1980
DOI: 10.1016/s0091-3057(80)80019-0
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Elevated blood acetaldehyde in alcoholics with accelerated ethanol elimination

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1982
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Cited by 110 publications
(19 citation statements)
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“…4 5 After drinking ethanol most acetaldehyde is not only formed in the liver, but is also immediately oxidised there, so that little enters the blood in normal subjects. 6 7 In alcoholics given infusions of ethanol, however, higher blood levels of acetaldehyde have been reported.7 Both a 'vicious cycle' theory of alcoholic liver injury mediated by acetaldehyde9 and a primary abnormality of acetaldehyde metabolism predisposing to alcoholism10 have been suggested to explain this difference, but the reason for it remains unclear, and the original studies have been criticised because the methods used to measure acetaldehyde were inadequate.1" More acetaldehyde may leave the liver in the blood if the rate of its formation from ethanol increases, or if the liver's capacity to oxidise acetaldehyde falls. In alcoholics both mechanisms are possible, as the rate of ethanol metabolism may be increased12 13 and the activity of hepatic acetaldehyde dehydrogenase (acetaldehyde dehydrogenase) is reduced.14 In the majority of biochemical reactions, however, enzyme activity is not the rate-limiting factor, so that a reduction in hepatic acetaldehyde dehydrogenase activity may not necessarily limit acetaldehyde oxidation in the liver, just as alcohol dehydrogenase activity is not ratelimiting for the oxidation of ethanol.…”
mentioning
confidence: 99%
“…4 5 After drinking ethanol most acetaldehyde is not only formed in the liver, but is also immediately oxidised there, so that little enters the blood in normal subjects. 6 7 In alcoholics given infusions of ethanol, however, higher blood levels of acetaldehyde have been reported.7 Both a 'vicious cycle' theory of alcoholic liver injury mediated by acetaldehyde9 and a primary abnormality of acetaldehyde metabolism predisposing to alcoholism10 have been suggested to explain this difference, but the reason for it remains unclear, and the original studies have been criticised because the methods used to measure acetaldehyde were inadequate.1" More acetaldehyde may leave the liver in the blood if the rate of its formation from ethanol increases, or if the liver's capacity to oxidise acetaldehyde falls. In alcoholics both mechanisms are possible, as the rate of ethanol metabolism may be increased12 13 and the activity of hepatic acetaldehyde dehydrogenase (acetaldehyde dehydrogenase) is reduced.14 In the majority of biochemical reactions, however, enzyme activity is not the rate-limiting factor, so that a reduction in hepatic acetaldehyde dehydrogenase activity may not necessarily limit acetaldehyde oxidation in the liver, just as alcohol dehydrogenase activity is not ratelimiting for the oxidation of ethanol.…”
mentioning
confidence: 99%
“…Moreover, ethanol metabolites (including acetaldehyde) were found to be probable activators of the NLRP3 inflammasome . However, toxicological monitoring of acetaldehyde is challenging, given the very low concentrations produced after alcohol consumption in humans . Indeed, acetaldehyde is rapidly cleared from blood and metabolized into acetic acid and other compounds .…”
Section: Discussionmentioning
confidence: 99%
“…Japanese men. The blood AERs in intoxicated alcoholics after massive alcohol intake are reportedly faster, compared with the AERs in nonalcoholics (Adachi et al, 1989;Keiding et al, 1983;Lindros et al, 1980). Adachi and colleagues (1989) investigated the blood AER in 94 intoxicated Japanese alcoholic men at the day of admission and showed a similar tendency of the AER to increase as the initial blood EtOH levels increased.…”
Section: Discussionmentioning
confidence: 99%