Effects Of Acute Ethanol Treatment Research Articles

Ethanol's fluidizing effects on RBC membranes from children at risk for alcoholism

The fluidizing effects of ethanol on membrane fluidity at 37 degrees C have been assessed using steady-state anisotropy measurements in both children at high risk for developing alcoholism and control children. Erythrocyte membranes were labeled with 1,6-diphenyl-1,3,5-hexatriene (DPH) and fluidity measurements recorded by steady-state fluorescence anisotropy for three ethanol concentrations--0, 0.5 M, and 1.0 M. The in vitro fluidizing effects of acute ethanol treatment by concentration were clearly shown in both groups. However, RBC membranes taken from children at high risk for developing alcoholism showed no significant differences in baseline membrane fluidity or to the fludizing effects of ethanol.

Maternal-fetal folate transfer: effect of ethanol and dietary folate deficiency

The effects of acute ethanol treatment and dietary folate deficiency on maternal-fetal folate transfer were studied to asses the hypothesis that the potentiation of ethanol's toxic effect on the fetus during ongoing folate deficiency was due to the impairment of folate transfer. Sprague-Dawley rats were fed either a folate-deficient diet (0.2 mg/kg) or a folate-sufficient diet (2 mg/kg) for an average of 11 weeks before pregnancy and continued until gestation day 11 when they were sacrificed. On gestation day 11, pregnant rats were treated with either ethanol (2.5 g/kg body weight) or isocaloric sucrose (control) followed by an intravenous administration of 3H-folate (2 muCi/100 g body weight) at 120 minutes. At 210 minutes, maternal blood and feto-placental tissues were removed for radioactivity measurement. Folate status and ethanol treatment had no effect on the distribution of 3H-folate in maternal circulation. However, contrary to the hypothesis, the uptake of 3H-folate by feto-placental tissues was increased in folate deficiency and by ethanol treatment, indicating that folate transfer was not impaired by the ethanol treatment. Other possibilities are discussed.

Ethanol influence on calcium uptake and insulin release by rat islets.

Effect of acute ethanol treatment on simultaneous 45Ca++ uptake and insulin response to glucose was measured in isolated rat pancreatic islets. Ethanol, given ip 1 gm/Kg 1 h prior to sacrifice of the animal, decreased significantly 45Ca++ uptake and insulin response to 8.3 and 16.7 mM glucose. Addition of ethanol to the incubation media inhibited 45Ca++ uptake and insulin release in a dose-related matter. Ionophore A23187, which is known to enhance 45Ca++ efflux, decreased 45Ca++ uptake without affecting insulin release. Inhibitory effects of ethanol and ionophore A23187 were not additive when islets were exposed to both test substances simultaneously. Forskolin, an activator of the adenylate cyclase system potentiated the glucose mediated insulin response in rat islets. However, ethanol decreased the insulin response of islets exposed to glucose and forskolin. The data show that ethanol inhibits 45Ca++ uptake response to glucose and that ethanol influence on insulin release may involve a site beyond the formation of cyclic AMP in the process of excitation-secretion coupling.

The effect of acute ethanol treatment on rates of oxygen uptake, ethanol oxidation and gluconeogenesis in isolated rat hepatocytes.

In hepatocytes isolated from fed rats, acute ethanol pretreatment (at a dose of 5.0 g/kg body wt.) did not change rates of O2 uptake. In cells from starved animals, acute ethanol pretreatment increased O2 uptake by 17-29%. The increased O2 uptake in hepatocytes from starved rats was not accompanied by increased rates of ethanol oxidation, but was accompanied by increased rates of gluconeogenesis under some conditions. The provision of ethanol (10 mM) as a substrate to cells from fed or starved rats decreased O2 uptake in the absence of other substrates or in the presence of lactate, and increased it in the presence of pyruvate or lactate and pyruvate. The results of this study show that the acute effects of ethanol on liver O2 uptake are dependent on the physiological state of the liver. Previously reported large (2-fold) increases in O2 uptake after acute ethanol pretreatment may have been an artefact owing to low control uptake rates (approximately 1.8 micromol/min per g wet wt. of cells) in the liver preparation used. The ATP contents (2.4-2.6 micromol/g wet wt. of cells) and rates of O2 uptake (2.5-5.0 micromol/min per g wet wt. of cells) of cells used in the present study were the same as values reported under conditions close to those in vivo. Therefore the increase in O2 uptake in cells from starved rats after acute ethanol pretreatment is likely to be of physiological significance.

Endorphins in inbred mice with variable sensitivity to ethanol: Effect of acute ethanol treatment

Resting levels of B-endorphin like immunoreactivity were determined in the hypothalamus, neurointermediate lobe and anterior lobe of the pituitary gland and the serum of inbred mice strains ( C57BL 6 , BALB C and DBA 2 ). C57BL 6 mice showed the highest content of B-endorphin like immunoreactivity in the neurointermediate lobe, anterior lobe and serum. Animals were injected i.p. with either an ethanol solution (3g ethanol/Kg b. wt.) or saline. 45 minutes post ethanol treatment the B-endorphin like immunoreactivity content was increased in the serum of all three strains of mice studied and was decreased in the hypothalamus of the C57BL 6 mice. Studies with reverse phace HPLC indicated some differences in the relative proportions of the various forms of B-endorphin in some tissues among the three strains of mice. These results suggest that genetically determined differences in endorphin levels may be involved in some of the genetically determined differences in responses to ethanol.

Effect of ethanol on dop amine synthesis in rat striatal synaptosomes

We have examined the effects of acute and chronic ethanol treatment and of ethanol withdrawal on dopamine synthesis in rat striatal synaptosomes in vitro. Our studies showed that acute exposure to ethanol produces a dose-related decrease in dopamine synthesis in synaptosomes. This effect of acute ethanol treatment is time-dependent, since there is an initial stimulation of dopamine synthesis, which then is followed by a depression of synthesis. Chronic exposure to ethanol in the form of a liquid diet for 2 weeks does not alter dopamine synthesis in striatal synaptosomes. After withdrawal from ethanol, dopamine synthesis in striatal synaptosomes is decreased.

Mechanism of the effect of acute ethanol on hexobarbital metabolism

The effect of acute ethanol treatment on hepatic metabolism of hexobarbital (Hb) was studied in the rat. Oral administration of 3 g/kg of ethanol (15% w/v) inhibited Hb hydroxylase activity 45–50 per cent. A dose-response relationship was found for ethanol inhibition of Hb metabolism. The overall hepatic microsomal protein content was not affected, but the hepatic cytochrome P-450 level was reduced approximately 42 per cent by this ethanol treatment. Corticosterone (12.5 mg/kg, i.p.) inhibited Hb hydroxylase activity 43 per cent. The combination of ethanol and corticosterone treatment further inhibited Hb hydroxylase activity. Study in vitro showed that corticosterone inhibited Hb metabolism competitively. Ethanol caused a 3-fold increase in the plasma corticosterone level but had no effect on plasma corticosterone of adrenalectomized rats. Hexobarbital metabolism was not affected by ethanol in adrenalectomized rats. Thus, the inhibition of hepatic Hb metabolism by acute ethanol was caused by the increased release of corticosterone induced by ethanol.

The effect of acute ethanol treatment on lipid-reesterifying enzymes of the rat small bowel.

The acute effects of intraduodenal administration of ethanol, 5 g/kg body weight, on intestinal activities of lipid-reesterifying and disaccharidase enzymes of the small bowel were studied. Results were compared to those produced in controls receiving isocaloric amounts of glucose by the same route. Acyl-CoA:monoglyceride acyltransferase, acyl-CoA synthetase (acid:CoA ligase (AMP) EC 6.2.1.3), sucrase, and lactase assays were performed on jejunal samples; acyl-CoA synthetase assay was performed on ileal samples. Ethanol produced greater activities of the lipid-reesterifying enzymes in the jejunum than did glucose. Ileal specific activity of acyl-CoA synthetase was also increased in the experimental group. No effect of ethanol on jejunal disaccharidase enzyme activities was noted. It is concluded that ethanol given acutely has a specific stimulating effect on intestinal enzymes involved in lipid absorption.