No description available.

The hypotheses of this research were (1) to test if the antagonistic effect of ethanol on liver copper could be seen within a short period when ethanol ingestion, low dietary copper and high metabolic demand represented by either pregnancy plus lactation or rapid growth are simultaneously present and (2) to test if ethanol ingestion would exaggerate a marginal dietary copper status to an obvious copper deficiency. Pregnant rats were fed liquid diets containing either 0.75 (low) or 3.75 (control) mg copper/L with or without 30% of kcal from ethanol throughout gestation and the first 15 days of lactation. Maternal ethanol intake failed to exaggerate a marginal copper status to a copper deficient anemia in both dams and pups as estimated by concentrations of hemoglobin and liver iron and oxidase activity of the copper-metalloenzyme ceruloplasmin. However, maternal ethanol intake did depress maternal liver copper concentration when diet copper was low (interactive effect P<0.05). This effect was specific for liver because other tissue copper concentration was unaffected by ethanol. Although ethanol depressed total pup liver copper concentration regardless of dietary copper level, the interactive effect seen in maternal liver was reflected in copper content of the pup liver metallothionein fraction eluted from a Sephadex G-75 column. At least part of the depressive effect of ethanol on pup liver copper can be explained by elevated pup serum corticosterone (r=-0.61, P<0.001), a hormone known to enhance loss of neonatal liver copper by way of biliary excretion. On the other hand, the copper status of weanling female rats which were fed liquid diets containing either 0.5 (low) or 2.5 (control) mg copper/L for 5 weeks was unaffected by ethanol. Results demonstrate that the depressive effect of ethanol on liver copper can be seen within a period of weeks rather than months when ethanol ingestion, low dietary copper and pregnancy plus lactation are simultaneously present in contrast to non-pregnancy. This ethanol and copper interaction during reproduction, however, can not be detected if only either serum copper or oxidase activity of ceruloplasmin is used as an indicator of copper status. / Graduation date: 1989

No description available.

Pregnant and weanling rats were fed liquid diets with or without 30 percent of total kcal from ethanol and varying levels of copper in order to determine if ethanol ingestion would exaggerate a marginal copper status to an obvious copper deficiency. Pregnant albino rats were fed either 0.75 or 3.75 mg Cu/L throughout gestation and the first 15 days of lactation while female weanling rats received 0.5 or 2.5 mg Cu/L for 5 weeks. Ethanol consumption exaggerated a marginal copper status during reproduction as evidenced by significant reductions in maternal liver copper concentration and enzymatic activity of the copper metalloprotein Copper-Zinc superoxide dismutase in offspring liver. Ethanol had little or no effect upon copper status in weanling rats. In addition, serum copper failed to reflect a developing depletion of liver copper when ethanol was being consumed. Since it is known that the average American diet is just adequate in copper content, and that copper balance is difficult to achieve during times of increased metabolic demand, pregnant subjects may be at a great risk to develop a copper deficiency when ethanol is being consumed. This ethanol and copper interaction, however, will likely go undetected if only serum copper is used as an indicator of copper status. / Graduation date: 1989

The effect of ethanol on the stress response in rats was examined. Experimental animals were given 0.25 ml of 28 percent ethanol or 0.25 ml of water orally once a day, five days a week, for a period of twelve months and were then subjected to fifteen minute cold stress. Corticosterone levels in ethanol-treated males following stress were significantly lower (22 percent) than in the sham group. Adrenal weights in sham-treated females were significantly higher (15 percent) than in the ethanol group at the end of twelve months. Mortality in sham-treated males was significantly higher (60 percent) than in ethanol-treated males. The effects observed may be due to the sedative action of ethanol on cortical centers controlling the hypothalmus.

by Wu Kwok Hang. / Thesis (M.Ph.)--Chinese University of Hong Kong, 1988. / Bibliography: leaves 213-229.

The effects of single injections and daily oral administration of ethanol on plasma levels of ACTH, beta endorphin, and corticosterone in response to cold stress were examined. The long-term experimental animals were given 0.25 ml of 28% ethanol or water orally once a day, five days a week, for fourteen months. Plasma levels of ACTH, beta endorphin, and corticosterone were lower in alcohol-treated rats as compared with water-treated rats when exposed to cold stress. The effects of a single injection of ethanol significantly elevated plasma levels of all three hormones. Mortality in sham-treated males was higher than ethanol-treated.

No description available.

The work in this dissertation aims to describe a simple new test for odor-recognition memory in rats that can be readily performed and results in an easily observable and lasting form of memory. This test has allowed for the demonstration of ethanol-induced retrograde memory impairments in rats when ethanol is administered during both the consolidation and reconsolidation phases of memory encoding. The observation that a high-dose of ethanol can cause retrograde memory impairments when administered immediately or within hours after learning has taken place is an original finding that may have implications for understanding human blackouts. Furthermore, the finding that ethanol can disrupt the reconsolidation of a previously consolidated memory has not been previously established. It is also demonstrated that caffeine can prevent ethanol’s memory impairing effects, a result that contributes a new piece of evidence for caffeine’s effects on the learning and memory process. This effect has been further investigated mechanistically and attributed to caffeine’s dual role as a phosphodiesterase type 5 inhibitor and adenosine A2A antagonist. Neither of these mechanisms alone appear to be sufficient enough to prevent the retrograde memory impairments seen with ethanol. It is hoped that this test and our findings will prove useful for future investigations into the effects of ethanol on learning and memory and the human phenomenon of alcohol-induced blackouts. / text

Alcohol abuse has been commonly associated with enhanced susceptibility to pathogens. Studies on the effects of ethanol on the immune system are complicated by a lack of consensus on whether ethanol activates, inhibits or has no effect on immune cells. We present data showing that acute exposure of T cells to ethanol elicits responses that broadly parallel responses seen in normally stimulated T cells such as the formation of the immune synapse, polarization of the microtubule organizing center (MTOC) to the synapse and tyrosine phosphorylation of signaling proteins as seen when the T cell Receptor (TcR) engages antigen-MHC. However, incomplete activation of the T cell signaling program leads to unresponsive or anergic T cells. Our data suggests the hypothesis that ethanol can activate T cells in a manner that leads to anergy. We have found that ethanol triggers calcium signaling and this has provided one of the primary tools for analyzing the effects of ethanol on T cells. Ethanol induced calcium transients are dose-dependent and are comparable to those triggered by low doses of anti-TcR antibody. This is important because it allows us to compare ethanol dependent signaling to that normally triggered through stimulation of the T cell receptors. Analysis of the calcium signaling pathway indicates that ethanol-stimulated calcium transients depend on calcium entry and are likely due to opening of CRAC type calcium channels. The observed calcium transients go a long way towards explaining how ethanol may stimulate T cells and provides a mechanism for immune suppression through the observed translocation of NF-AT in ethanol pulsed cells. The translocation of NF-AT is particularly important because of reports that it plays a crucial role in triggering anergy and immunosuppression. Taken together, these data can help explain how ethanol can both activate T cells and cause immunosuppression.