Alcohol metabolism during development

In conlcusion, the rates of ethanol metabolism and the activity of hepatic alcohol dehydrogenase are both reduced in fetal life and in the newborn when compared with values obtained in the adult. Significant microsomal ethanol oxidizing system and catalase activities are detected early in fetal life and do not increase during further fetal development However, the contribution of these two enzymes to the m vivo metabolism of ethanol during development remains to be evaluated. 

Heavy drinking—and especially "binge" drinking—are associated with both atrial and ventricular arrhythmias. Patients undergoing alcohol withdrawal syndrome can develop severe arrhythmias that may reflect abnormalities of potassium or magnesium metabolism as well as enhanced release of catecholamines. Seizures, syncope, and sudden death during alcohol withdrawal may be due to these arrhythmias. 

Maturation effected the following changes In enzymes and metabolites in orange fruit ethanol and acetaldehyde accumulated to levels of 10 mM and 0.08 mM, pyruvate decreased about 30%, pyruvate decarboxylase increased over 4 fold, alcohol dehydrogenase increased about 2 fold, the NADH to NAD ratio increased 21/2 fold and the terminal oxidase developed CN-insensitivity. The fraction of the total alternative respiratory pathway in actual use increased from 0.46 to 1.08. Induction of the alternative, CN-insensitive oxidase during maturation was interpreted as indicating that membrane function was modified which affected metabolic pathways resulting in the accumulation of ethanol and acetaldehyde. 

More than 90% of the body s supply of vitamin A is stored in the liver. The hepatic parenchymal cells are involved in its uptake, storage, and metabolism. Retinyl esters are transferred to hepatic fat-storing cells (also called Ito cells or lipocytes) from the parenchymal cells. The capacity of these fat-storing cells may determine when vitamin A toxicosis becomes symptomatic. During the development of hepatic fibrosis (e.g., in alcoholic liver disease), vitamin A stores in Ito cells disappear and the cells differentiate to myofibroblasts. These cells appear to be the ones responsible for the increased collagen synthesis seen in fibrotic and cirrhotic livers. 

Unpleasant odors may sometimes develop in wine during alcoholic fermentation, due to the formation of sulfur compounds by yeast. In view of the complexity of yeast s sulfur metabolism, there are many biochemical mechanisms capable of producing these malodorous molecules. For this reason, theories that attempt to explain the appearance of reduction defects in fermenting wines are often contradictory, and of practically no use to winemakers wishing to implement reliable preventive measures (Rankine, 1963 Eschenbruch, 1974). 

Beer, on the other hand, is produced by more complex biochemical and technological processes, which all affect its flavor. Yeast amino acid metabolism, a key to the development of beer flavor as described earlier, is affected by process temperature and use of cell immobilization techniqnes. Therefore, technologies based on these features as well as other process conditions and strain selection have been developed to control beer flavor. The combination of immobilized yeast and low-temperature primary fermentation was found to produce beers with low diacetyl amounts, therefore indicating potential of low-cost industrial application since maturation is a high-energy-consuming process. Finally, Perpete and Collin showed that during alcohol-free beer production, the enzymatic reduction of worty flavor (caused by Strecker aldehydes) by brewer s yeast was improved by cold contact fermentation. 

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