dinoprost and Alcoholism

dinoprost has been researched along with Alcoholism* in 5 studies

Other Studies

5 other study(ies) available for dinoprost and Alcoholism

ArticleYear
[The level of 8-iso-prostaglandin F2 alpha, 4-hydroxynonenal and malondialdehyde in alcohol dependent men during combined therapy].
    Psychiatria polska, 2002, Volume: 36, Issue:2

    The aim of the study was the estimation of intensity of lipid peroxidation in alcohol dependent male patients after three months of therapy with naltrexone or tianeptine and the next three months follow-up. 61 males with clinical diagnosis of alcohol dependence (ICD-10) have been examined. The investigated parameters have been determined in blood serum, the 8-iso-prostaglandin F2 alpha by means of immunoenzymatic assay (ELISA) and malondialdehyde with 4-hydroxynonenal by means of colorimetric method. In alcohol dependent men before pharmacotherapy the mean concentration of 8-iso-PGF2 alpha and [MDA + 4-HNE] was higher than the reference interval. Both, after three months of applied drugs and the next three months follow-up, the concentration of studied parameters decreased considerably. The above results show intensification of lipid peroxidation in alcohol abusers and advantageous influence of abstinence from alcohol and treatment of naltrexone or tianeptine on free-radical changes of lipids as well.

    Topics: Adult; Alcoholism; Aldehydes; Antidepressive Agents, Tricyclic; Dinoprost; Drug Therapy, Combination; Enzyme-Linked Immunosorbent Assay; F2-Isoprostanes; Humans; Lipid Peroxidation; Male; Malondialdehyde; Middle Aged; Naltrexone; Narcotic Antagonists; Thiazepines; Time Factors

2002
Alcohol-induced pancreatic oxidative stress: protection by phospholipid repletion.
    Free radical biology & medicine, 1999, Volume: 26, Issue:5-6

    Oxidative stress is considered to be a forerunner of pancreatitis. Since we had found polyenylphosphatidylcholine, a mixture of polyunsaturated phosphatidylcholines extracted from soybeans, to protect against hepatic oxidative stress, we now tested its effects on the pancreas. Sprague-Dawley rats were pair-fed for two months nutritionally adequate liquid diet containing ethanol (36% of energy) or isocaloric carbohydrate, with either polyenylphosphatidylcholine (3 g/1000 kcal) or safflower oil, with or without 5 g/1000 kcal carbonyl iron. Parameters of oxidative stress (F2-isoprostanes, 4-hydroxynonenal, reduced glutathione), ubiquinol-10, ubiquinol-9 and vitamin E, as well as phosphatidylcholine species, were assessed by GC/MS and/or HPLC. Alcohol feeding increased pancreatic 4-hydroxynonenal three-fold, F2-isoprostanes and ubiquinol-9 by more than 70%, whereas it decreased total phospholipids, several phosphatidylcholine species, ubiquinol-10 and glutathione, especially in iron fed rats. Polyenylphosphatidylcholine prevented the rise in 4-hydroxynonenal and F2-isoprostanes, the decrease in dilinoleoylphosphatidylcholine and oleoyllinoleoylphosphatidylcholine and opposed the alcohol-induced decrease of glutathione; alpha-tocopherol remained unchanged. Iron had no significant effect except for decreasing ubiquinol-10 in the pancreas and increasing aminotransferases in the plasma. Thus, the alcohol-induced oxidative stress in the pancreas was shown to be prevented by polyenylphosphatidylcholine which may act, in part, by correcting the depletion of several phosphatidylcholine species.

    Topics: Alcoholism; Aldehydes; Animals; Chromatography, High Pressure Liquid; Diet; Dietary Supplements; Dinoprost; Ethanol; Gas Chromatography-Mass Spectrometry; Glutathione Disulfide; Glycine max; Iron; Lipid Peroxidation; Oxidative Stress; Pancreas; Phosphatidylcholines; Rats; Rats, Sprague-Dawley; Safflower Oil

1999
Prostaglandin E2 and prostaglandin F2 alpha biosynthesis in human gastric mucosa: effect of chronic alcohol misuse.
    Gut, 1996, Volume: 39, Issue:3

    The results of experimental studies support the hypothesis that decreased prostaglandin production might play a part in the gastric mucosal injury induced by alcohol. In this study, it was investigated whether alcohol misuse impairs the synthesis of prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) in gastric mucosa.. Fifty six alcoholic patients and 66 subjects without alcohol misuse were included in the study.. Mucosal biopsy specimens were obtained from the antrum and body of the stomach. Maximal synthesis rates of PGE2 and PGF2 alpha were determined in the microsomal fraction of the biopsy specimens.. The rates of synthesis of both prostaglandins in biopsy specimens from the antrum were not significantly different from those obtained in the body. Synthesis of both prostaglandins was significantly reduced in alcoholic patients who abstained less than five days compared with the non-alcoholic group with normal mucosa (PGE2-40%, PGF2 alpha-42% respectively). In non-alcoholic patients with severe gastritis PGE2 synthesis was increased (+30%, p < 0.05) and PGF2 alpha synthesis was decreased (-42.5%, p < 0.025). In alcoholic patients with severe gastritis PGE2 synthesis was depressed by almost 60% (p < 0.001) compared with the non-alcoholic group with severe gastritis. Neither colonisation of Helicobacter pylori nor smoking had a significant influence on the prostaglandin synthesis.. Chronic alcohol misuse is associated with significantly reduced capacity for prostaglandin synthesis in gastric mucosa and this alcohol induced decrease in prostaglandin synthesis is modulated by the presence and degree of gastritis.

    Topics: Alcoholism; Dinoprost; Dinoprostone; Female; Gastric Mucosa; Gastritis; Helicobacter pylori; Humans; Male; Middle Aged; Pyloric Antrum; Smoking; Temperance

1996
GC/MS assay of prostaglandins in cerebrospinal fluid from humans and monkeys.
    Advances in alcohol & substance abuse, 1988, Volume: 7, Issue:3-4

    The objective of this project has been to develop a sensitive and specific assay for prostaglandins in human cerebrospinal fluid (CSF) from patients with alcoholism and appropriate controls using gas chromatography/mass spectrometry. This study was initiated because numerous literature reports strongly suggest that a relationship exists between ethanol's central nervous system effects and the central production of prostaglandins. In both human and animal studies, administration of prostaglandin synthesis inhibitors prior to administration of ethanol attenuated central nervous system effects of ethanol. Samples from alcoholics after a three week period of abstinence and normals contained none of the measured prostaglandins (PGE2, PGE1, PGF1a, PGF2a, 6-keto-PGF1a) at a concentration more than twice the limit of quantification (3 pg/mL CSF). Comparison of GC/MS and radioimmunoassay methods provided further validation for these results. Literature reports of much higher levels of prostaglandins in normal controls, i.e., tens to hundreds of pg/mL CSF, appear to be incorrect. Examination of monkey CSF provided a positive control, since several of the prostaglandins were easily quantifiable in these samples.

    Topics: 6-Ketoprostaglandin F1 alpha; Alcoholism; Animals; Dinoprost; Dinoprostone; Gas Chromatography-Mass Spectrometry; Humans; Macaca mulatta; Prostaglandins; Radioimmunoassay

1988
Prostaglandin synthesis and response to alcoholism treatment.
    Alcohol and alcoholism (Oxford, Oxfordshire), 1987, Volume: 22, Issue:4

    Serum prostaglandin F2 (PGF2) was assayed in 27 alcoholic patients and in 18 control subjects. No significant difference was observed in mean basal PGF2 titers of patients and controls. However, patients who completed four months of alcoholism treatment had a mean titer that was significantly higher than that of treatment dropouts. Patients who maintained continuous abstinence for 2 years following treatment had a mean titer that was significantly higher than that of patients who returned to pre-treatment drinking levels.

    Topics: Adult; Alcoholism; Dinoprost; Follow-Up Studies; Humans; Male; Prostaglandins F; Temperance

1987