Effects Of Alcohol Administration Research Articles

Mixing Misery and Gin: The Effect of Alcohol Administration on Ostracism Response.

Williams's need-threat model proposes that ostracism responses are reflexive and, because of their evolutionary significance, difficult to diminish. Alcohol is widely consumed in social contexts and for reasons of coping with social stress, and major theories of alcohol propose that intoxication disrupts cognitive appraisal of environmental threats, leading to stress relief. Surprisingly, though, no well-powered experimental research has examined the impact of alcohol intoxication on distress from social ostracism. In three studies across two independent laboratories (N = 438), participants were randomly assigned to receive either an alcoholic or nonalcoholic (i.e., no-alcohol control or placebo) beverage and were exposed to an ostracism (or social inclusion) manipulation. Results, which emerged as remarkably consistent across all studies, indicated strong and consistent effects of ostracism on mood and needs satisfaction among both intoxicated and sober participants. Findings have important implications for ostracism theory and speak to boundary conditions for alcohol's ability to relieve stress.

ALCOHOL ABOLISHES POST-STRESSOR AVERSION IN MALE RATS (POTENTIAL ROLE OF к-OPIOID RECEPTORS)

The probability of alcohol consumption by humans and experimental animals increases immediately after impact of stressors and remains at high level for some time. Neurobiological basis of this pattern is the effect of stress hormones on the mesolimbic system which is the core of the reward system in the brain that initiates learning processes. Literature data suggest that formation of aversive reactions depends on the system of dynorphin and к-opioid receptors which activates during the stress reaction. The purpose of this study was to investigate effect of alcohol administration on the post-stressor condition of the reward system and to clarify the role of к-opioid receptors in this. Experiment 1 aimed to investigation of post-stressor condition of the reward system in male and female rats and the influence of alcohol administration on it. Experiment 2 aimed to study whether alcohol affects the known from the literature aversive effect of che mical stimulation of к-opioid receptors as a model of post-stressor aversion. Methods. Appearance of preference or aversion to place where the rats were after action of the stressor was the indicator of the state of their reward syste m (place preference test). Result of the experiment 1. Condition of the reward syste m in the male rats was aversive 15 minutes after the end of the stressor action that caused avoidance of the context of environment in the future. Administration of alcohol after the end of the stressor action ceased this effect. Result of the experiment 2. Unlike the post-stressor aversion alcohol does not influence the aversion caused by stimulation of к-opioid receptors. Conclusion. Results of the study suggest that there is the aversive phase of the post-stressor state in the male rats that leads to formation of aversive associative reaction to the context of environment. Alcohol administration abolishes this phase. The involve ment of к- opioid receptors in this effect of alcohol is doubtful. But the final conclusion is possible only after direct experiment using antagonists.

Analysis of liver damage from radon, X-ray, or alcohol treatments in mice using a self-organizing map.

In our previous studies, we found that low-dose radiation inhibits oxidative stress–induced diseases due to increased antioxidants. Although these effects of low-dose radiation were demonstrated, further research was needed to clarify the effects. However, the analysis of oxidative stress is challenging, especially that of low levels of oxidative stress, because antioxidative substances are intricately involved. Thus, we proposed an approach for analysing oxidative liver damage via use of a self-organizing map (SOM)—a novel and comprehensive technique for evaluating hepatic and antioxidative function. Mice were treated with radon inhalation, irradiated with X-rays, or subjected to intraperitoneal injection of alcohol. We evaluated the oxidative damage levels in the liver from the SOM results for hepatic function and antioxidative substances. The results showed that the effects of low-dose irradiation (radon inhalation at a concentration of up to 2000 Bq/m3, or X-irradiation at a dose of up to 2.0 Gy) were comparable with the effect of alcohol administration at 0.5 g/kg bodyweight. Analysis using the SOM to discriminate small changes was made possible by its ability to ‘learn’ to adapt to unexpected changes. Moreover, when using a spherical SOM, the method comprehensively examined liver damage by radon, X-ray, and alcohol. We found that the types of liver damage caused by radon, X-rays, and alcohol have different characteristics. Therefore, our approaches would be useful as a method for evaluating oxidative liver damage caused by radon, X-rays and alcohol.

The effect of alcohol administration on social behavior of rats with experimental schizophrenia

Experimental animal modeling of schizophrenia and alcoholism allows understanding the mechanisms of comorbid pathology formation. The aim was to investigate the effect of ethanol administration on social relations in rats with experimental schizophrenia.The study was carried out on 30 Wistar adult male rats aged. After 2 weeks isolation rat social ranks were determined. Alcohol preference was evaluated in the two-bottle test. Schizophrenia was modeled by administering to rats (n = 15) dopamine precursor levodopa-carbidopa (LC) during 5 days each month in four months experiment. The control animals (n = 15) received water. All animals were subjected to intermittent alcoholization throughout the experiment after the introduction of the LC. The behavioral parameters evaluated in the “open field” and “despair” tests.It was found out that the experimental rats who received alcohol did not differ in the number of interactions compared to the rats who received only alcohol. In the rats with experimental schizophrenia a significantly higher social interactions were observed compared to the control group. This is consistent with the results of the clinical studies, which have shown that patients often drink alcohol to relieve anxiety and tension. The two-bottle test has shown the difference between the experimental and control groups only in the first week of the experiment. Apparently, this can be explained by the prolonged isolation. In the despair test, before the alcoholization, the rats with experimental schizophrenia were completely immobilized, compared to the controls. After alcoholization the differences in the despair test were not observed.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Effect of Alcohol Administration on Mg2+ Homeostasis in H9C2 Cells.

Alcoholic cardiomyopathy represents one of the main clinical complications in chronic alcoholics. This pathology contrasts the seemingly beneficial effect of small doses of alcohol on the cardiovascular system. Studies carried out in liver cells exposed acutely or chronically to varying doses of EtOH indicate that intrahepatic alcohol metabolism results in a major loss of cellular Mg2+. To investigate whether EtOH administration also induced Mg2+ extrusion in cardiac cells, H9C2 cells were exposed to varying doses of EtOH for short- or ling-term periods of time. The results indicate that H9C2 cells exposed to EtOH doses higher than 0.1% (v/v, or 15 mM) extruded Mg2+ into the extracellular medium on a time- and dose-dependent manner. Consistent with the involvement of cyP4502E1 in metabolizing EtOH, administration of chloro-methiazole (CMZ) as an inhibitor of the cytochrome prevented EtOH-induced Mg2+ loss to a large extent. EtOH-induced Mg2+ extrusion was also prevented by the administration of di-thio-treitol (DTT) and n-acetyl-cysteine (NAC), two agents that prevent the negative effects of ROS formation and free radicals generation associated with EtOH metabolism by cyP4502E1.Taken together, our data indicate that Mg2+ extrusion also occur in cardiac cells exposed to EtOH as a result of alcohol metabolism by cyP4502E1 and associated free radical formation. Interestingly, Mg2+ extrusion only occurs at doses of EtOH higher than 0.1% administered for an extended period of time. The significance of Mg2+ extrusion for the onset of alcoholic cardiomyopathy remains to be elucidated.

The effect of alcohol administration on human timing: A comparison of prospective timing, retrospective timing and passage of time judgements

Previous research suggests that human timing may be affected by alcohol administration. The current study aimed to expand on previous research by examining the effect of alcohol on prospective timing, retrospective timing and passage of time judgements. A blind between-subjects design was employed in which participants were either administered 0 g of alcohol per kilogramme of body weight (placebo), 0.4 g/kg (low dose) or 0.6 g/kg (high dose). Participants completed four types of temporal task; verbal estimation and temporal generalisation, a retrospective timing task and a passage of time judgement task. A high dose of alcohol resulted in overestimations of duration relative to the low dose and placebo group in the verbal estimation task. A high dose of alcohol was also associated with time passing more quickly than normal. Alcohol had no effect on retrospective judgements. The results suggest that a high dose of alcohol increases internal clock speed leading to over-estimations of duration on prospective timing tasks, and the sensation of time passing more quickly than normal. The absence of an effect of alcohol on retrospective timing supports the suggestion that retrospective judgements are not based on the output of an internal clock.

Prenatal exposure to ethanol: A specific effect on the H19 gene in sperm

Alcohol exposure during pregnancy induces a range of disorders in the offspring. Methylation changes in imprinted genes may play a role in the teratogenic effects of alcohol. We evaluated the possible effects of alcohol administration in pregnant mice on the methylation pattern of 5 imprinted genes (H19, Gtl2, Peg1, Snrpn and Peg3) in somatic and sperm cell DNAs of the male offspring. The effects observed were a 3% ( p < 0.005) decrease in the number of methylated CpGs of H19 in the F1 offspring sperm, a 4% ( p < 0.005) decrease in the number of methylated CpGs of H19 in the F2 offspring brain and a 26% ( p < 0.05) decrease in the mean sperm concentration. CpGs 1 and 2 of the H19 CTCF-binding site 2 exhibited significant methylation percentage losses. H19 CTCF-binding sites are important for the regulation of Igf2 gene expression. The hypomethylation of H19 may contribute to the decreased spermatogenesis in the offspring.

Functional biomarkers for the acute effects of alcohol on the central nervous system in healthy volunteers

The central nervous system (CNS) effects of acute alcohol administration have been frequently assessed. Such studies often use a wide range of methods to study each of these effects. Unfortunately, the sensitivity of these tests has not completely been ascertained. A literature search was performed to recognize the most useful tests (or biomarkers) for identifying the acute CNS effects of alcohol in healthy volunteers. All tests were grouped in clusters and functional domains. Afterwards, the effect of alcohol administration on these tests was scored as improvement, impairment or as no effect. Furthermore, dose-response relationships were established. A total number of 218 studies, describing 342 different tests (or test variants) were evaluated. Alcohol affected a wide range of CNS domains. Divided attention, focused attention, visuo-motor control and scales of feeling high and of subjective drug effects were identified as the most sensitive functional biomarkers for the acute CNS effects of alcohol. The large number of CNS tests that are used to determine the effects of alcohol interferes with the identification of the most sensitive ones and of drug-response relationships. Our results may be helpful in selecting rational biomarkers for studies investigating the acute CNS effects of alcohol or for future alcohol- interaction studies.

The Pathogenesis of Aseptic Necrosis of the Femoral Head Associated with Alcohol Drinking —The Effects of Alcohol Administration on the Osteocytes of the Rabbit—

The Pathogenesis of Aseptic Necrosis of the Femoral Head Associated with Alcohol Drinking —The Effects of Alcohol Administration on the Osteocytes of the Rabbit—

Effect of Alcohol Administration on the Liver and Serum Lipid Levels of Rats Fed with High Cholesterol or High Tocopherol Diets

Effect of Alcohol Administration on the Liver and Serum Lipid Levels of Rats Fed with High Cholesterol or High Tocopherol Diets

Effects of alcohol administration during adulthood on parvalbumin and glial fibrillary acidic protein immunoreactivity in the rat cerebral cortex

The pathology of brain atrophy mediated by alcohol was investigated in all parts of the cerebral cortex (the frontal, parietal, temporal lobes and occipital cortex) by using two markers: parvalbumin (PV) and glial fibrillary acidic protein (GFAP). Three-month old male Wistar rats were divided into control (C) and alcohol-exposed groups. The control group received distilled water, whereas the alcohol-exposed groups received either a low dose (2g/kg body wt) or a high dose (5g/kg) of ethanol for periods of 21 days, 3 or 6 months. The brains of the animals were processed for immunohistochemistry using anti-parvalbumin and anti-GFAP antibodies and the number of PV immunoreactive (PV-ir) neurons and GFAP immunoreactive (GFAP-ir) astrocytes were counted per unit area. Results showed that all groups exposed to ethanol had significantly reduced numbers of PV-ir neurons in all parts of the cerebral cortex compared to those of the control group (p<0.05). In contrast, the numbers of GFAP-ir astrocytes were increased in all parts of the cerebral cortex following the exposure to a high dose of ethanol after 21-days (but not a low dose) and both high and low doses of ethanol after 3-months or 6-months treatment compared to those of age-matched control groups (p<0.05). This indicated that in young rats (21-days), PV-ir neurons in all cerebral cortex areas seemed to be more sensitive to alcohol than GFAP-ir astrocytes. Moreover, the change in densities of both PV-ir neurons and GFAP-ir astrocytes became more apparent after exposure to prolonged and high doses of ethanol. The decrease of PV-ir neurons and the increase of GFAP-ir astrocytes indicated that alcohol may induce pathology in broad areas of the cerebral cortex. This may explain the underlying mechanism of brain atrophy and other impairments found in alcoholics. For investigations of the effects of alcohol on mediating brain pathology, we recommend the use of the two markers (PV and GFAP).

Cholinergic alterations following alcohol exposure in the frontal cortex of Aldh2-deficient mice models

We investigated the effects of alcohol (EtOH) and acetaldehyde (ACe) on choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) in the frontal cortex of Aldh2-/- (KO) mice. KO mice were used as models of Aldh2-deficient humans to examine ACe effects. Brain samples were analyzed at 40 and 120 min after 2- and 4-g/kg intraperitoneal EtOH administration by RT-PCR and Western blot. Wild-type (WT) mice exhibited a remarkable decrease in ChAT and AChE mRNA expression at both time points only after 4-g/kg EtOH treatment compared with the naive control, whereas KO mice showed a considerable reduction in cholinergic markers after 2- and 4-g/kg EtOH treatment. The 4-g/kg EtOH-induced decrease in ChAT and AChE RNA expression at both time points was significantly greater than that in obtained with the administration of 2-g/kg at 40 min in WT mice. KO mice showed a significant difference in ChAT mRNA at 40 min between the EtOH groups. The findings regarding the ChAT mRNA levels are consistent with the results of Western blot in both types of mice, with some exceptions. EtOH-induced ChAT and AChE expression in KO mice was significantly lower than that in WT mice. This genotype effect occurred mostly at 40 min after EtOH dosing. Only ACe was quantified in the brains of KO mice, whereas EtOH was detected in both types of mice in vivo. These results suggest that EtOH and ACe combined or high EtOH alone alters cholinergic markers expression via changes in presynaptic and postsynaptic processes in the mice frontal cortex, thus indicating that central cholinergic neurons may be sensitive to EtOH and ACe.

Effects of alcohol on the levels of parvalbumin in rat hearts

Chronic excessive alcohol administration has been reported to be associated with diastolic dysfunction. Parvalbumin (PV) is a calcium-binding protein present in cardiac myocytes and involved in mediating relaxation. Therefore, alteration of PV levels may affect relaxation in cardiac myocytes. This study investigated the effects of alcohol administration on the levels of PV in the rat heart. Male Wistar rats weighing 200-250 g were divided into 2 groups: control (C) and alcohol-treated groups. The control group was provided with distilled water and the alcohol groups were provided with either a low dose (LD, 2g/kg) or high dose of ethanol (HD, 5 g/kg) once daily for 21 days, 3 months or 6 months. The PV levels in the ventricles were investigated by immunohistochemistry and Western blot analysis. In the 21-day ethanol-treated groups, parvalbumin immunoreactivity (PV-ir) and protein levels were not different when compared to the C, LD and HD groups. In the 3-month ethanol-treated groups, PV-ir and PV protein levels were decreased in both the LD and HD groups compared to that of the control group. In the 6-month ethanol-treated groups, PV-ir and PV protein levels decreased significantly in both the LD and HD groups (P<0.05). This indicates that short-term ethanol treatment may not affect PV levels, whereas, long-term ethanol treatment clearly reduced PV levels. The decrease of PV was predominantly due to the direct toxic effects of alcohol rather than malabsorption caused by pathological changes in the duodenum and liver. The toxic effects of alcohol leading to a reduction of PV levels may lead to diastolic impairment.

Effect of Vitamin E Deficiency on Inhibition of Liver Regeneration by Long‐Term Administration of Alcohol

The effects of vitamin E (VE) deficiency on liver regeneration suppressed by long-term administration of alcohol were studied. Male rats were divided into two groups: the alcohol group and the control group. In addition, each group was subdivided into two groups according to the presence or not of VE. Altogether, four groups were provided: a group maintained on the VE-deficient alcohol diet (group EA), a group maintained on the VE-deficient control diet (group EC), a group maintained on the ordinary alcohol diet (group A), and a group maintained on the ordinary control diet (group C). After pair-feeding for 6 weeks, partial hepatectomy was performed to determine the omithine decarboxylase (ODC) activity, polyamine levels, lipid peroxide levels, and DNA synthesis, DNA synthesis at 24 hr after partial hepatectomy was suppressed significantly in the alcohol administration group, regardless of the presence or not of VE DNA synthesis at 48 hr after partial hepatectomy tended to show low values in group EA, compared with group A. As for the hepatic ODC activity, group EA showed the lowest value at 4 hr after partial hepatectomy. Of polyamines, the putrescine level in group EA at 4 hr after partial hepatectomy was significantly low, compared with the other three groups. The levels of spermidine and spermine decreased by long-term administration of alcohol, but the effect of VE deficiency was not found. The lipid peroxide level increased significantly in the VE-deficient diet administration group, but the effect of alcohol administration was not found. These results suggested that the decrease in putrescine after ODC suppression by VE deficiency in addition to the decrease in spermidine and spermine caused by long-term alcohol administration were concerned with suppression of DNA synthesis later.

Anxiety sensitivity and anticipation of a self-disclosing interview as determinants of alcohol consumption.

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Effects of alcohol administration on psychophysiological and subjective-emotional responses to aversive stimulation in anxiety-sensitive women.

Effects of alcohol administration on psychophysiological and subjective-emotional responses to aversive stimulation in anxiety-sensitive women.

Effects of alcohol administration on psychophysiological and subjective-emotional responses to aversive stimulation in anxiety-sensitive women.

Effects of alcohol administration on psychophysiological and subjective-emotional responses to aversive stimulation in anxiety-sensitive women.

Effects of alcohol administration on the disinhibition of racial prejudice.

Eighty-two white male undergraduate social drinkers were selected from high and low scorers on the Modern Racism Scale. Subjects were randomly assigned to 1 of 3 balanced placebo design conditions. After consuming their beverages, subjects viewed a videotape interaction between a Black and a White confederate. The subjects were told to rate the behaviors of the confederates, including an ambiguous shove of the White confederate by the Black confederate. It was expected, according to attribution theory, that high racism subjects would label the shove as more aggressive when they believed they had consumed alcohol, because alcohol could be used as an excuse for the socially unacceptable behavior of racial discrimination. A mood measure was also administered. Significant main effects of racism group and alcohol dosing were found for seriousness of aggression ratings, with high racism subjects and those expecting alcohol reporting more serious aggression, but the racism group by dosing condition interaction was not significant. A significant racism group by dosing condition interaction was found for the tension/anxiety mood scale, with greater tension being reported by high racism subjects who received alcohol. The results were related to theories of alcohol's disinhibiting and attention-limiting properties.

Breath acetone concentrations in fasting male volunteers: further studies and effect of alcohol administration.

This paper reports the concentration of acetone in end-expired breath of male volunteers as determined by gas chromatography. It also explores the effect of small doses of ethanol, given orally and intravenously, on breath acetone concentrations and their variations with time after intake. When subjects drank a small dose of alcohol (0.25 g/kg) after 12 h fasting, their breath acetone concentration decreased abruptly by 40%. The breath acetone time profile was almost a mirror image of the blood ethanol time course. After 36 h without food, the ethanol-induced drop in breath acetone was 18%. Ethanol given intravenously likewise caused a significant lowering of breath acetone concentration.

Effect of alcohol administration on plasma growth hormone response to insulin-induced hypoglycemia

Plasma growth hormone (HGH) response to insulin-induced hypoglycemia was assessed in a group of normal adult volunteers, with and without prior consumption of ethanol. A significant difference was found in peak HGH concentrations on the two occasions, indicating that prior consumption of ethanol attenuates the normal HGH response to insulin-induced hypoglycemia. It is suggested that ethanol may deplete catecholamine stores in the neurons of the ventromedial nucleus of the hypothalamus and may thereby impair secretion of growth hormone releasing factor. Under certain circumstances this could be of importance in the pathogenesis of alcohol-induced hypoglycemia.