking group, A more extensive study will most likely determine the potential of these modified proteins and antibodies as markers of alcohol abuse. Serious liver damage (alcoholic hepatitis and liver cirrhosis) does not develop in all individuals that chronically abuse alcohol. For this reason there must be a factor(s) other than alcohol consumption that affects the generation of alcoholic liver disease. As mentioned above, acetaldehyde is produced after the ingestion of ethanol and can react with proteins to form immunogenic products. A model system was established where rats underwent a partial hepatectomy and cytosolic proteins from the excised portion of liver were modified with acetaldehyde. The rats were placed on an ethanol-containing liquid diet and immunised with their own acetaldehyde-modified cytosolic proteins for periods of ten or twenty weeks. At the end of the treatment period, the rats were killed and the degree of liver damage was scored by histological analysis. Alanine and aspartate aminotransferase activities were also measured. The results showed that the groups immunised with the acetaldehyde-modified proteins and fed ethanol had significantly more liver damage than the control groups. In addition, the liver damage was greater in the animals in the twenty week treatment group compared with the ten week treatment group. The liver damage produced was typified by the presence of microvesicular fat, and small areas of necrosis generally surrounding a lymphocytic infiltrate. While there are some differences in the liver damage seen in the current experiment and that seen in alcoholic hepatitis and cirrhosis, this model shows that the formation of acetaldehyde-modified proteins and their related antibodies results in liver damage in rats and may be significant in the early stages of alcoholic liver disease in humans. Fatty acid ethyl esters are a family of non-oxidative metabolites of ethanol present in many tissues after ethanol consumption. Demonstrated here is the existence in human liver of an acyl-CoA: ethanol acyltransferase activity which may be responsible for the synthesis of these compounds in vivo. The effects of oleoyl-CoA and ethanol concentrations, presence or absence of bovine serum albumin and detergent, pH and enzyme concentration on this activity have been determined. Acyl-CoA: ethanol acyltransferase is localised in the membrane-bound fraction. Using inhibitors directed against related enzyme activities, it has been shown that the activity is not related to serine-dependent carboxylesterases or acyl-CoA: cholesterol acyltransferase, but that it may be associated with acyl-CoA hydrolase activity, A comparison of acyl-CoA: ethanol acyltransferase and fatty acid ethyl ester synthase activity in microsomes and cytosol from the same liver suggests that these activities are comparable in vitro (on a units/g liver basis), and that both activities may be significant in vivo." @default.
• W176273816 created "2016-06-24" @default.
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• W176273816 date "2003-01-01" @default.
• W176273816 modified "2023-09-27" @default.
• W176273816 title "Ethanol metabolites in alcohol abuse" @default.
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