Biochemical and Biophysical Approaches in the Study of Ethanol-Membrane Interaction

Sun, Albert Y.

doi:10.1007/978-1-4684-3450-7_6

Cited by 16 publications

(3 citation statements)

References 88 publications

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“…The "A" system of transport, which is Na+-dependent and requires energy, serves mainly for short-chain amino acids such as alanine, glycine, and Annu. Rev (175). These changes appear to be caused by alterations in the composition of membrane phospholipids (182).…”

Section: Amino Acidsmentioning

confidence: 94%

Liver Disease and Protein Needs

Mezey

1982

Annu. Rev. Nutr.

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Protein deficiency is often associated with liver disease. The principal cause of protein deficiency is decreased dietary intake. Deficiencies in digestion and absorption that are common in alcoholics contribute to protein deficiency in alcoholic liver disease. The protein requirements in most patients with compensated chronic liver disease are not different from normal, but increase during episodes of hepatocellular deterioration. An increased demand for protein after liver injury drains nitrogen from other organs such as muscle. Aromatic amino acids released from muscle in increased amounts accumulate in the circulation of patients with chronic liver disease because of their decreased hepatic metabolism. By contrast branched chain amino acids decrease in the circulation because of their preferential uptake by extrahepatic tissues. Decreases in urea synthesis in liver disease result in the accumulation of ammonia. The causes of the decrease in urea synthesis include decreases in the enzymes and substrates of the urea cycle, alterations in portal blood flow, and a decrease in total hepatic mass. The resulting increase in ammonia in association with an increased accumulation and entry of aromatic amino acids into the brain are important factors in the pathogenesis of hepatic encephalopathy. Circulating proteins synthetized by the liver, such as albumin and clotting factors, are frequently decreased in chronic liver disease. Vitamin deficiencies that are common in liver disease contribute to abnormalities of protein metabolism. Hepatic regeneration following hepatic resection or injury is adversely affected by protein and vitamin deficiencies and by alcohol ingestion.

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Section: Amino Acidsmentioning

confidence: 94%

Liver Disease and Protein Needs

Mezey

1982

Annu. Rev. Nutr.

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“…31 Alcohol is known to inhibit Ca 2+ -ATPase in several tissues, which extrudes calcium from the cell. 32 Consequently, chronic alcohol administration would result in an increase in intracellular calcium by influencing the cellular calcium transport system. In addition, alcohol can influence the metabolism of other cellular ions.…”

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confidence: 99%

Magnesium supplementation prevents the development of alcohol-induced hypertension.

et al. 1992

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The effect of chronic alcohol administration on blood pressure was investigated in 7-week-old Wistar rats. Tail-cuff blood pressure was significantly higher in rats who received 15% ethanol in drinking water than in control rats. Intracellular free calcium concentration of lymphocytes was increased, while magnesium concentration of erythrocyte, aorta, and skeletal muscle and erythrocyte ouabain-sensitive u Na efflux rate constant (K m ) were decreased in alcohol-induced hypertensive rats but not in control rats. Extracellular fluid volume was also increased in alcohol-administered rats. Oral magnesium supplementation (1% MgO in rat chow) attenuated the development of alcohol-induced hypertension accompanied by increased magnesium concentration of erythrocyte, aorta, skeletal muscle, and K a and decreased intraerythrocyte sodium concentration. Norepinephrine half-life time of the heart and spleen was also increased in magnesium-supplemented rats. Blood pressure significantly correlated positively with intracellular calcium concentration and extracellular fluid volume, negatively with magnesium concentration of erythrocyte, aorta, skeletal muscle, and K n . These results suggest that increased intracellular calcium, which was partly due to magnesium depletion and suppressed sodium pump activity, and expanded body fluid volume had a possible role in the development of alcohol-induced hypertension. It is also suggested that oral magnesium supplementation had a hypotensive effect on alcohol-induced hypertension possibly through decreased intracellular sodium concentration caused by an activation of sodium pump and decreased sympathetic nervous activity. {Hypertension 1992;19:175-182)

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“…The advance of research on the molecular mechanisms involved in central nervous system neurotransmission has permitted a better understanding of the neurotransmitter systems involved in the actions of ethanol. Ethanol can induce primary perturbations of neuronal membranes (Sun, 1979;Goldstein, 1979;Littleton, 1980;Franks & Lieb, 1984) as well as alterations in calcium influx through voltage sensitive calcium channels (Little, Dolin & Whittington, 1988;Wang et al, 1991). It can also influence the release of several neurotransmitters such as dopamine (Kiianmaa & Tabakoff, 1983), acetylcholine (Erickson & Graham, 1973), norepinephrine (Shefner & Tabakoff, 1985) and serotonin (Tabakoff, Hoffman & Moses, 1977).…”

Section: Introductionmentioning

confidence: 99%

Influence of age and of pre‐treatment with D‐cycloserine on the behavior of ethanol‐treated rats tested in the elevated plus‐maze apparatus

Ferreira

Morato

1996

Addiction Biology

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There is evidence that ethanol is able to influence central functions through the antagonism of the NMDA-receptor system. It has been shown that this system is also involved in the modulation of anxiety-related behavior in rats. Recently, we observed gender- and age-related behavioral influences in rats tested on the elevated plus-maze apparatus The present study was undertaken in order to investigate: (1) the effects of ethanol (0.8, 1.0 or 1.2 g/kg, i.p.) on the behavior of male and female rats tested on the elevated plus-maze at 2, 3, 4 or 5 months of age; (2) the effect of the pre-treatment with D-cycloserine (3.0 or 6.0 mg/kg), an agonist of the glutamate NMDA-receptor system, 30 min before the ethanol (1.2 g/kg) injections, in rats tested in the elevated plus-maze at 2 months or 4 months of age. The results demonstrated that ethanol did not affect the time spent and the frequency of entries on the open arms of the elevated plus-maze in rats tested at 2 months of age, but increased these parameters in older animals. Moreover, the results showed that D-cycloserine, at doses that did not affect the behavior of control animals, antagonized the increased frequency of entries and time spent on open arms produced by ethanol in rats tested at 4 months of age. Our results suggest an age-related influence on the anxiolytic action of ethanol in rats tested in the elevated plus-maze. Moreover, the results suggest that the NMDA-receptor system can be involved in this effect, and strengthens the evidence for the participation of the NMDA-receptor system in anxiety-related behavior.

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Biochemical and Biophysical Approaches in the Study of Ethanol-Membrane Interaction

Cited by 16 publications

References 88 publications

Liver Disease and Protein Needs

Liver Disease and Protein Needs

Magnesium supplementation prevents the development of alcohol-induced hypertension.

Influence of age and of pre‐treatment with D‐cycloserine on the behavior of ethanol‐treated rats tested in the elevated plus‐maze apparatus

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