Describe And Explain Ethanol Catabolism Pathways In Humans,
1597 WordsFeb 28, 20177 Pages
Describe and explain ethanol catabolism pathways in humans, the metabolic effects of excessive alcohol consumption and describe the long-term treatment and prognosis of this disease.
Ethanol is a small two-carbon molecule, referred to as alcohol (1, 4); it comes from the fermentation of grains such as cane sugar molasses etc. Fermentation is the process by which a substance such as carbohydrates for example, sugars are turned into alcohol by the action of microorganisms such as yeast, that eventually dies as alcohol levels rise during fermentation (1).
Upon consumption and digestion of alcohol, different metabolic pathways are triggered to aid in elimination. Therefore, after alcohol is swallowed, it is absorbed primarily from the small…show more content… Oxidation of ethanol to acetaldehyde involves NAD+, an intermediate electron carrier, reduced by two electrons to form NADH (2). The oxidation of alcohol therefore, involves the generation of a cytosolic environment, which is extremely reduced in liver; this in turn leaves the cells of the liver cells in a condition that is highly susceptible to damage from the by-products of ethanol metabolism, such as acetaldehyde and free radicals (2, 4).
The second oxidative pathway involved in metabolising ethanol induced by individuals who chronically consume alcohol, is the microsomal ethanol oxidising system (MEOS), which involves a cytochrome P450, to be specific, the CYP2E1 isozyme, which is mainly present in the microsome and requires the electron carrier NADPH+ instead of NAD+ as for ADH (4). The induction of CYP2E1 by excessive alcohol consumption plays a vital role in metabolizing ethanol to acetaldehyde at elevated levels of ethanol concentrations (2, 3, 4). In addition to CYP2E1, inducing ethanol oxidation in the liver, CYP2E1¬ dependent ethanol oxidation may also occur in other tissues, such as the brain, where there is low levels of ADH activity. CYP2E1 also produces ROS, which increase the risk of tissue damage. Induction of the MEOS pathways, which involves CYP2E1, can lead to the production