Effects of Acute and Chronic Ethanol Administration and its Withdrawal on the Level and Binding of Somatostatin in Rat Brain

1990 ◽  
Vol 79 (5) ◽  
pp. 451-456 ◽  
Author(s):  
V. Barrios ◽  
M. N. Rodríguez-Sánchez ◽  
E. Arilla
Keyword(s):  
Nervous System ◽  
Specific Binding ◽  
Somatostatin Receptors ◽  
Chronic Administration ◽  
Ethanol Administration ◽  
Actual Number ◽  
Brain Areas ◽  
Frontoparietal Cortex ◽  
Acute Ethanol ◽  
Chronic Ethanol Administration

1. Acute ethanol administration resulted in an increase in the total number of specific somatostatin receptors in rat frontoparietal cortex and hippocampus, and a decrease in the level of somatostatin-like immuno-reactivity in the hippocampus but not in the frontoparietal cortex. 2. Chronic administration of ethanol caused a decrease in the number of somatostatin receptors in the frontoparietal cortex but not in the hippocampus, although the level of somatostatin-like immunoreactivity was unchanged in both brain areas. 3. A week after suppressing ethanol the value for specific binding of tracer to somatostatin receptors in the frontoparietal cortex was not significantly different from that of the control rats, although the actual number of receptors was slightly lower. 4. These results suggest a possible role for somatostatin in the nervous system during alcoholism and the post-withdrawal reaction.

Effect of haloperidol withdrawal on somatostatin level and binding in rat brain

1990 ◽  
Vol 10 (1) ◽  
pp. 15-22 ◽  
Author(s):  
E. Perez-Oso ◽  
M. P. Lopez-Ruiz ◽  
E. Arilla
Keyword(s):  
Side Effects ◽  
Rat Brain ◽  
Specific Binding ◽  
Somatostatin Receptor ◽  
Somatostatin Receptors ◽  
Chronic Administration ◽  
Brain Areas ◽  
Frontoparietal Cortex ◽  
Receptor Number ◽  
Haloperidol Treatment

The effects of withdrawal on the level and specific binding of somatostatin in the frontoparietal cortex and hippocampus of the rat after chronic haloperidol treatment were examined using125I-Tyr11 somatostatin as tracer. One week after haloperiodol withdrawal the number of specific somatostatin receptors in both brain areas returned to control values, after having decreased as the result of chronic administration. Neither administration of haloperidol nor withdrawal of it affected the levels of somatostatin-like immunoreactivity (SLI) in the two brain areas studied. The return of the somatostatin receptor number to control values after haloperidol withdrawal may be related to the motor side-effects that are clinically observed when the haloperidol treatment is terminated.

Acute and chronic ethanol administration on specific 3H-GABA binding in different rat brain areas

1980 ◽  
Vol 67 (3) ◽  
pp. 261-264 ◽  
Author(s):  
A. Reggiani ◽  
M. L. Barbaccia ◽  
P. F. Spano ◽  
M. Trabucchi
Keyword(s):  
Rat Brain ◽  
Chronic Ethanol ◽  
Ethanol Administration ◽  
Brain Areas ◽  
Gaba Binding ◽  
Chronic Ethanol Administration

Ethanol in Liquid Preparations Intended for Children

PEDIATRICS ◽  
1984 ◽  
Vol 73 (3) ◽  
pp. 405-407 ◽  
Author(s):  
Keyword(s):  
Clinical Importance ◽  
Alcoholic Beverages ◽  
Ethanol Administration ◽  
Metabolizing Enzymes ◽  
Cardiac Arrythmias ◽  
Passive Exposure ◽  
Acute Ingestion ◽  
Acute Ethanol ◽  
Chronic Ethanol Administration ◽  
Inert Solvent

Ethanol is present in more than 700 pharmaceutical liquid preparations, ostensibly as an "inert" solvent on diluent.1 Despite recent voluntary efforts by several pharmaceutical companies to replace alcohol or reduce its content, there remain on the market an excessive number of liquid medications containing alcohol in concentrations ranging from 0.3% to 68%, eg, teething preparations, decongestants, and cough medicines. The presence of ethanol in children's medication is of major toxicologic interest with respect to both acute ingestion and passive exposure that occurs during therapy with ethanol-containing products. This commentary focuses upon the toxicology of ethanol in children and the determination of acceptable alcohol concentrations in children's medication. INTERACTION WITH OTHER DRUGS When taken in conjunction with other drugs, medicines containing alcohol may produce undesirable interactions. Acute ethanol administration may alter drug absorption2 or impair the degradation of other drugs.3 When taken with sedating drugs, it may result in enhanced psychomotor impairment.4,5 Chronic ethanol administration, which induces drug-metabolizing enzymes (such as P-450), may be of clinical importance by altering the clearance of several drugs (phenobarbital, phenytoin, meprobamate, and warfarin).3 Disulfiram (Antabuse) reactions, symptoms of which include flushing, tachycardia, nausea, vomiting, and, in severe forms, cardiac arrythmias, cardiovascular collapse, respiratory depression, and convulsions, may also be induced by alcohol-containing medicines. Of more direct importance to pediatricians are recent reports of disulfiram-like reactions that occur in some individuals after the simultaneous use of antibacterial drugs such as moxalactam, metronidazole, sulfonamides, chloramphenicol on cefamandole, and alcoholic beverages or medicinal elixirs.6-9 ESTABLISHING CRITERIA FOR ALCOHOL CONTENT IN CHILDREN'S MEDICATION

scholarly journals Alteration of oxidative-stress and related marker levels in mouse colonic tissues and fecal microbiota structures with chronic ethanol administration: Implications for the pathogenesis of ethanol-related colorectal cancer

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0246580
Author(s):  
Hideo Ohira ◽  
Atsuki Tsuruya ◽  
Daiki Oikawa ◽  
Wao Nakagawa ◽  
Rie Mamoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Colorectal Cancer ◽  
Chronic Administration ◽  
Ethanol Consumption ◽  
Treg Cells ◽  
Fecal Microbiota ◽  
Chronic Ethanol ◽  
Ethanol Administration ◽  
Chronic Ethanol Consumption ◽  
Chronic Ethanol Administration

Chronic ethanol consumption is a risk factor for colorectal cancer, and ethanol-induced reactive oxygen species have been suggested to play important roles in the pathogenesis of ethanol-related colorectal cancer (ER-CRC). In this study, the effects of 10-week chronic administration of ethanol on the colonic levels of oxidative stress and advance glycation end product (AGE) levels, as well as fecal microbiota structures, were examined in a mouse model. Chronic oral administration of ethanol in mice (1.0 mL of 1.5% or 5.0% ethanol (v/v) per day per mouse, up to 10 weeks) resulted in the elevation of colonic levels of oxidative stress markers (such as 8-hydroxy-2’-deoxyguanosine and 4-hydroxynonenal) compared to control mice, and this was consistently accompanied by elevated levels of inflammation-associated cytokines and immune cells (Th17 and macrophages) and a decreased level of regulatory T (Treg) cells to produce colonic lesions. It also resulted in an alteration of mouse fecal microbiota structures, reminiscent of the alterations observed in human inflammatory bowel disease, and this appeared to be consistent with the proposed sustained generation of oxidative stress in the colonic environment during chronic ethanol consumption. Moreover, the first experimental evidence that chronic ethanol administration results in elevated levels of advanced glycation end products (AGEs) and their receptors (RAGE) in the colonic tissues in mice is also shown, implying enhanced RAGE-mediated signaling with chronic ethanol administration. The RAGE-mediated signaling pathway has thus far been implicated as a link between the accumulation of AGEs and the development of many types of chronic colitis and cancers. Thus, enhancement of this pathway likely exacerbates the ethanol-induced inflammatory states of colonic tissues and might at least partly contribute to the pathogenesis of ER-CRC.

scholarly journals Prevention by pyrazole of the effects of chronic ethanol administration on the redox states of the hepatic nicotinamide–adenine dinucleotide (phosphate) couples and on liver and brain tryptophan metabolism in the rat

1979 ◽  
Vol 184 (1) ◽  
pp. 165-168 ◽  
Author(s):  
N F Punjani ◽  
A A B Badawy ◽  
M Evans
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Chronic Administration ◽  
Chronic Ethanol ◽  
Tryptophan Metabolism ◽  
Ethanol Administration ◽  
Redox States ◽  
Chronic Effects ◽  
Chronic Ethanol Administration ◽  
Tryptophan Pyrrolase

Chronic administration of pyrazole in the diet of rats does not cause toxicity and prevents the chronic effects of ethanol on: (1) the redox states of the hepatic NAD(P) couples; (2) liver tryptophan pyrrolase activity; (3) brain tryptophan and 5-hydroxytryptamine metabolism.

scholarly journals Mate Tea Prevents Oxidative Stress in the Blood and Hippocampus of Rats with Acute or Chronic Ethanol Administration

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Bianca Scolaro ◽  
Daniela Delwing-de Lima ◽  
José Geraldo Pereira da Cruz ◽  
Débora Delwing-Dal Magro
Keyword(s):  
Oxidative Stress ◽  
Chronic Administration ◽  
Thiobarbituric Acid ◽  
Treated Group ◽  
Chronic Ethanol ◽  
Ethanol Administration ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Chronic Ethanol Administration ◽  
Mate Tea

Objective. The aim of this study was to evaluate the influence of acute and chronic intake of mate tea on the effects elicited by acute and chronic administration of ethanol.Methods. Oxidative stress was evaluated by measuring thiobarbituric acid-reactive substances (TBARS), as well as the activities of the antioxidant enzymes, catalase (CAT), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) in the hippocampus and blood of rats. Male Wistar rats were randomly assigned to four groups, for both acute and chronic treatment: (1) control group, (2) treated group, (3) intoxicated group, (4) and intoxicated group treated with mate tea.Results. Both ethanol administrations significantly increased TBARS in plasma and hippocampus of rats and altered antioxidant enzyme activities, changes which were reverted by mate tea administration.Conclusions. Data indicate that acute and chronic ethanol administration induced oxidative stress in hippocampus and blood and that mate tea treatment was able to prevent this situation.

Effect of acute ethanol administration on histone acetylation in mouse brain

2010 ◽  
Vol 68 ◽  
pp. e422-e423
Author(s):  
Keisuke Mizuo ◽  
Yoko Nishitani ◽  
Ryuichi Katada ◽  
Shunichiro Okazaki ◽  
Kenji Tateda ◽  
...  
Keyword(s):  
Histone Acetylation ◽  
Mouse Brain ◽  
Ethanol Administration ◽  
Acute Ethanol
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