Characterization of the effects of clomiphene citrate on reproductive physiology in male rats of various ages

1988 ◽  
Vol 118 (3) ◽  
pp. 437-443 ◽  
Author(s):  
Janine L. Brown ◽  
Prabir K. Chakraborty
Keyword(s):  
Seminal Vesicle ◽  
Clomiphene Citrate ◽  
Prostate Gland ◽  
Age Groups ◽  
Reproductive Function ◽  
Male Rats ◽  
Testis Weight ◽  
Lh Receptor ◽  
Serum Lh ◽  
Prepubertal Rats

Abstract. Clomiphene citrate (clomiphene) inhibits reproduction in male rats; however, stimulatory effects have been reported at low doses. Male rats were implanted at 60 (adult), 35 (peripubertal) or 10 (prepubertal) days of age with pellets that delivered 0,0.05, 0.5 or 5.0 mg clomiphene · kg−1 · day−1 and were sacrificed after 7 or 14 days of treatment. Testis weight was unaffected by clomiphene in adult and peripubertal rats, but was reduced by all doses in prepubertal rats. Seminal vesicle and prostate gland weights were decreased to varying degrees by clomiphene in all animals, except seminal vesicle weight in peripubertal rats. Serum LH and testosterone were decreased by most doses in all age groups, whereas pituitary LH was decreased in prepubertal rats only. Pituitary GnRH and testicular LH receptor concentrations were reduced in all treated animals. Serum and pituitary FSH were decreased in pre- and peripubertal rats, whereas testicular FSH receptor concentrations were unaffected by treatment. In summary, 1) reproductive function was compromised by clomiphene and many responses were age-dependent, 2) reductions in gonadotropins suggest that clomiphene decreased their synthesis and/or release, and 3) decreased serum LH and testicular LH receptor concentrations were coupled to reduced testosterone secretion.

scholarly journals Antiperoxidative Activity ofTetracarpidium conophorumLeaf Extract in Reproductive Organs of Male Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Seun Funmilola Akomolafe ◽  
Ganiyu Oboh ◽  
Afolabi Akintunde Akindahunsi ◽  
Anthony Jide Afolayan
Keyword(s):  
Body Weight ◽  
Seminal Vesicle ◽  
Clomiphene Citrate ◽  
Prostate Gland ◽  
Reproductive Organs ◽  
Cellular Damage ◽  
Male Rats ◽  
Standard Drug ◽  
Percentage Decrease ◽  
Accessory Glands

Tetracarpidium conophorum(Mull. Arg.) Hutch. & Dalz is one of the many medicinal plants used in folklore as male fertility enhancers. This research was aimed at evaluating the anti-peroxidative activity of the leaves of this plant by determining their capacity to reduce malondialdehyde (MDA) level in reproductive organs and accessory glands of rats. Adult male rats were administered orally with the aqueous leaf extract fromT. conophorumat 50, 500 and 1000 mg/kg body weight for 21 consecutive days while clomiphene citrate (1.04 mg/kg body weight), a fertility drug was used as standard. The results of the study indicated that there was increase in relative organ weight, body weight, mean total food and water consumed by the treated groups. Testicular MDA level was highly significantly different from that of the control (p<0.0001) although a tentatively decreased MDA level was observed. However, MDA levels in the reproductive accessory glands, epididymis, seminal vesicle and prostate gland were insignificantly (p<0.05) lower than those of controls. The highest percentage decrease of MDA level (66.35, 42.68, 62.50 and 63.36%) was observed at the highest concentration of the extract (1000 mg/kg) in the testis, epididymis, seminal vesicle and prostate gland respectively. These values were two-fold greater than the values obtained for the standard drug. Interestingly, the treatment of rats with the extract significantly increased the activities of superoxide dismutase, catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and the levels of GSH, vitamin C and total protein. Collectively, the results suggest that the extract fromT. conophorumleaves had greater capacity to reduce lipid peroxidation in reproductive organs and accessory glands and thus, this plant may be useful in the treatment/management of reproductive cellular damage involving reactive oxygen species.

Acute and short-term actions of serotonin administration on the pituitary-testicular axis in the adult rat

1995 ◽  
Vol 7 (5) ◽  
pp. 1101 ◽  
Author(s):  
MP Hedger ◽  
S Khatab ◽  
G Gonzales ◽  
Kretser DM de
Keyword(s):  
Serum Testosterone ◽  
Fold Increase ◽  
Significant Inhibition ◽  
Male Rats ◽  
Minor Role ◽  
Testis Weight ◽  
Serum Concentrations ◽  
Adult Rat ◽  
Serum Lh ◽  
A Minor

In this study, adult male rats were injected intraperitoneally with a single dose of serotonin (5-hydroxytryptamine, 5HT; 10 mg kg-1 bodyweight) for 2 h or 18 h, or daily with graded doses of 5HT (0.1-10 mg kg-1) for four days before being killed. Serum and testicular interstitial fluid (IF) concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone and immunoreactive-inhibin were measured by radioimmunoassay, and one testis was removed for histological examination. At 2 h after a single injection, 5HT caused a significant inhibition of serum concentrations of LH and inhibin, recovered IF volume and intratesticular testosterone concentrations; testis weight and serum concentrations of testosterone and FSH were unaffected. At 18 h after injection, all parameters had returned to normal, with the exception of intratesticular testosterone concentration which remained lower than normal. The lowest 5HT dose (0.1 mg kg-1) had no effect on any parameter following four daily injections. At a dose of 1.0 mg kg-1 5HT, there was a four-fold increase in the concentration of serum LH, but testis weight, recovered IF volume, testosterone and inhibin concentrations and serum concentrations of FSH were not significantly affected. At the highest dose of 5HT (10 mg kg-1) after four daily injections, testis weight decreased, and IF volume increased nearly three-fold. Testis concentrations of inhibin and serum testosterone were reduced, whereas serum concentrations of both LH and FSH were elevated; intratesticular testosterone concentrations did not differ from controls. Only at the highest dose of 5HT was disruption to the seminiferous epithelium observed, with focal damage ranging in severity from increased degeneration of spermatogenic cell profiles, to complete loss of the germinal epithelium; however, many tubule profiles displayed completely normal spermatogenesis. The acute IF volume reduction and spermatogenic disruption in 5HT-treated rats were consistent with localized ischaemia due to constriction of the testicular arterial supply. The eventual increase in IF volume observed after 5HT treatment appeared to be secondary to the loss of germ cells. Although 5HT also inhibited pituitary LH release and Leydig cell steroidogenesis, these effects appeared to play only a minor role in the induction of spermatogenic damage.

INFLUENCE OF VARIOUS STEROIDS ON TESTES AND ACCESSORY SEX ORGANS IN THE RAT

1965 ◽  
Vol 49 (1) ◽  
pp. 145-154 ◽  
Author(s):  
Fred A. Kind ◽  
M. Maqueo ◽  
Ralph I. Dorfman
Keyword(s):  
Seminal Vesicle ◽  
Treatment Period ◽  
Post Treatment ◽  
Testicular Atrophy ◽  
Male Rats ◽  
Ventral Prostate ◽  
Testis Weight ◽  
Intact Male ◽  
Seminal Vesicle Weight ◽  
Testicular Histology

ABSTRACT Various neutral steroids were studied in intact male rats for their ability to influence testicular function, particularly spermatogenesis. The compounds were injected once daily for 21 days, starting at 21 days of age. One day after the last injection, testicular histology and testis, ventral prostate, and seminal vesicle weights were determined. In some experiments, after the standard 21 day treatment period, testicular histology and function were evaluated after 30 and 60 day post-treatment recovery periods. 2α-Hydroxymethyl-17β-hydroxy-5α-androstan-3-one, 2-hydroxy-5α-androst-2-en-17β-ol, 2,17α-dimethyl-5α-androst-2-en-17β-ol and 2-formyl5α-androst-2-en-17β-ol caused decreases in testicular, ventral prostate and seminal vesicle weight and produced arrest of spermatogenesis. These effects were reversible and testis weight and histology, as well as fertility, were restored in the post-treatment period. 19-Norprogesterone, which did not produce convincing testicular atrophy, did cause significant decreases in ventral prostate and seminal vesicle weight. Chlormadinone showed a similar picture, although direct antagonistic testicular effects were also seen. The lowered ventral prostate and seminal vesicle weights produced by these compounds may be an expression of their antiandrogenic activity.

HYPOTHALAMIC-PITUITARY-TESTICULAR SYSTEM FOLLOWING TESTICULAR X-IRRADIATION

1976 ◽  
Vol 83 (1) ◽  
pp. 190-200 ◽  
Author(s):  
H. L. Verjans ◽  
K. B. Eik-Nes
Keyword(s):  
Interstitial Cell ◽  
Serum Testosterone ◽  
Male Rats ◽  
Ventral Prostate ◽  
Testis Weight ◽  
X Ray ◽  
Serum Lh ◽  
Testicular Weight ◽  
Unknown Factor ◽  
X Irradiation

ABSTRACT Testes of adult, male rats were exposed to a total dose of 1500 R of X-irradiation. Testicular weight decreased from day 8 after X-ray treatment. This decrease was, however, preceded by an increment of the testis weight on day 4 following treatment. X-ray treatment of testes was associated with significant increases in serum FSH. Testicular irradiation had, however, no effect on ventral prostate and seminal vesicles weights. Serum testosterone increased only on day 1, 2 and 4 after irradiation, while serum LH levels tended to increase from day 8 post-irradiation. These changes were not significant, however, when compared with non-irradiated controls. At 7, 13 and 20 days following 1500 R of bilateral, testicular X-irradiation, the hypothalamic-pituitary unit was still capable of responding to exogenous gonadotrophin releasing factor. Serum FSH may in male rats be regulated at least partly by circulating steroids of testicular origin and partly by an unknown factor of non-interstitial cell nature.

Leydig cell resistance to the cytotoxic effect of ethylene dimethanesulphonate in the adult rat testis

1985 ◽  
Vol 105 (3) ◽  
pp. 311-NP ◽  
Author(s):  
I. D. Morris
Keyword(s):  
Seminal Vesicle ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Serum Testosterone ◽  
Male Rats ◽  
Cell Physiology ◽  
Testis Weight ◽  
Endocrine Activity ◽  
Adult Rat ◽  
Seminal Vesicle Weight

ABSTRACT Weekly doses of the Leydig cell cytotoxic ethylene dimethanesulphonate (EDS) were administered to adult male rats in an attempt to study the endocrine activity of the testis in the absence of Leydig cells. One week after the first dose serum testosterone and LH concentrations and seminal vesicle weights were close to levels in castrated rats and testicular human chorionic gonadotrophin (hCG) binding was severely depressed. These changes were maintained for a further week but subsequently began to return to, but did not achieve, control levels. After six weekly doses seminal vesicle weight and serum testosterone concentrations were significantly higher than in the castrated rats. Serum LH concentrations were declining towards control values at 4 weeks but had risen again at 6 weeks. Serum FSH concentrations were raised to about 50% of the value in castrated rats throughout the period studied. Testis weight and hCG binding, which initially fell, were partially restored at 6 weeks and spermatogenesis was recovering. The data show that responses of the testis to multiple doses of EDS are similar to those after a single dose. This apparent resistance indicates that the regenerating Leydig cells are functionally different from the mature Leydig cell. The similarities between the maturing Leydig cell seen after EDS destruction and those in the immature rat suggest that EDS will provide a valuable model for the investigation of Leydig cell physiology. J. Endocr. (1985) 105, 311–316

scholarly journals Simultaneous Effect of Kisspeptin and Galanin on Serum Luteinizing Hormone and Testosterone Levels in Male Rats

2017 ◽  
Vol 6 (1) ◽  
pp. 23-29
Author(s):  
Maliheh Talebolhosseini ◽  
Homayoun Khazali
Keyword(s):  
Luteinizing Hormone ◽  
Reproductive Function ◽  
Hormonal Control ◽  
Male Rats ◽  
Testosterone Concentration ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Wide Range ◽  
Male Wistar Rats ◽  
The Mean

Background: Galanin is a neuropeptide with a wide range of physiological functions that also has stimulatory effects on the reproductive axis. Kisspeptin is a crucial neuropeptide for the stimulation of the reproductive function. In the present study, the interaction of kisspeptin and the galanin signaling system was investigated on the mean serum luteinizing hormone (LH) and the testosterone concentrations in rats. Materials and Methods: Fifty-five male Wistar rats in 11 groups (n=5 per group) received saline, kisspeptin (1nmol), P234(1nmol), galanin(1nmol), galantide (1nmol) or simultaneous injections of them via third cerebral ventricle at 07:00 - 07:30. Blood samples were collected at 30 min following the injections. Hormone concentrations were measured using rat kit and the method of the radio-immunoassay (RIA). Results: Kisspeptin or galanin injection significantly increased both the mean serum LH and the testosterone concentration compared to saline (P<0.05). The co-administration of kisspeptin/galanin increased the mean serum LH and the testosterone concentration significantly compared to galanin or saline (P<0.05). The co-administration of kisspeptin/galanin decreased the mean serum LH concentration compared to kisspeptin, this reduction, however, was not statistically significant. Also, testosterone concentration declined in the kisspeptin/galanin group compared to kisspeptin group. Galantide or p234 injection decreases the mean serum LH and the testosterone concentration compared to galanin and kisspeptin, respectively. The co-administration of galantide/p234 lowers the mean serum LH concentration compared to saline. Conclusion: The interaction of hypothalamic galanin and kisspeptin signaling pathways may play an important role in the modulation of hormonal control of the hypothalamus-pituitary-gonadal axis. [GMJ. 2017;6(1):23-29]

scholarly journals Effects of Chronic Hyperghrelinemia on Puberty Onset and Pregnancy Outcome in the Rat

Endocrinology ◽  
2005 ◽  
Vol 146 (7) ◽  
pp. 3018-3025 ◽  
Author(s):  
R. Fernández-Fernández ◽  
V. M. Navarro ◽  
M. L. Barreiro ◽  
E. M. Vigo ◽  
S. Tovar ◽  
...  
Keyword(s):  
Pregnancy Outcome ◽  
Energy Homeostasis ◽  
Reproductive Function ◽  
Chronic Administration ◽  
Serum Levels ◽  
Male Rats ◽  
Gestational Length ◽  
Serum Lh ◽  
Puberty Onset ◽  
Key Aspects

Abstract Ghrelin, the endogenous ligand of the GH secretagogue receptor, has been recently involved in a wide array of biological functions, including signaling of energy insufficiency and energy homeostasis. On the basis of the proven reproductive effects of other regulators of energy balance, such as the adipocyte-derived hormone leptin, we hypothesized that systemic ghrelin may participate in the control of key aspects of reproductive function. To test this hypothesis, the effects of daily treatment with ghrelin were assessed in rats, pair-fed with control animals, in two relevant reproductive states, puberty and gestation, which are highly dependent on proper energy stores. Daily sc injection of ghrelin (0.5 nmol/12 h; between postnatal d 33 and 43) significantly decreased serum LH and testosterone levels and partially prevented balanopreputial separation (as an external index of puberty onset) in pubertal male rats. On the contrary, chronic administration of ghrelin to prepubertal females, between postnatal d 23 and 33, failed to induce major changes in serum levels of gonadotropins and estradiol, nor did it modify the timing of puberty, as estimated by the ages at vaginal opening and first estrus. Moreover, females treated with ghrelin at puberty subsequently displayed normal estrous cyclicity and were fertile. Conversely, ghrelin administration (0.5 nmol/12 h) during the first half of pregnancy (d 1–11) resulted in a significant decrease in pregnancy outcome, as estimated by the number of pups born per litter, without changes in the number of successful pregnancies at term or gestational length. Overall, our data indicate that persistently elevated ghrelin levels, as a putative signal for energy insufficiency, may operate as a negative modifier of key reproductive states, such as pregnancy and (male) puberty onset.

Effect of acute and chronic administration of clonidine on hypothalamic content of growth hormone-releasing hormone and somatostatin in the rat

1991 ◽  
Vol 131 (3) ◽  
pp. 381-385 ◽  
Author(s):  
I. Gil-Ad ◽  
Z. Laron ◽  
Y. Koch
Keyword(s):  
Age Groups ◽  
Chronic Administration ◽  
Feedback Mechanism ◽  
Male Rats ◽  
Releasing Hormone ◽  
Negative Feedback Mechanism ◽  
Gh Secretion ◽  
Pubertal Stages ◽  
Prepubertal Rats ◽  
A Chain

ABSTRACT Hypothalamic GH-releasing hormone (GHRH) and somatostatin contents were determined in male rats at pre- and mid-pubertal stages following acute (0·15 mg/kg) or chronic (0·1 mg/kg twice daily for 7 days) administration of clonidine. Hypothalamic GHRH content increased markedly during transition from pre- to mid- and late-pubertal stages (2·05±0·17vs 3·13±0·26 and 3·46±0·20 ng/hypothalamus respectively, means ±s.e.m.). Hypothalamic GHRH content was markedly decreased 1 h after clonidine administration in mid-pubertal but not in prepubertal rats (3·67±0·23 vs 2·65±0·22 ng/hypothalamus). Hypothalamic somatostatin content, on the other hand, decreased in both age groups, although the decrease in the mid-pubertal group was more pronounced (51% and 38% respectively). In addition, the GH responsiveness to clonidine was higher at mid-puberty than at prepuberty. Determination of hypothalamic somatostatin and GHRH content in the chronic experiment 4 h after the last drug administration revealed a marked decrease in GHRH in the mid-pubertal rats and a slight decrease in the prepubertal rats (1·78±0·32 vs 3·15±0·31 and 2·01±0·30 vs 2·35±0·15 ng/hypothalamus; P < 0·005 and P<0·05 respectively) whereas somatostatin levels were not altered. It is suggested that the clonidineinduced GH secretion is modulated by a chain of events which involves primary stimulation of GHRH release resulting in increased GH secretion which, via a negative-feedback mechanism, triggers an enhancement of somatostatin release which ultimately normalizes the system. This mechanism is age-dependent and reaches full maturity only at the onset of puberty. Journal of Endocrinology (1991) 131, 381–385

Testosterone maintains pituitary and serum FSH and spermatogenesis in gonadotrophin-releasing hormone antagonist-suppressed rats

1986 ◽  
Vol 108 (1) ◽  
pp. 101-107 ◽  
Author(s):  
M. A. Rea ◽  
G. R. Marshall ◽  
G. F. Weinbauer ◽  
E. Nieschlag
Keyword(s):  
Serum Testosterone ◽  
Treated Group ◽  
Male Rats ◽  
Testis Weight ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Hypophysectomized Rats ◽  
Gonadotrophin Releasing Hormone ◽  
Vehicle Treated Control

ABSTRACT Groups of adult male rats were treated continuously for 30 days with either vehicle or the potent gonadotrophin-releasing hormone (GnRH) antagonist, (N-Ac-d-Nal(2)1,d-pCl-Phe2,d-Trp3,d-hArg (Et2)6,d-Ala10)-GnRH (RS 68439; 35 μg/day). In addition, groups of vehicle- and antagonist-treated rats received s.c. testosterone implants sufficient to maintain serum testosterone concentrations 3·5- to 5-fold higher than those of vehicle-treated control rats. After 30 days of antagonist treatment serum LH, FSH and testosterone concentrations were at or below the detection limits of their respective assays and pituitary FSH content and GnRH receptor binding were reduced, relative to control animals, by 77 and 98% respectively. Testis weight in antagonist-treated rats was reduced by 75% and spermatogenesis was suppressed to an extent comparable to that observed in hypophysectomized rats. Testosterone, which caused a 40% reduction in serum FSH relative to control animals, prevented the antagonist-induced fall in both serum and pituitary FSH, but not GnRH receptors, below that observed in the vehicle plus testosterone-treated group. Furthermore, spermatogenesis in the antagonist plus testosterone-treated group was indistinguishable from that observed in control animals. It is concluded that testosterone is capable of maintaining serum and pituitary FSH levels in vivo, under conditions which presumably render the pituitary insensitive to hypothalamic GnRH. J. Endocr. (1986) 108, 101–107

REGULATION OF PROLACTIN BINDING SITES IN THE SEMINAL VESICLE, PROSTATE GLAND, TESTIS AND LIVER OF INTACT AND CASTRATED ADULT RATS: EFFECT OF ADMINISTRATION OF TESTOSTERONE, 2-BROMO-α-ERGOCRYPTINE AND FLUPHENAZINE

1979 ◽  
Vol 81 (1) ◽  
pp. 11-18 ◽  
Author(s):  
R. J. BARKEY ◽  
J. SHANI ◽  
D. BARZILAI
Keyword(s):  
Seminal Vesicle ◽  
Binding Sites ◽  
Specific Binding ◽  
Prostate Gland ◽  
Male Rats ◽  
Male Rat ◽  
Serum Prolactin ◽  
Testosterone Replacement Therapy ◽  
Adult Rats ◽  
Intact Rats

The effect of hormonal manipulations on prolactin binding to its specific binding sites in the seminal vesicle, prostate gland, testis and liver of adult male rats was studied. Castration significantly reduced prolactin binding to the seminal vesicle and prostate, whereas it greatly increased its binding to the liver. Testosterone replacement therapy restored the reduced level of binding to that found in the liver of intact rats, whereas binding to the seminal vesicle and the prostate was raised to the high levels found in the testosterone-treated intact rats. In contrast, testosterone administration to intact rats significantly reduced the binding of prolactin to the testicular homogenate. The administration of 2-bromo-α-ergocryptine (CB 154) to either intact or testosterone-treated castrated rats caused no significant change in binding of prolactin to any of the organs tested. Fluphenazine enanthate or CB 154 +ovine prolactin increased the binding of prolactin to the liver, when compared with untreated rats, whereas in the testis these treatments resulted in a minor decrease as compared with untreated rats. In the testosterone-treated castrated rats, fluphenazine caused no apparent effect on the binding of prolactin to any of the organs tested. In conclusion, testosterone is essential for the maintenance of prolactin binding sites in the seminal vesicle and prostate of the adult rat. Prolactin, however, does not appear to regulate its own receptor in the accessory sex glands, neither alone nor in synergism with testosterone. In the testis, exogenous testosterone exerted a negative effect on prolactin binding, as did raised serum prolactin levels. In the liver of the male rat, testosterone seemed to be the major cause of the low level of prolactin binding sites, while prolactin was capable of inducing its own sites in that organ.

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