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The effect of combined administration of ethanol and manganese on the brain tissue of rats was investigated to evaluate the role of alcohol ingestion in inducing susceptibility to manganese poisoning. Ethanol and manganese alone and the combination of the two were administered orally daily to the rats for 30 days. Almost identical increase in the brain contents of manganese in rats receiving the metal alone and in combination with ethanol indicates that ethanol administration does not influence the accumulation of manganese in that organ. The copper contents of brain also increased to almost the same extent in these two groups. Synergistic effect of ethanol and manganese was noticed on increasing the activity of ATPase and RNase while marked antagonistic effect was observed on the activity of MAO. The mechanism and the significance of these neurochemical alterations occurring after the administration of ethanol and manganese have been discussed.

Concentrations of corticosterone in brain areas of TO strain mice were measured by radioimmunoassay. The studies examined the effects of routine laboratory maneuvers, variation during the circadian peak, adrenalectomy, social defeat and acute injections of alcohol on these concentrations. Brief handling of mice increased corticosterone levels in plasma but not in striatum and reduced those in the hippocampus. Single injections of isotonic saline raised the plasma concentrations to a similar extent as the handling, but markedly elevated concentrations in the three brain regions. Five minutes exposure to a novel environment increased hippocampal and cerebral cortical corticosterone levels and striatal concentrations showed a larger rise. However, by 30 min in the novel environment, plasma concentrations rose further while those in striatum and cerebral cortex fell to control levels and hippocampal corticosterone remained elevated. Over the period of the circadian peak the hippocampal and striatal concentrations paralleled the plasma concentrations but cerebral cortical concentrations showed only small changes. Adrenalectomy reduced plasma corticosterone concentrations to below detectable levels after 48 h but corticosterone levels were only partially reduced in the hippocampus and striatum and remained unchanged in the cerebral cortex. Single or repeated social defeat increased both brain and plasma concentrations after 1 h. Acute injections of alcohol raised the regional brain levels in parallel with plasma concentrations. The results show that measurements of plasma concentrations do not necessarily reflect the levels in brain. The data also demonstrate that corticosterone levels can change differentially in specific brain regions. These results, and the residual hormone seen in the brain after adrenalectomy, are suggestive evidence for a local origin of central corticosterone.

Administration of low amounts of ethanol for a prolonged period increases rat brain synaptosomal (Na+-K+)-ATPase activity, the increase being less in the protein deficient rats. The adaptive mechanism to offset the stress imposed by the continued presence of ethanol seems to be depressed by low plane of nutrition. In vivo and in vitro effects of ethanol on (Na+-K+)ATPase seems to be different.

Glutathione (GSH) and other non-protein sulfhydryls (NPS) are known to protect cells from oxidative stress and from potentially toxic electrophiles formed by biotransformation of xenobiotics. This study examined the effect of a simultaneous administration of styrene and ethanol on NPS content and lipid peroxidation in rat liver and brain. Hepatic cytochrome P450 and cytochrome b5 content, aniline hydroxylase and aminopyrine N-demethylase activities as well as the two major urinary metabolites of styrene, mandelic and phenylglyoxylic acids were also measured. Groups of rats given ethanol for 3 weeks in a liquid diet were exposed, starting from the second week, to 326 ppm of styrene (6 h daily, 5 days a week, for 2 weeks). In control pair-fed animals, styrene produced about 30% depletion of brain NPS and 50% depletion of hepatic NPS. Subchronic ethanol treatment did not affect hepatic NPS levels, but caused 23% depletion of brain NPS. Concomitant administration of ethanol and styrene caused a NPS depletion in brain tissue in the order of 60%. These results suggest that in the rat, simultaneous exposure to ethanol and styrene may lead to considerable depletion of brain NPS. This effect is seen when both compounds are given on a subchronic basis, a situation which better resembles possible human exposure.

Cellular morphology, macromolecular composition, (DNA, RNA and Protein content) marker enzyme activities for neurons [neuron specific enolase (NSE)] and astrocytes [glutamine synthetase (GS)] and plasma membrane protein profiles in the bulk isolated neurons and astrocytes from control and ethanol treated rats were studied. One month aged Wistar rats were given ethanol as sole drinking fluid for 10 weeks. Scanning electron microscopy revealed a characteristic cell surface smoothening in astrocytes due to ethanol treatment. DNA levels were unaltered, while RNA and Protein contents were decreased in astrocytes and neurons. Further, 3H-leucine incorporation into proteins was decreased in neurons and astrocytes derived from ethanol treated rats indicating reduced protein synthesis in neurons and astrocytes. GS activity was affected severely suggesting impairment in astrocytic functions. Plasma membrane protein composition was analyzed by 2-D electrophoresis. The analysis indicated several protein defects in the plasma membranes of neurons and astrocytes, which might be involved in 'membrane disorder' during ethanol challenge. 125I-Wheat Germ agglutinin binding studies showed three prominent proteins (160, 116 and 97 kDa) in astrocyte membrane fraction suggesting the possible involvement of N-terminal glycoproteins in altered astrocyte morphology during ethanol ingestion. Impairment in the astrocyte cell functions, protein changes in plasma membrane and cellular morphology studies suggest that astrocytes may be more vulnerable than neurons for ethanol effects.

The effects of 50% ethanol extract of one formulated ayurvedic product, consisting of a mixture of medicinal plant species, was investigated on behavioral despair test (forced swimming test, FST), central dopaminergic and serotonergic activity in rats. The effects on the forced swimming test were assessed along with the levels of dopamine (DA), serotonin (5-HT) and its metabolites homovanillic acid (HVA) and 5-hydroxyindoleaceticacid (5-HIAA) in striatum, frontal cortex, hippocampus, hypothalamus and brain stem after 21 days of chronic oral administration of the extract (500 and 1500 mg/kg-body weight). The extract significantly increased climbing behavior at 500 mg/kg and increased swimming behavior by reducing immobility time at 1500 mg/kg when compared with the control group in forced swimming test (P<0.05). This showed that the active substances present in 50% ethanol extract of the ayurvedic preparation possess antidepressant activity and their specificity towards particular behavior, depends on the concentration of the extract. Further it showed that the enhancement of active behavior in FST is not due to generalized motor activity. The neurochemical estimations revealed the swim stressor inducing alterations in the levels of DA, 5-HT and their metabolites HVA and 5-HIAA in the brain regions assayed as compared with the non-stressed control rats. These changes were prevented extract treated rats. The 500 mg/kg extract treated group had significantly increased the levels of DA in frontal cortex, hypothalamus and hippocampus whereas the 5-HT in hypothalamus (P<0.05). However, there were no significant changes in the levels of HVA and 5-HIAA. These behavioral and biochemical results indicate antidepressant properties of the extract, which may be mediated by the dopaminergic and serotonergic mechanisms in rat brain.

The protective effect of Piper betle, a commonly used masticatory, has been examined in the brain of ethanol-administered Wistar rats. Brain of ethanol-treated rats exhibited increased levels of lipids, lipid peroxidation, and disturbances in antioxidant defense. Subsequent to the experimental induction of toxicity (i.e., the initial period of 30 days), aqueous P. betle extract was simultaneously administered in three different doses (100, 200, and 300 mg kg(-1)) for 30 days along with the daily dose of alcohol. P. betle coadministration resulted in significant reduction of lipid levels (free fatty acids, cholesterol, and phospholipids) and lipid peroxidation markers such as thiobarbituric acid reactive substances and hydroperoxides. Further, antioxidants, like reduced glutathione, vitamin C, vitamin E, superoxide dismutase, catalase, and glutathione peroxidase, were increased in P. betle-coadministered rats. The higher dose of extract (300 mg kg(-1)) was more effective, and these results indicate the neuroprotective effect of P. betle in ethanol-treated rats.

Ethanol is a widely consumed substance throughout the world. During development it can substantially damage the human fetus, whereas the developing brain is particularly vulnerable. The brain damage induced by prenatal alcohol exposure may lead to a variety of long-lasting behavioral and neurochemical problems. However, there are no data concerning the effects of developmental ethanol exposure on the glutamatergic system, where extracellular glutamate acts as signaling molecule. Here we investigated the effect of ethanol exposure for 2h (concentrations of 0.0%, 0.1%, 0.25%, 0.50%, and 1.00%) in embryos at 24h post-fertilization (hpf) by measuring the functionality of glutamate transporters in the brain of adult (4 months) zebrafish. However, ethanol 0.1%, 0.25% and 0.50% decreased transport of glutamate to 81.96%, 60.65% and 45.91% respectively, when compared with the control group. Interestingly, 1.00% was able to inhibit the transport activity to 68.85%. In response to the embryonic alcohol exposure, we found impairment in the function of cerebral glutamate transport in adult fish, contributing to long-term alteration in the homeostasis glutamatergic signaling.

These studies were aimed at correlating the effects of ethanol on operant behavior and on locomotor activity with its distribution in selected tissues in the body. One group of male rats was trained on a continuous reinforcement schedule for intracranial self-stimulation (ICSS) with electrodes in the lateral hypothalamus. Another group was studied in a locomotor activity apparatus, and both groups were given ethanol intraperitoneally over the dose-range 0.3-1.7 g/kg. Urine was collected 15 min and 60 min after ethanol administration and samples of blood, brain, heart, lung, liver, muscle and testis were obtained at both time points. Depressions of ICSS and of locomotor activity occurred, and these changes in behavior were correlated with increasing concentrations of ethanol in blood, urine and tissue. Thus, the disrupting effects of ethanol on behavior which occurred shortly after its acute administration were closely linked to its concentrations throughout the body.