beta-endorphin and Alcoholic-Intoxication

Acute alcohol intoxication (AAI) is a frequent emergency, but therapeutic drugs with superior efficacy and safety are lacking. Panax ginseng (PG) and Hippophae rhamnoides (HR) respectively has a wide application as a complementary therapeutic agent in China for the treatment of AAI and liver injury induced by alcohol. We investigated the effects of aqueous extracts from PG and HR (AEPH) on AAI mice and identified its underlying mechanisms.. Models of AAI were induced by intragastric administration of ethanol (8g/kg). Seventy-two Specific pathogen-free (SPF) male Kunming mice were randomly divided into six groups: normal group, positive control group, AEPH of low dosage (100mg/kg) group, AEPH of medium dose (200mg/kg) group, AEPH of high dosage (400mg/kg) group and model group. The mice were treated with metadoxine (MTD, 500mg/kg) and AEPH. Thirty minutes later, the normal group was given normal saline, while the other groups were given ethanol (i.g., 8g/kg). The impact of AEPH was observed. In the same way, another seventy-two Kunming mice were randomly divided into six groups equally. The blood ethanol concentration at 0.5, 1, 1.5, 2, 3 and 6h after ethanol intake was determined by way of gas chromatography. The activity of alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH) and microsomal ethanol oxidase (EO) in liver, and the concentration of β-endorphin (β-EP), leucine-enkephalin (LENK) in the brain were determined by enzyme-linked-immunosorbent serologic assay (ELISA).. AEPH markedly prolonged alcohol tolerance time and shortened sober-up time after acute ethanol administration. AEPH decreased blood ethanol levels in six tests after ethanol intake. The 7-day survival rate of AEPH group was obviously superior to model group. AEPH increased the activities of ADH, ALDH, and decreased EO activity in liver. The crucial find was that AEPH markedly decreased β-EP and LENK concentration in the brain.. AEPH can markedly increase the levels of ADH, ALDH, decrease EO activity in liver and decrease the concentration of β-EP and LENK in the brain to against acute alcohol intoxication in mice.

Topics: Alcohol Dehydrogenase; Alcohol Oxidoreductases; Alcoholic Intoxication; Aldehyde Dehydrogenase; Animals; beta-Endorphin; Blood Alcohol Content; Brain; Cytochrome P-450 Enzyme System; Disease Models, Animal; Dose-Response Relationship, Drug; Enkephalin, Leucine; Ethanol; Gas Chromatography-Mass Spectrometry; Hippophae; Liver; Male; Mice; Panax; Phytotherapy; Plant Extracts; Plants, Medicinal; Solvents; Time Factors; Water

Teenage drinking continues to be a major problem in industrialized countries, where almost 35% of alcohol drinkers are under 16 years old. In the present paper we studied the effects of acute alcohol intoxication (AAI) on the pituitary-gonadal (PG) axis hormones, and the possible contribution of pituitary-adrenal (PA) axis hormones, beta-endorphin (BEND), and prolactin (PRL) to the alcohol-induced dysfunction of PG axis hormones. Blood samples were drawn from adolescents that arrived at the emergency department with evident behavioral symptoms of drunkenness (AAI) or with nil consumption of alcohol (controls [C]). Our results demonstrated that AAI produces in adolescents a high increase in plasma PRL, ACTH, and cortisol (F), and a contradictory behavior of testosterone (T) according to gender: plasma T was increased in females and decreased in males. ACTH and PRL correlated positively with F, dehydroepiandrosterone-sulphate (DHEAS) and T in females, which suggests that PRL and ACTH could synergistically stimulate adrenal androgen production. In contrast, the decrease in T and increase in BEND in males suggests that AAI could have an inhibitory effect on testicular T, perhaps mediated by BEND. The hormones studied are involved in the development of secondary sexual characteristics and the growth axis during adolescence. The deleterious effects of alcohol abuse should be made known to adolescents and the appropriate authorities.

Topics: Acute Disease; Adolescent; Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Alcoholic Intoxication; beta-Endorphin; Dehydroepiandrosterone Sulfate; Ethanol; Female; Follicle Stimulating Hormone; Gonadotropins, Pituitary; Humans; Hydrocortisone; Luteinizing Hormone; Male; Ovary; Pituitary-Adrenal System; Prolactin; Regression Analysis; Sex Factors; Testis; Testosterone

To study the therapeutical mechanism of traditional Chinese medicine Xingnaojing injection (XNJI) for acute alcohol intoxication.. XNJI was used in treating the experimental model rabbits (n = 26) and the patients (n = 8) admitted to the emergency department with acute alcoholism. Before and after the treatment, beta-EP, superoxide anion (free radicals) and SOD were measured.. XNJI could enhance the regaining consciousness of rabbits and patients, simultaneously reduce the concentration of beta-EP in plasma to the normal level (drunk rabbits 127.09 +/- 13.67 ng/L, normal rabbits 41.48 +/- 7.46 ng/L. P < 0.01, drunk patients 292.97 +/- 14.85 ng/L, normal people 221.60 +/- 15.95 ng/L, P < 0.01). The concentration change of superoxide anion (free radicals) in plasma of rabbits and patients was similar to beta-EP (drunk rabbits 313.39 +/- 15.64 u/L, normal rabbits 254.27 +/- 21.71 u/L, P < 0.01; drunk patients 278.47 +/- 11.48 u/L, normal people 159.92 +/- 11.51 u/L, P < 0.01), and SOD was inversely changed (drunk rabbits 53.57 +/- 6.48%, normal rabbits 77.18 +/- 7.89%, P < 0.01; drunk patients 43.76 +/- 7.84%, normal people 82.53 +/- 4.33%, P < 0.01).. XNJI is similar to Naloxone in pharmacologic action. And it is an effective antioxidant. It can be used for treating alcoholism.

Topics: Adult; Alcoholic Intoxication; Animals; Antioxidants; beta-Endorphin; Drugs, Chinese Herbal; Female; Humans; Male; Middle Aged; Rabbits; Superoxide Dismutase

We are interested in the characterization of the effects of alcohol on human T-cell activation, maturation, and migration, because this cell population is crucial in the initiation, regulation, and propagation of cellular immunity. We and others have described the effects of both acute and chronic exposure of human immune cells to ethanol (EtOH) in vitro. Herein, we briefly, review these reports and expand this body of literature with the inclusion of new data recently obtained in our laboratory. We confirm the blunting effects of EtOH on the production of interleukin-2 and mitogen proliferative response following T-cell mitogen stimulation, and on the expression of membrane markers of activation. We show that EtOH significantly alters the expression of the CD4 cell-associated marker of activation, CD26. We report the effect of EtOH on the expression of the homing receptor CD62L by CD4+ cells, and on their ability to adhere by a CD18-mediated process to a defined cellular substratum. Furthermore, we demonstrate the effects of EtOH and EtOH and beta-endorphin pretreatment on the activation of CD4+ lymphocytes endowed with the homing receptor CD62L.

Topics: Alcoholic Intoxication; Alcoholism; beta-Endorphin; CD4 Antigens; CD4-Positive T-Lymphocytes; Cell Adhesion; Cell Line; Cell Movement; Dipeptidyl Peptidase 4; Ethanol; Humans; Immunocompetence; In Vitro Techniques; Interleukin-2; Lymphocyte Activation; Receptors, Immunologic; Recombinant Proteins; T-Lymphocytes; Tumor Cells, Cultured

Plasma beta-endorphin, met-enkephalin and ACTH concentrations were measured in 20 male alcoholics (age: 32-60 yr; duration of ethanol addiction: 13.2 +/- 6.2 yr; mean +/- SE) immediately after admission to the hospital (at a time not exceeding 8 hr from the last ethanol consumption) and after 5 weeks of forced abstinence. The results were compared with those obtained in 12 age-matched normal controls. Plasma ACTH and met-enkephalin levels were normal in alcoholics on both occasions. In contrast, in samples taken at admission to the hospital, the circulating concentrations of beta-endorphin in alcoholics were half (17.1 +/- 5.3 pg/ml; mean +/- SE) of those observed in the normal controls (34.1 +/- 6.0). beta-endorphin levels rose significantly after 5 weeks of abstinence (30.1 +/- 4.9); at this time, they were not significantly different from those observed in normal controls. These data indicate that acute alcohol consumption induces significant alterations in plasma beta-endorphin, but not met-enkephalin levels, which are reversed after 5 weeks of abstinence.

Topics: Adrenocorticotropic Hormone; Adult; Alcoholic Intoxication; Alcoholism; beta-Endorphin; Enkephalin, Methionine; Humans; Male; Middle Aged; Substance Abuse Treatment Centers

Beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) plasma concentrations were examined in ten chronic alcohol abusers, eight men and two women aged 25-56 years with histories of continuously elevated ethanol consumption dating from 5-30 years. Plasma levels of the two peptides were measured after acute alcohol consumption and then after 3, 6 and 9 days of forced abstinence, during chlordiazepoxide treatment. Beta-EP and beta-LPH concentrations were normal on all four occasions. A reduced sensitivity of opioid receptors to acute alcohol administration due to chronic alcohol consumption is suggested.

Topics: Adult; Alcohol Withdrawal Delirium; Alcoholic Intoxication; Alcoholism; beta-Endorphin; beta-Lipotropin; Female; Humans; Male; Middle Aged; Naloxone; Psychoses, Alcoholic; Receptors, Opioid

Intracerebroventricular (icv) administration of neurotensin produced a dose-dependent increase in ethanol sensitivity as measured by blood ethanol concentration at loss of righting reflex in SS/Ibg (SS) but not in LS/Ibg (LS) mice. Central administration of calcium also enhanced ethanol sensitivity of SS and to a lesser extent LS mice. Concurrent icv administration of calcium and neurotensin resulted in an additional enhancement of sensitivity to ethanol over that seen with either substance alone in both mouse lines. A dose-dependent increase in ethanol sensitivity was also produced in response to central administration of beta-endorphin in SS mice. No additional increase in sensitivity was noted following administration of beta-endorphin plus calcium. These results suggest a specific interaction of calcium and neurotensin may be involved in the mechanism through which ethanol elicits intoxication. The difference in response of LS and SS mice to neuropeptide and calcium-induced alterations in ethanol sensitivity may be related to the genetically selected differences to the acute narcotic actions of ethanol in these mice.

Topics: Alcoholic Intoxication; Animals; beta-Endorphin; Calcium; Drug Interactions; Endorphins; Ethanol; Injections, Intraventricular; Male; Mice; Mice, Inbred Strains; Neurotensin; Reflex