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Alcohol-Induced Hepatotoxicity
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
Ethanol forms ethyl esters in vivo. Laposata and Lange (1986) found that concentrations of fatty acid ethyl esters in pancreas, liver, heart, and adipose tissue were significantly higher in acutely intoxicated subjects than in controls. Since this nonoxidative ethanol metabolism occurs in the organs most commonly injured by alcohol abuse, and since some of these organs lack an oxidative ethanol metabolizing system, it was postulated that fatty acid ethyl esters and their metabolism may play a role in the production of alcohol-induced injury.
Drug Testing of Meconium: Determination of Prenatal Drug Exposure
Published in Steven H. Y. Wong, Iraving Sunshine, Handbook of Analytical Therapeutic Drug Monitoring and Toxicology, 2017
After extraction, the specimen has been most often analyzed by an immunoassay. The immunoassays used have included RIA (Diagnostics Products Corporation Coat-a-Count®, Roche Abuscreen®), Syva Emit®, Abbott FPIA (known as fluorescence polarization immunoassay), Roche ONTRAK™, and Roche Online™. (Although in one study, this last technique, which uses latex beads, demonstrated many unconfirmed positive results apparently caused by interaction of the beads with the comparably sized [1 to 5 μm] lipid droplets in the extracted and methanolic buffer reconstituted meconium specimens).53 The chromatographic techniques used have been primarily GC/MS and occasionally HPLC. Drugs and metabolites that have been detected in meconium include opiates (morphine and morphine glucuronide, codeine, and hydrocodone), methadone, meperidine and normeperidine, cocaine and metabolites (norcocaine, benzoylecgonine, benzoyl-norecgonine, ecgonin methyl ester, m-hydroxybenzoylecgonine, and cocaethylene), THC (parent and major acid metabolite, and other immunoreactive metabolites), amphetamine and methamphetamine, phencyclidine (PCP), benzodiazepines, and cotinine (nicotine metabolite). In addition, fetal exposure to ethanol has been determined by meconium analysis for various fatty acid ethyl esters: ethyl laurate, ethyl palmitate, and ethyl stearate.54
The Metabolism of Alcohol and Its Implications for the Pathogenesis of Disease
Published in Victor R. Preedy, Ronald R. Watson, Alcohol and the Gastrointestinal Tract, 2017
The possible pathogenic role of a nonoxidative pathway of alcohol metabolism to form fatty acid ethyl esters was suggested by Laposata and Lange.147 The capacity of alcohol to form ethyl esters in vivo had been demonstrated by Goodman and Deykin148 and also by Lange149 who purified the enzyme.150 Laposata and Lange147 found that in acutely intoxicated subjects, concentrations of fatty acid ethyl esters in pancreas, liver, heart, and adipose tissue were significantly higher than in controls. Since this nonoxidative alcohol metabolism occurs in humans in the organs most commonly injured by alcohol abuse, and since some of these organs lack oxidative alcohol metabolism, Laposata and Lange147 postulated that fatty acid ethyl esters may have a role in the production of alcohol-induced injury. Further experiments are needed to verify this interesting hypothesis.
High alcohol-producing Klebsiella pneumoniae causes fatty liver disease through 2,3-butanediol fermentation pathway in vivo
Published in Gut Microbes, 2021
Nan-Nan Li, Wei Li, Jun-Xia Feng, Bing Du, Rui Zhang, Shu-Heng Du, Shi-Yu Liu, Guan-Hua Xue, Chao Yan, Jing-Hua Cui, Han-Qing Zhao, Yan-Ling Feng, Lin Gan, Qun Zhang, Wei-Wei Zhang, Di Liu, Chen Chen, Jing Yuan
Under normal conditions, ethanol is constantly produced by the intestinal microbiota in the human gut, as increased blood alcohol concentrations were detected after the intake of alcohol-free food,20,21 but the endogenous ethanol is rapidly and almost completely removed from portal blood by liver ADHs, catalases, and the microsomal ethanol-oxidizing system. It remained to be determined whether HiAlc Kpn utilizes the 2,3-butanediol fermentation pathway to produce high-level endogenous alcohol in vivo, which would be different from the alcohol-production pathway used by yeast. Considering all of the potential alcohol-producing pathways in bacteria, we found that the majority of the enriched proteins and metabolites were associated with the 2,3-butanediol fermentation pathway (Figure 4d), which is a neglected pathway for alcohol production from glucose and glycerol metabolism in vivo. Accordingly, the key upregulated enzymes and metabolites all belonged to this pathway (Figure 4d). On the one hand, the pathway is capable of efficiently transforming sugar and glycerol into alcohols and acids. On the other hand, the metabolites derived from alcohol catabolism, including acetaldehyde, acetic acid and fatty acid ethyl esters, may also cause tissue injury and hepatic steatosis.
Molecular mechanisms of ethanol biotransformation: enzymes of oxidative and nonoxidative metabolic pathways in human
Published in Xenobiotica, 2020
Grażyna Kubiak-Tomaszewska, Piotr Tomaszewski, Jan Pachecka, Marta Struga, Wioletta Olejarz, Magdalena Mielczarek-Puta, Grażyna Nowicka
A number of toxic effects of ethanol result not only from its direct impact on the body constituents, but is the result of the action of toxic metabolites formed during its biotransformation. Acetaldehyde formed during the aerobic metabolism of ethanol with the help of alcohol dehydrogenase (ADH), microsomal ethanol oxidizing system (MEOS) or, to a much lesser extent by hepatic catalase (CAT), plays a special role here. Acetaldehyde corresponds to, among others for the development of alcoholic liver disease (ALD), which is a sequence of alcoholic hepatitis, alcoholic cirrhosis (AC) and hepatocellular carcinoma (HCC). By-products of ethanol oxidation, such as oxygen free radicals (ROS), are also dangerous (Teschke, 2018). Also products of non-oxidative ethanol metabolism may be toxic. For example, fatty acid ethyl ester (FAEE) has been shown to be responsible for pancreatic acinar cell injury and myocardial damage (Laposata et al., 2002). Important for clinical and diagnostic reason is also the polymorphism of enzymes involved in ethanol biotransformation, as it determines not only the efficiency of metabolic processes, but also its organ specificity.
The interpretation of hair analysis for drugs and drug metabolites
Published in Clinical Toxicology, 2018
Eva Cuypers, Robert J. Flanagan
Regarding the Society of Hair Testing consensus for the use of alcohol markers in hair for assessment of both abstinence and chronic excessive alcohol consumption [91], the direct determination of ethanol itself in hair is not possible due to its volatility and its potential absorption from external sources. Instead, the minor ethanol metabolites ethyl glucuronide, ethyl sulfate, and/or fatty acid ethyl esters can be measured in hair as indirect markers of alcohol consumption. The fatty acid ethyl esters measured were ethyl myristate, ethyl palmitate, ethyl oleate, and ethyl stearate. For the interpretation of results prior to 2016 the Society of Hair Testing recommended that the sum of the concentrations of these four esters should be used when testing for alcohol use, but the 2016 consensus guidelines now suggest that only ethyl palmitate should be used. The fact that legal judgments will have been made based on the earlier, superseded guidelines inevitably raises questions as to the reliability of the decisions made.