Distribution and utilization of alcohol-derived acetate in the rat.

Suokas, Antti; Forsander, Olof A.; Lindros, Kai O.

doi:10.15288/jsa.1984.45.381

Cited by 27 publications

(16 citation statements)

References 32 publications

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“…So long as ethanol is present, the acetate concentrations were almost constant, 1-2 mM, but ethanol concentrations seemed to be no effect on blood acetate levels. This increased acetate level in the blood might be used as an indicator of ethanol consumption [13,14].…”

Section: Practical Applicationsmentioning

confidence: 99%

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Simultaneous determination of formate and acetate in whole blood and urine from humans using gas chromatography–mass spectrometry

Kage¹,

Kudo

Ikeda

et al. 2004

Journal of Chromatography B

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Section: Practical Applicationsmentioning

confidence: 99%

“…Formate is considered to be an indicator for formaldehyde [1][2][3], methanol [4][5][6][7][8][9][10], and formic acid poisoning [11,12] since methanol and formaldehyde are metabolized to formic acid. As ethanol is metabolized to acetic acid, acetate is considered to be an indicator for oral ingestion of ethanol [13,14].…”

Section: Introductionmentioning

confidence: 99%

Simultaneous determination of formate and acetate in whole blood and urine from humans using gas chromatography–mass spectrometry

Kage¹,

Kudo

Ikeda

et al. 2004

Journal of Chromatography B

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“…Because the liver is the primary organ for ethanol metabolism, hepatocytes are exposed to rather high acetate concentrations in vivo following ethanol administration, with the rate of acetate production from ethanol in the rat liver estimated to be about 1.4 mmol/min per 10 8 cells, or approximately 3.5-7 mmol/min per milliliters of cell volume (assuming a typical per cell volume of 2 to 4 Â 10 29 cm 3 per cell) (Buckley and Williamson, 1977). Perfusion of liver in live rat with ethanol has been shown to result in acetate concentrations as high as 10 mM in the perfusate (Topping et al, 1984), and blood levels of acetate can reach 2.5-3 mM in rats and rabbits following acute administration of ethanol (Suokas et al, 1984;Fujimiya et al, 2003). In human chronic alcoholics, blood acetate levels close to 2 mM have been reported (Nuutinen et al, 1985).…”

Section: Actions Of Ethanol and Acetate In Hepatocytes Resultsmentioning

confidence: 99%

Different Mechanisms for Histone Acetylation by Ethanol and Its Metabolite Acetate in Rat Primary Hepatocytes

Shukla

Restrepo

Fish

et al. 2015

J Pharmacol Exp Ther

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Ethanol and its major metabolite acetate both induced histone H3 acetylation in primary culture of rat hepatocytes. The acetylation by ethanol was dependent on the reactive oxygen species and mitogen-activated protein kinase pathway, whereas that by acetate was independent of both pathways. Ethanol increased CYP2E1 protein expression but acetate had negligible effect. The level of phospho-H2AX, an indicator of DNA breaks, was elevated by ethanol but not by acetate. Ethanol and acetate differentially activated mRNA expression for different genes, e.g., IL-6, PPARg, c-Fos, Egr-1, and PNPLA3 in hepatocytes. The most striking increase (3-fold) was in PNPLA3 mRNA by ethanol with little change by acetate. It was further shown that acetate inhibited histone deacetylase activity. Taken together, these data establish for the first time that ethanol and acetate exhibit differences in their effects on hepatocytes in gene expression, P-H2AX levels, and the mechanism of histone H3 acetylation. The implications of these differences in the actions of ethanol in liver are discussed.

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“…For the measurement of ethanol and acetate, blood samples (or gastric contents) were immediately deproteinized with 2 vol ofcold 0.6 N perchloric acid and then centrifuged at 40C for 10 min at 13,000 g ( 18). Acetate was esterified to methylacetate and quantified by head space GC, essentially as described by Giles et al (19).…”

Section: Methodsmentioning

confidence: 99%

First-pass gastric mucosal metabolism of ethanol is negligible in the rat.

Smith¹,

DeMaster²,

Furne³

et al. 1992

J. Clin. Invest.

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Ethanol metabolism by gastric alcohol dehydrogenase (ADH) is thought to be an important determinant of peripheral ethanol time-concentration curves (AUCs) in rats and humans. We quantitated this metabolism in rats by measuring the gastric absorption of oral ethanol (0.25 g/kg) and the gastric venousarterial (V-A) difference of ethanol versus ethanol metabolites (acetate, acetaldehyde, and bicarbonate). Over 1 h, -20% of the ethanol was absorbed from the stomach and 70% was emptied into the duodenum. The gastric V-A difference of ethanol metabolites was < 4% of that of ethanol. Thus, gastric metabolism accounted for < 1% (< 4% of 20% absorbed) of the dose. This negligible metabolism was predictable from the low affinity of gastric ADH for ethanol. In contrast, gastric ADH has a high affinity for octanol, and 66% ofthis compound was metabolized during gastric absorption. Evidence supporting gastric metabolism of ethanol largely derives from the lower AUCs observed after oral than after intravenous administration; however, we observed increasingly higher AUCs with increasingly rapid portal vein infusions of identical ethanol doses. We conclude that gastric metabolism of ethanol is negligible in the rat, and differences in AUCs ascribed to gastric metabolism may reflect differences in ethanol absorption. (J. Clin. Invest. 1992.

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Distribution and utilization of alcohol-derived acetate in the rat.

Cited by 27 publications

References 32 publications

Simultaneous determination of formate and acetate in whole blood and urine from humans using gas chromatography–mass spectrometry

Simultaneous determination of formate and acetate in whole blood and urine from humans using gas chromatography–mass spectrometry

Different Mechanisms for Histone Acetylation by Ethanol and Its Metabolite Acetate in Rat Primary Hepatocytes

First-pass gastric mucosal metabolism of ethanol is negligible in the rat.

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