Effects of Acute Alcohol Administration on Reproductive Endocrinology in the Male Rat (original) (raw)
Related papers
Effects of alcohol on the hypothalamic-pituitary-gonadal axis in the male rat
PubMed, 1977
The effects of acute and chronic alcohol administration on serum testosterone and luteinizing hormone (LH) levels were examined in the male rat. Chronic alcohol administration resulted in depressed serum testosterone and LH levels when alcohol-fed rats were compared with rats maintained, ad libitum, on rat chow and water. However, neither testosterone nor LH levels were significantly lower in alcohol-treated rats when comparisons were made to pair-fed control animals, indicating that the nutritional deficits imposed by the chronic alcohol-feeding regimen contributed heavily to the observed reductions in the two hormones. To avoid the problems associated with a chronic drug delivery model, we injected rats with a single acute injection of alcohol. LH levels dropped significantly within 2 hours after the injection of a 2.5 g/kg dose of alcohol and remained depressed, at a level between 25 and 30% of control values, from 2 to 4 hours. By 6 hours after the injection, LH levels had returned to base-line levels. Testosterone levels were also reduced by alcohol, but this drop was not significant until at least 3 hours after the injection. Testosterone levels did not return to control levels throughout the 6-hour course of the experiment. Dose-response determinations revealed that alcohol produced a biphasic effect on serum testosterone and LH: low doses of alcohol significantly increased testosterone and LH, whereas high doses decreased the levels of both hormones. The results of these studies suggest that the ability of alcohol to depress serum testosterone levels, and thus produce symptoms of hypogonadism in the male of several species, is due to a primary effect of alcohol on the hypothalamic-pituitary aspect of the hypothalamic-pituitary-gonadal axis.
Alcohol's Effects on Male Reproduction
Alcohol Health and Research World, 1998
: AODE (alcohol and other drug effects); hypothalamus; pituitary gland; male genitals; reproductive function; testosterone; hormone metabolism; heavy AOD use; cell type; luteinizing hormone; follicle stimulating hormone; gonadotropin RH; secretion; animal model; male; literature review article by Hiller-Sturmhöfel and Bartke, pp. 153-164.) Among other hormones, the hypothalamus produces gonadotropinreleasing hormone (GnRH). GnRH is MARY ANN EMANUELE, M.D., is a professor in the EMANUELE, M.A.; KIRSTEINS, L.; REDA, D.; EMANUELE, N.V.; AND LAWRENCE, A.M. In vitro effect of ethanol exposure on basal and GnRHstimulated LH secretion from pituitary cells. Endocrine Research 15:293-401, 1989. EMANUELE, M.A.; TENTLER, J.J.; REDA, D.; KIRSTEINS, L.; EMANUELE, N.V.; AND LAWRENCE, A.M. The effect of in vitro ethanol exposure on 201 LHRH release from perfused rat hypothalami. Endocrine Research 16:313-321, 1990. EMANUELE, M.A.; TENTLER, J.; EMANUELE, N.V.; AND KELLEY, M.R. In vivo effects of acute EtOH on rat α and β luteinizing hormone gene expression. Alcohol 8:345-348, 1991.
Alcohol and the male reproductive system
Alcohol Research Health the Journal of the National Institute on Alcohol Abuse and Alcoholism, 2001
: hypothalamic-pituitary-gonadal axis; reproductive effects of AODU (alcohol and other drug use); male; reproductive system; testicles; nitric oxide; oxidation; ethanol-to-acetaldehyde metabolism; apoptosis; luteinizing hormone-releasing hormone; fertility; opioids MARY ANN EMANUELE, M.D., is a professor in
Hypogonadism precedes liver feminization in chronic alcohol-fed male rats
Hepatology, 2000
Men who chronically abuse alcohol may display a spectrum of endocrine abnormalities including hypogonadism and feminization, with elevated serum estradiol and low serum testosterone. We examined factors that may result in disruption of hepatic sex hormone homeostasis in alcoholfed male rats and possible consequences of such changes. Rats were fed alcohol-containing or isocaloric diets for 30, 60, and 90 days. In alcohol-fed rats, serum testosterone levels and hepatic activity of 2 androgen-dependent estrogen metabolizing enzymes were reduced (P F .05) at all times, as was activity of androgen receptor. There was also a significant early and progressive decrease in testes/body ratio in alcohol-fed rats. Compared with this early decrease in testosterone-related parameters, there was a significant increase in serum estrogen levels (at 30 and 90 days, 132% and 168% of control values, respectively). An increase in serum ceruloplasmin, an estrogen-responsive liver protein, was apparent at 60 and 90 days, but not at 30 days of alcohol exposure, suggesting that hypogonadism precedes liver feminization. Hepatic estrogen receptor activity was decreased in alcohol-fed rats at 60 and 90 days, the latter despite elevated serum estrogen levels. Hepatic aromatase was slightly increased in alcohol-fed rats, an elevation probably not sufficient to account for observed increases in serum estrogen. Taken together, these data suggest that (1) alcohol induces profound reduction of serum testosterone, resulting in loss of androgen-regulated hepatic functions such as estrogen-metabolizing enzyme activity and activity of androgen receptors; and (2) such alcohol-induced hypogonadism precedes changes in hepatic sex hormone homeostasis and subsequent feminization. (HEPATOLOGY 2000;31:
Alcoholism: Clinical and Experimental Research, 2003
The interaction of alcohol and testosterone has long been of interest, mainly due to the effect of alcohol on aggression and sexual behavior. To date, there have been very few, if any, studies examining the effect of acute alcohol administration on testosterone concentrations in the brain. The administration of 1,1-dideuteroethanol ([1,1-2 H 2 ]ethanol) provided the opportunity to trace the deuterium label into newly synthesized deuterotestosterone in brain samples to determine whether ethanol oxidation was directly linked to testosterone synthesis.
The Journal of steroid biochemistry and molecular biology, 1990
The mechanisms by which ethanol (EtOH, 1.5 g/kg) inhibits testicular testosterone synthesis were studied in nonstimulated and human chorionic gonadotropin (hCG, 50 IU/kg)-treated male rats. To dissociate the effects caused by ethanol metabolism, the alcohol dehydrogenase inhibitor 4-methylpyrazole (4MP, 10 mg/kg) was given to half of the rats 30 min before EtOH. The 4MP had little or no effect in the nonstimulated rats on the EtOH-induced decreases in the concentrations of serum testosterone and of the intratesticular steroids of the testosterone biosynthetic pathway measured, but reduced the EtOH-induced elevation in the intratesticular pregnenolone-to-progesterone ratio. In contrast, 4MP pretreatment markedly reversed the EtOH-induced decrease in serum and intratesticular testosterone and increase in intratesticular pregnenolone concentrations in the hCG-stimulated rats. Simultaneously, the EtOH-induced elevations in the intratesticular pregnenolone/progesterone and androstenedion...
Alcoholism: Clinical and Experimental Research, 1997
It is the purpose of this study to investigate the effects of acute ethanol (EtOH) on the female rat hypothalamic-pituitary-gonadal (HPG) axis. The molecular and cellular mechanistic details of such effects have been studied intensively in the male rat. However, there has been relatively little in-depth study of EtOH's effects on the adult, postpubertal female rat. Adult female rats with confirmed 4-or &day estrous cycles were given a single injection of EtOH or saline between noon and 1:00 PM on proestrous and were killed at 400 PM. EtOH caused a sharp 97% reduction in luteinizing hormone (LH) serum levels (p c 0.001), cornpared with controls with no concomitant change in LH mRNA EtOH also significantly reduced hypothalamic LH releasing hormone (LHRH) by 49% (p c 0.01), with no change in content of the precursor pro-LHRH compared with saline-injected controls. The ratio of LHRH to pro-LHRH was also significantly reduced by EtOH (p c 0.05), compared with control. There was no EtOH-induced change in LHRH mRNA Compared with saline, EtOH reduced both serum estradiol by 37% (p c 0.02) and progesterone by 47% (p c 0.001). These results show that EtOH has profound disruptive effects on the female HPG axis. Our data suggests that EtOH decreases the releasable LHRH pool either by decreasing conversion of pro-LHRH to LHRH andor by increasing local LHRH degradation. This acutely restricts the release of LH and subsequent estradol and progesterone secretion.
Notulae Scientia Biologicae, 2020
This study evaluated the influence of human chorionic gonadotropin on hormonal and haematological profile of postpubertal male albino rats exposed to chronic oral administration of alcohol. Twenty-four mature male albino rats were assigned to four groups (n=6). Group A was the control, given distilled water, Group B was given 30% ethanol (8 ml/kg) orally 3 times a week, Group C was given human chorionic gonadotropin (HcG) (50 IU/kg) subcutaneously 3 times a week and Group D was given HcG (50 IU/kg) subcutaneously + 30% ethanol (8 ml/kg) orally 3 times a week. The study was for 10 weeks, and hormonal profile and haematology were determined. The follicle stimulating hormone of Group B decreased significantly (P<0.05) when compared to Groups A, C and D. The luteinizing hormone was significantly lower (P<0.05) in Group B when compared to Groups A, C and D. The testosterone level was significantly higher (P<0.05) in Group D when compared to Groups A, B and C. The results obtaine...
Interaction of Ethanol and Nitric Oxide in the Hypothalamic-Pituitary-Gonadal Axis in the Male Rat
Alcoholism: Clinical and Experimental Research, 1998
Ethanol (EtOH) exerts deleterious actions on reproductive function at all three levels: the hypothalamus, pituitary, and gonad (HPG). Nitric oxide (NO), a newly identified messenger molecular in a variety of biological systems, has been suggested as playing a role in HPG hormone regulation. NO stimulates luteinizing hormone releasing hormone secretion from the hypothalamus and has variable effects on luteinizing hormone release from the pituitary. NO is inhibitory to testosterone production, and it may also directly inhibit some steroidogenic enzymes. Related studies in the accompanying paper have demonstrated that inhibiting NO synthase (NOS) using various NOS inhibitors can prevent the EtOH-induced suppression of testosterone on the male HPG axis, and this action is mainly, although not entirely, due to a direct gonadal effect. To further investigate the role of NO in the HPG axis, we assessed the HPG NO-NOS system by determining NOS mRNA levels, protein levels, and enzyme activity in the presence and absence of EtOH. At the testicular level, EtOH's action did not appear to be mediated by increasing NO content. However, EtOH was able to potentiate NO'S suppressive effect on the testicular synthesis system. One locus where EtOH and NO interacted was at the steroidogenic enzyme level. fl-nitro-L-arginine methyl ester, a NOS inhibitor, was found to antagonize the EtOHinduced fall on P-450 17a-hydroxylase/C17-20 lyase mRNA levels when administered along with EtOH. EtOH had no apparent effect on the pituitary NO-NOS system and its effects on the hypothalamic NO-NOS system do not explain its ability to reduce luteinizing hormone releasing hormone secretion.