The human pathway for metabolizing alcohol starts with the enzyme alcohol dehydrogenase, which catalyzes the conversion...

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The human pathway for metabolizing alcohol starts with theenzyme alcohol dehydrogenase, which catalyzes the conversion ofethanol (C2H5OH) to acetaldehyde (CH3CHO). This is followed by thealdehyde dehydrogenase 2 (ALDH2, the enzyme of interest in thisproblem), which catalyzes the conversion of acetaldehyde and HS-CoAto acetyl-CoA (CH3COâ€“Sâ€“CoA). The TCA cycle starts and oxidizes theacetyl-CoA to CO2. Draw two diagrams of this pathwayâ€”one for anindividual without AFS and another for an individual with AFS. HowALDH2 deficiency combined with ethanol input into the bloodstreamcould culminate in the accumulation of acetaldehyde in the blood ofthe patient.

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This is the explaintion thatThe primary enzymes involved in alcohol metabolism are alcoholdehydrogenase ADH and aldehyde dehydrogenase ALDH Both enzymesoccur in several forms that are encoded by different genesmoreover there are variants ie alleles of some of these genesthat encode enzymes with different characteristics and which havedifferent ethnic distributions Which ADH or ALDHalleles a person carries influence his or her level of alcoholconsumption and risk of alcoholism Researchers to date primarilyhave studied coding variants in the ADH1B ADH1C andALDH2 genes that are associated with altered kineticproperties of the resulting enzymes For example certainADH1B and ADH1C alleles encode particularlyactive ADH enzymes resulting in more rapid conversion of alcoholie ethanol to acetaldehyde these alleles have a protectiveeffect on the risk of alcoholism A variant of the ALDH2 geneencodes an essentially inactive ALDH enzyme resulting inacetaldehyde accumulation and a protective effect It is becomingclear that noncoding variants in both ADH andALDH genes also may influence alcohol metabolism andconsequently alcoholism risk the specific nature and effects ofthese variants still need further studyAlcohol and other drug AOD use AODU abuse and dependencealcoholism genetics and heredity genetic theory of AODU ethnicgroup protective factors ethanol metabolism liver alcoholdehydrogenase ADH aldehyde dehydrogenase ALDH risk factorsprotective factors alcohol flush reactionThe effects of ingested beverage alcohol ie ethanol ondifferent organs including the brain depend on the ethanolconcentration achieved and the duration of exposure Both of thesevariables in turn are affected by the absorption of ethanol intothe blood stream and tissues as well as by ethanol metabolism Themain site of ethanol metabolism is the liver although somemetabolism also occurs in other tissues and can cause local damagethere The main pathway of ethanol metabolism involves itsconversion ie oxidation to acetaldehyde a reaction that ismediated ie catalyzed by enzymes known as alcoholdehydrogenases ADHs In a second reaction catalyzed by aldehydedehydrogenase ALDH enzymes acetaldehyde is oxidized to acetateOther enzymes such as cytochrome P450 eg CYP2E1 metabolize asmall fraction of the ingested ethanolThere are multiple ADH andALDH enzymes that are encoded by different genes Some of thesegenes occur in several variants ie alleles1 and the enzymes encoded by thesealleles can differ in the rate at which they metabolize ethanol oracetaldehyde or in the levels at which they are produced Thesevariants have been shown to influence a persons drinking levelsand consequently the risk of developing alcohol abuse ordependence Studies have shown that people carrying certainADH and ALDH alleles are at significantly reducedrisk of becoming alcohol dependent In fact these associations arethe strongest and most widely reproduced associations of any genewith the risk of alcoholism As will be discussed later in thisarticle the alleles encoding the different ADH and ALDH variantsare unevenly distributed among ethnic groupsMethodsMethods will be Wild type and ALDH2 deficient mice were fed16 in LieberDeCarli diet for 4 weeks Gut permeability invivo measured by plasmatoluminal flux of FITCinulin tightjunction and adherens junction integrity analyzed by confocalmicroscopy and liver injury was assessed by analysis of plasmatransaminase activity histopathology and liver triglycerideResultIn Ethanol feeding elevated colonic mucosal acetaldehyde whichwas significantly greater in ALDH2 deficient mice ALDH2 miceshowed a drastic reduction in the ethanol diet intake Thereforethis study was continued only in wild type and ALDH2 miceEthanol feeding elevated mucosal inulin See Answer

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