By W. K. Lelbach (auth.), Priv. Doz. Dr. med. Helmut Karl Seitz, Professor Dr. med. Burkhard Kommerell (eds.)
Alcohol abuse ranks one of the commonest and likewise the main critical environmental dangers to human healthiness. Its importance is heightened by means of the potential for prevention through removing of the behavior, although, infrequently exerted. The prevalence of deleterious results on human future health has relentlessly risen long ago years for quite a few elements. They comprise migration of populations and, rather, elevated urbanization. hence, in a few elements of the realm, inhabitants teams formerly spared became concerned, that's additionally re flected within the expanding variety of breweries and distilleries within the constructing nations. Social, spiritual, and gender-related boundaries to alcohol intake are loosening, and the monetary development of a few segments of populations now allow them to shop for alcoholic drinks. hence the best percent upward thrust within the usa has lately been in black girls. children and adolescents drink extra alcoholic drinks than ever, and starting to be alcohol abuse via pregnant girls has enable to a rise of the prevalence of the fetal alcohol syndrome. whereas the social and behavioral, together with psychiatric, results of alcoholism are incredible, the gastrointestinal and, fairly, hepatic manifestations are the main frequent somatic results, and persistent hepatic sickness in alcoholics appears to be like to reason the best rate to society. certainly, mortality from liver cirrhosis is taken into account a competent index of alcohol intake in a country.
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Extra resources for Alcohol Related Diseases in Gastroenterology
Mitochondria of alcohol-fed animals have a reduction in cytochrome a and b content (Koch et al. 1977; Rubin et al. 1970) and in succinic dehydrogenase activity (Oudea et al. 1970; Rubin et al. 1970). The respiratory capacity of the mitochondria was found to be depressed (Gordon 1973; Hasumura et al. 1975b; Kiessling and Pilstrom 1968; Rubin et al. 1972) using pyruvate, succinate, and acetaldehyde as substrates. After chronic alcohol consumption, the liver mitochondria are unusually susceptible to the toxic effects of acetaldehyde, and a variety of important mitochondrial functions, such as fatty acid oxidation, are depressed, even in the presence of relatively low acetaldehyde concentrations (Matsuzaki and Lieber 1977).
S. Lieber Blomstrand R, Kager L, Lantto 0 (1973) Studies on the ethanol-induced decrease of fatty acid oxidation in rats and human liver. Life Sci 13: 1131-1141 Bode JC, Zelder 0, Rumpelt HJ, Wittkamp U (1973a) Depletion of liver adenosine phosphates and metabolic effects of intravenous infusion of fructose or sorbitol in man and in the rat. Eur J Clin Invest 3: 436-441 Bode JC, Bode C, Rumpelt HJ, Zelder 0 (1973b) Loss of hepatic adenosine phosphates and metabolic consequences following fructose or sorbital administration in man and in the rat.
1975). More direct proof was obtained from studies of microsomal proteins (Ohnishi and Lieber 1977). The rise in cytochrome P-450 involved a hemoprotein different from those induced by phenobarbital or 3-methylcholanthrene treatment. Studies by Joly et al. (1976, 1977) also showed that chronic ethanol administration to rats is associated with the appearance of a form of cytochrome P-450 with spectral and catalytic properties different from those of the cytochrome P-450 of control, phenobarbital-treated, and methylcholan-threne-treated rats.