The influence of aliphatic alcohols and their halogen derivatives on the coenzyme A in the liver of mice

Ammon, H. P. T.; Heim, F.; Estler, C.-J.; Fickeis, G.; Wagner, Moshe

doi:10.1016/0006-2952(67)90130-x

Cited by 11 publications

(6 citation statements)

References 3 publications

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“…Indeed, the specific enzymatic procedure employed in this study gives CoA values for controI mouse liver about half of those reported by Ammon et al (4). The CoA concentrations we obtained in normal rat liver, however, agree well with data reported by others for …”

supporting

confidence: 90%

“…Our studies, therefore, do not support the concept that alcohol lowers the hepatic CoA concentration. Diverse methodology probably explains our inability to corroborate the prior findings of Ammon et al (4,5 ) . The CoA assay used by these investiga-ALCOHOL AND HEPATIC COA A N D ACETYL COA …”

contrasting

confidence: 57%

“…In these studies we paralleled the protocol of Ammon et al (4,5 ) but applied it to rats. Table I11 shows that rats given disulfiram and alcohol exhibited the same hepatic CoA concentration as controls given disulfiram alone or together with isocaloric glucose.…”

Section: Ministrationmentioning

confidence: 99%

“…The results of these investigations, however, have been contradictory. As regards CoA, Ammon et al (4,5 ) have shown that alcohol given intravenously to mice induces a striking depression of hepatic CoA, and this was felt to be due to complexing of the CoA with acetaldehyde generated by alcohol metabolism. On the other hand, no decrease of hepatic CoA has been demonstrated by Williamson et al (2), using a rat liver perfusion system and employing a relatively low alcohol concentration in the perfusate; or by Bode et al ( 6 ) , 2 hr after the oral administration of a single large alcohol load to rats kept on a standard diet.…”

mentioning

confidence: 99%

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The Acute Effect of Alcohol on Hepatic Coenzyme A and Acetyl CoA Concentrations

Breen¹,

Shaw²,

Levinson³

et al. 1971

Experimental Biology and Medicine

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Several investigations have shown convincingly that ethanol' inhibits the citric acid cycle in the liver (1, 2 ) , but the exact nature of this effect is still uncertain ( 3 ) . One prior study employing low alcohol levels in a perfused liver system has suggested t-hat the impairment of the citric acid cycle is due to a coordinated inhibition of citrate synthase and isocitrate dehydrogenase mediated by an increased NADH/NAD ratio ( 2 ) . It is not established, however, whether these observations apply also to the in vivo situation and to higher blood alcohol levels. Another aspect of this problem previously studied has dealt with the effect of ethanol on hepatic coenzyme A (COX) and acetyl-CoA concentrations. The results of these investigations, however, have been contradictory. As regards CoA, Ammon et al. (4, 5 ) have shown that alcohol given intravenously to mice induces a striking depression of hepatic CoA, and this was felt to be due to complexing of the CoA with acetaldehyde generated by alcohol metabolism. On the other hand, no decrease of hepatic CoA has been demonstrated by Williamson et al.(2), using a rat liver perfusion system and employing a relatively low alcohol concentration in the perfusate; or by Bode et al. ( 6 ) , 2 hr after the oral administration of a single large alcohol load to rats kept on a standard diet. The available data regarding the effect of ethanol on hepatic acetyl-CoA are equally confusing. Decreased ( 7 ) , increased (8), or unaltered ( 2 ) liver acetyl-CoA concentrations have been reported after alcohol administration to rats. These various inconsistencies have been so far either left unanswered or have been attributed to differences in species or manner of alcohol administration. Since the concentration of 1 Alcohol and ethanol 'are used interchangeably.CoA and acetyl-CoA in liver may influence importantly the citric acid cycle, it was the purpose of this study to resolve the present controversy by assessing in detail the acute effect of alcohol on hepatic CoA and acetyl-CoA levels.Materials and Methods. Two sets of experiments were carried out using nonfasted female Sprague-Dawley rats (80-100 g ) and female and male Swiss Albino mice (20 g).In the first studies, groups of rats and mice were given alcohol in various doses orally, intraperitoneally, or intravenously; and at specified times thereafter, liver CoA and acetyl-CoA concentrations and pyruvate decarboxylase activity were measured and correlated with the blood alcohol level. Pyruvate decarboxylase activity was investigated, since this enzyme participates in the reaction wherein pyruvate is converted to acetyl-CoA. In the second group of studies, we assessed the concept of Ammon et a,?. ( 5 ) that acetaldehyde derived from alcohol binds and depresses hepatic CoA. Accordingly, some animals were given disulfiram (which inhibits acetaldehyde metabolism) prior to being injected with alcohol, while other rats were given acetaldehyde directly. Controls consisted of uninjected animals and those given isocaloric glucose or sa...

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supporting

confidence: 90%

contrasting

confidence: 57%

Section: Ministrationmentioning

confidence: 99%

mentioning

confidence: 99%

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The Acute Effect of Alcohol on Hepatic Coenzyme A and Acetyl CoA Concentrations

Breen¹,

Shaw²,

Levinson³

et al. 1971

Experimental Biology and Medicine

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“…In vitro experiments have shown that at high concentrations acetaldehyde impairs mitochondrial function [13], protein synthesis and secretion [14], reacts with thiol amino acids [15] and inactivates coenzyme A [16]. Firstly acetaldehyde like other aldehydes, is chemically highly reactive.…”

mentioning

confidence: 99%

Acetaldehyde: Its Role in Alcoholic Toxicity and Dependence

Thomas

1981

British Journal of Addiction

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The role of acetaldehyde in the pathogenisis of alcohol-induced tissue damage and of alcoholism is discussed. Although there are technical difficulties in the measurement of plasma acetaldehyde, the levels appear to be elevated in chronic alcoholics and this may reflect the reduced hepatic activity of acetaldehyde dehydrogenase in these patients. Even though acetaldehyde can form morphine-like adducts with certain CNS biogenic amines, it remains to be demonstrated that these phenomena are important in alcoholics. The role of acetaldehyde toxicity in alcoholism remains at present not proven. Pathway of hepatocyte ethanol oxidation EthanolNAD ->. Alcohol ' dehydrogenase NADH nase J r H2O2 Catalase r H2O NAD NADH Acetaldehyde Acetaldehyde dehydrogenase NADPH MEOS NADP Acetate

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Alcohol

Wallgren¹

1971

Alterations of Chemical Equilibrium in the Nervous System

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The influence of aliphatic alcohols and their halogen derivatives on the coenzyme A in the liver of mice

Cited by 11 publications

References 3 publications

The Acute Effect of Alcohol on Hepatic Coenzyme A and Acetyl CoA Concentrations

The Acute Effect of Alcohol on Hepatic Coenzyme A and Acetyl CoA Concentrations

Acetaldehyde: Its Role in Alcoholic Toxicity and Dependence

Alcohol

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