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Acetaldehyde determination in wine --- Acidimetry

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Alcool. --- Acétaldéhyde. --- Psychobiologie. --- Alcool --- effets secondaires.

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Liver diseases related to chronic alcohol consumption are not only due to malnutrition but mainly to the hepatotoxicity of ethanol. This toxicity stems from its metabolism by alcohol dehydrogenase and cytochrome P450 2E1 (CYP2E1). The metabolism results in a production of acetaldehyde, which is toxic to the organism, but also results in an increase of NADH. This promotes steatosis by stimulating the synthesis of fatty acids and preventing their oxidation. In addition, CYP2E1 is induced by ethanol. Excess of ethanol metabolism generates free radicals leading to oxidative stress with lipid peroxidation, membrane damage and alteration of the activity of certains enzymes. All these mechanisms contribute to inflammation and necrosis of liver cells and a progressive fibrosis and cirrhosis. Therefore, prevention and therapy of steatosis and more severe hepatic lesions, requires a multifactorial approach: control of alcohol consumption and the addition for instance, of S-adenosylmethionine and phosphatidylcholine by taking PPC Les maladies hépatiques liées à une consommation chronique d’alcool ne sont pas dues uniquement à une malnutrition mais essentiellement à l’hépatotoxicité de l’éthanol. Cette toxicité provient de son métabolisme par l’alcool déshydrogénase et le cytochrome P450 2E1 (CYP2E1). Son métabolisme résulte en une production d’acétaldéhyde qui est toxique pour l’organisme mais aussi une augmentation de taux de NADH. Ceci induit la stéatose par stimulation de la synthèse d’acides gras et l’inhibition de leur oxydation.
De plus, le CYP2E1 est induit par l’éthanol. L’excès de métabolisation de l’éthanol génère des radicaux libres qui mènent à un stress oxydatif avec une peroxydation lipidique, des dommages membranaires et une altération de l’activité de certains enzymes.
Tous ces mécanismes contribuent à une nécrose et une inflammation des cellules du foie et progressivement à une fibrose et une cirrhose.
C’est pourquoi, la prévention et la thérapie de la stéatose et des lésions hépatiques plus sévères, passent par une approche multifactorielle : contrôle de la consommation d’alcool et par exemple, la reconstruction de réserve de GSH en administrant un précurseur de la cystéine comme l’acétylcystéine ou le S-adenosylmethionine (SAM) ainsi que la protection des phosphatidylcholines dans les membranes par administration de PPC.

Alcohol-Related Disorders --- Cytochrome P-450 CYP2E1 --- Alcohol Dehydrogenase --- Acetaldehyde --- Liver Diseases --- Liver Cirrhosis

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Ethanol, the main psychopharmacologically active ingredient of alcoholic drinks, represents a paradigmatic example of a research subject intrinsically able to perpetually self-generate interdisciplinary cutting-edge investigations. This eBook was inspired by the aim of providing an up-to-date characterization of the diverse effects of ethanol, of the possible mechanisms of action on different intracellular systems as well as of the hypothesized actions of ethanol and/or its metabolites on various neurotransmitters and neuromodulators. Indeed, the eBook provides a factual example of an excellent synthesis on the complex relationship between ethanol and its main biologically active metabolites (Chapter 1), on the behavioral and molecular consequences of early exposure to them (Chapter 2), on the recent proposals, advanced by the preclinical research, for new therapeutic approaches to distinct aspects of alcoholism (Chapter 3) and on the most recent and original preclinical evidence of the interactions between ethanol and/or its metabolites and the dopaminergic, adenosinergic and endocannabinoidergic systems (Chapter 4). Overall we believe that this eBook accomplishes its main goals of widening the perspective on this research subject and offering the readership a newer and, simultaneously, up-to-date and comprehensive scenery on ethanol’s and ethanol's active metabolites neurophysiological and behavioral effects.

UchB --- Prenatal-exposure --- Self-administration --- Salsolinol --- Motivation --- Ehanol --- Stress --- Acetaldehyde --- Caffeine --- Nicotine

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Methanol. --- Methanol --- Acetone. --- Acetaldehyde. --- forests --- Gas exchange --- Air flow --- pollutant emission --- Belgium