Acute effect of EtOH on Mg2+homeostasis in liver cells:  evidence for the activation of an Na+/Mg2+exchanger

The acute administration of ethanol mobilizes a considerable amount of Mg2+ from perfused rat livers and isolated hepatocytes in a dose-dependent fashion in the absence of release of cellular K+ or lactate dehydrogenase (LDH) in the extracellular medium. Mg2+extrusion becomes detectable within 2 min and reaches the maximum within 8 min after ethanol addition, declining toward the basal value thereafter irrespective of the persistence of alcohol in the perfusion system and the dose of ethanol administered. The effect is the result of a specific impairment of Mg2+transport and/or regulatory mechanisms. In fact, Mg2+ extrusion does not occur under conditions in which 1) ethanol is replaced by an equivalent dose of DMSO, 2) amiloride or imipramine are used as inhibitors of the Na+/Mg2+exchanger, 3) extracellular Na+ is replaced by an equimolar concentration of choline chloride, and 4) 4-methylpyrazole is used to specifically inhibit alcohol dehydrogenase and cytochrome P-4502E1. Finally, the observation that the cellular level of ATP is markedly reduced after acute ethanol administration would suggest that Mg2+ extrusion results from a decreased buffering capacity of cytosolic Mg-ATP complex.

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The role of free serum tryptophan in the biphasic effect of acute ethanol administration on the concentrations of rat brain tryptophan, 5-hydroxytryptamine and 5-hydroxyindol-3-ylacetic acid

Biochemical Journal ◽

10.1042/bj1600315 ◽

1976 ◽

Vol 160 (2) ◽

pp. 315-324 ◽

Cited By ~ 59

Author(s):

A A Badawy ◽

M Evans

Keyword(s):

Rat Brain ◽

Tryptophan Metabolism ◽

Ethanol Administration ◽

Acute Administration ◽

Free Tryptophan ◽

Biphasic Effect ◽

Acute Ethanol ◽

Comparison Of The Results ◽

Ylacetic Acid

1. Acute administration of ethanol exerts a biphasic effect on the concentrations of rat brain tryptophan, 5-hydroxytryptamine and 5-hydroxyindol-3-ylacetic acid. Both effects are associated with corresponding changes in the availability of circulating free tryptophan. 2. The initial increases in the above concentrations are prevented by ergotamine, are unaltered by allopurinol and are potentiated by theophylline, whereas the later decreases are prevented by both ergotamine and allopurinol. 3. It is suggested that the initial enhancement by ethanol of brain tryptophan metabolism is caused by catecholamine-mediated lipolysis followed by displacement of protein-bound serum tryptophan, whereas the activation of liver tryptophaan pyrrolase, which is produced by the same mechanism, leads to the later decreases in the brain concentrations of tryptophan and its metabolites. 4. The initial effects of ethanol can be reproduced by an equicaloric dose of sucrose, and a comparison of the two treatments alone could therefore be misleading. 5. The effects of ethanol on liver and brain tryptophan metabolism have also been examined in mice, and a comparison of the results with those previously reported suggests that the ethanol effects are strain-dependent.

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Effect of ethanol on amino acid absorption across in vivo rat intestine

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1981.241.2.g176 ◽

1981 ◽

Vol 241 (2) ◽

pp. G176-G181

Author(s):

R. S. Green ◽

R. G. MacDermid ◽

R. L. Scheig ◽

J. J. Hajjar

Keyword(s):

Amino Acid ◽

Acute Effect ◽

Ethanol Administration ◽

Rat Intestine ◽

Single Pass ◽

Acid Absorption ◽

Amino Acid Absorption ◽

Acute Ethanol

The acute effect of ethanol on amino acid absorption across the in vivo rat intestine was studied using single-pass continuous perfusion and recirculation techniques. The single-pass steady-state perfusion was used to examine the effect on the entire small intestine and recirculation perfusion to examine the effect on short intestinal segments and to limit ethanol absorption. Unlike the in vitro findings of other investigators, ethanol does not cause inhibition of net amino acid absorption in vivo unless the alcohol is perfused in 2 M or higher concentrations. The inhibition that is observed at these concentrations is very likely due to severe injury and shedding of intestinal cells as evidenced by an increased recovery of DNA in the perfusates. The findings suggest that acute ethanol administration, in concentrations that are comparable to those found in the upper intestines of humans after the ingestion of moderate doses of alcohol, does not have a prominent effect on amino acid absorption across the in situ rat intestine. Under these conditions, the ethanol inhibition of active absorption is masked by enhanced diffusion of the amino acids across the intestine.

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Regulation of brain anandamide by acute administration of ethanol

Biochemical Journal ◽

10.1042/bj20061898 ◽

2007 ◽

Vol 404 (1) ◽

pp. 97-104 ◽

Cited By ~ 74

Author(s):

Belen Ferrer ◽

Francisco Javier Bermúdez-Silva ◽

Ainhoa Bilbao ◽

Lily Alvarez-Jaimes ◽

Irene Sanchez-Vera ◽

...

Keyword(s):

Fatty Acid ◽

Nucleus Accumbens ◽

Time Course ◽

Intraperitoneal Administration ◽

Ethanol Exposure ◽

In Vivo Studies ◽

Ethanol Administration ◽

Acute Administration ◽

Peripheral Tissues ◽

Acute Ethanol

The endogenous cannabinoid acylethanolamide AEA (arachidonoylethanolamide; also known as anandamide) participates in the neuroadaptations associated with chronic ethanol exposure. However, no studies have described the acute actions of ethanol on AEA production and degradation. In the present study, we investigated the time course of the effects of the intraperitoneal administration of ethanol (4 g/kg of body mass) on the endogenous levels of AEA in central and peripheral tissues. Acute ethanol administration decreased AEA in the cerebellum, the hippocampus and the nucleus accumbens of the ventral striatum, as well as in plasma and adipose tissue. Parallel decreases of a second acylethanolamide, PEA (palmitoylethanolamide), were observed in the brain. Effects were observed 45–90 min after ethanol administration. In vivo studies revealed that AEA decreases were associated with a remarkable inhibition of the release of both anandamide and glutamate in the nucleus accumbens. There were no changes in the expression and enzymatic activity of the main enzyme that degrades AEA, the fatty acid amidohydrolase. Acute ethanol administration did not change either the activity of N-acyltransferase, the enzyme that catalyses the synthesis of the AEA precursor, or the expression of NAPE-PLD (N-acylphosphatidylethanolamine-hydrolysing phospholipase D), the enzyme that releases AEA from membrane phospholipid precursors. These results suggest that receptor-mediated release of acylethanolamide is inhibited by the acute administration of ethanol, and that this effect is not derived from increased fatty acid ethanolamide degradation.

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Effect of acute ethanol administration on histone acetylation in mouse brain

Neuroscience Research ◽

10.1016/j.neures.2010.07.1873 ◽

2010 ◽

Vol 68 ◽

pp. e422-e423

Author(s):

Keisuke Mizuo ◽

Yoko Nishitani ◽

Ryuichi Katada ◽

Shunichiro Okazaki ◽

Kenji Tateda ◽

...

Keyword(s):

Histone Acetylation ◽

Mouse Brain ◽

Ethanol Administration ◽

Acute Ethanol

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Bradykinin has no acute effect on the response of forearm blood flow to sympathetic stimulation in man

Clinical Science ◽

10.1042/cs0780399 ◽

1990 ◽

Vol 78 (4) ◽

pp. 399-401 ◽

Cited By ~ 2

Author(s):

M. J. Cullen ◽

J. R. Cockcroft ◽

D. J. Webb

Keyword(s):

Blood Flow ◽

Angiotensin Ii ◽

Negative Pressure ◽

Enzyme Inhibitor ◽

Lower Body Negative Pressure ◽

Acute Effect ◽

Acute Administration ◽

Lower Body ◽

Resistance Vessels ◽

Sympathetic Responses

1. Six healthy male subjects received 0.9% (w/v) NaCl (saline) followed by incremental doses of bradykinin (1, 3 and 10 pmol/min), via the left brachial artery. Blood flow and the response of blood flow to lower-body negative pressure were measured in both forearms during infusion of saline and each dose of bradykinin. 2. Bradykinin produced a moderate and dose-dependent increase in blood flow in the infused, but not the non-infused, forearm. Lower-body negative pressure produced an approximately 15–20% reduction in blood flow in both forearms, and this response was unaffected by local infusion of bradykinin. 3. Bradykinin, in contrast to angiotensin II, had no acute effect on peripheral sympathetic responses to lower-body negative pressure. We conclude that, in forearm resistance vessels in man, withdrawal of angiotensin II, rather than accumulation of bradykinin, is likely to account for the attenuation of peripheral sympathetic responses after acute administration of a converting-enzyme inhibitor.

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Biphasic effect of acute ethanol administration on rat liver tyrosine-2-oxoglutarate aminotransferase activity

Biochemical Journal ◽

10.1042/bj1860755 ◽

1980 ◽

Vol 186 (3) ◽

pp. 755-761 ◽

Cited By ~ 5

Author(s):

A A B Badawy ◽

B M Snape ◽

M Evans

Keyword(s):

Enzyme Activity ◽

Rat Liver ◽

Actinomycin D ◽

Tyrosine Aminotransferase ◽

Ethanol Metabolism ◽

Ethanol Administration ◽

Aminotransferase Activity ◽

Biphasic Effect ◽

Initial Decrease ◽

Acute Ethanol

1. Acute ethanol administration causes a biphasic change in rat liver tyrosine aminotransferase activity. 2. The initial decrease is significant with a 200 mg/kg dose of ethanol, is prevented by adrenoceptor-blocking agnets and by reserpine, but not by inhibitors of ethanol metabolism, and exhibits many of the characteristics of the inhibition caused by noradrenaline. 3. The subsequent enhancement of the enzyme activity by ethanol is not associated with stabilization of the enzyme, but is sensitive to actinomycin D and cycloheximide. 4. It is suggested that the initial decrease in aminotransferase activity is caused by the release of catecholamines, whereas the subsequent enhancement may be related to the release of glucocorticoids.

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