Prolactin In Male Rats Research Articles

Rapid prolactin induction in adult male rats after treatment with diethylstilbestrol.

Diethylstilbestrol (DES) is a synthetic oestrogen known to disrupt the endocrine system and to cause reproductive toxicity mediated via the hypothalamic-pituitary-adrenal axis; however, its molecular mechanism of action is poorly understood. In the present study, we found that, after only 1week of exposure to DES, blood testosterone dramatically decreased and that this decrease was associated with a strong induction of prolactin (PRL). Even with the increase in PRL, the luteinising hormone and follicle-stimulating hormone mRNAs slightly decreased. Our results show that, after 48hours of a single dose of DES, there was a six-fold increase in PRL expression. After exploring the upstream mechanisms, we determined that dopamine, which inhibits PRL secretion in male rats, did not decrease in the pituitary gland of DES-treated rats, whereas vasoactive intestinal peptide (VIP), which mediates the acute release of PRL, was elevated. Serotonin (5-HT) increased in the brain of male rats 24hours after a single DES treatment; however, PRL, VIP or 5-HT was not induced by DES in female rats. Our results indicate that DES induces the expression of pituitary PRL in male rats by stimulating VIP in the hypothalamus and 5-HT in the central nervous system.

Prosocial effects of prolactin in male rats: Social recognition, social approach and social learning

Prolactin (PRL) and oxytocin (OT) are pituitary hormones essential for lactation, but also promote sexual behavior. OT stimulates social behaviors, such as recognition, approach, and learning, but less is known about PRL in these behaviors. Since PRL and OT have complementary functions in reproduction, we hypothesized that PRL increases social recognition, approach, and learning. Male Long-Evans rats received ovine PRL (oPRL; 0.5, 2.0 or 5.0mg/kg), the PRL antagonist bromocriptine (0.1, 3.0 or 5.0mg/kg) or saline 20 mins before testing for recognition of familiar vs. unfamiliar stimulus males. Saline controls preferred the unfamiliar male (p<0.05), while bromocriptine blocked this preference. oPRL did not increase preference. To measure social approach, we determined if PRL restores approach 2h after defeat by an aggressive male. Defeated rats avoided the aggressive male. 2mg/kg oPRL, before or after defeat, restored approach towards the aggressive male (p<0.05). In non-defeated rats, oPRL or 3mg/kg bromocriptine had no effect. To determine if PRL increases social learning, we tested social transmission of food preference. Rats choose between two unfamiliar flavors, one of which they have previously been exposed to through interaction with a demonstrator rat. Vehicle controls preferred chow with the demonstrated flavor over the novel flavor. oPRL-treated rats were similar. Bromocriptine-treated rats failed to show a preference. When tested one week later, only oPRL-treated rats preferred the demonstrated flavor. The results suggest that PRL is required for social recognition and learning, and that increasing PRL enhances social memory and approach, similar to OT.

Effect of Soybean (Glycine max L.) on the Hormonal Milieu of Male Rats

Effect of soybean (Glycine max) on serum level of some sex hormones: testosterone, follicle stimulating hormone (FSH), luteinizing hormone/interstitial cell stimulating hormone (LH/ICSH), estradiol and prolactin in male rats was investigated. Twenty male albino rats of 12 weeks old with similar body weights were assigned to four groups of 5 rats each and treatment with soybean meal at 100, 200 and 300 mg kg(-1) body weight, respectively daily for 8 weeks. Blood samples collected through cardiac puncture were assayed for levels of hormones. There were dose-dependent effects of the soybean meal on the serum concentration of the hormones. The treatment significantly reduced the levels of testosterone and FSH in the serum while it significantly increased the levels of estradiol, LH/ICSH and prolactin. The results show that soybean (Glycine max) had strong capability to disrupt hormonal functions. Hence, its indiscriminate use could increase the risk of infertility in males.

Central Administration of Orexin A Suppresses Basal and Domperidone Stimulated Plasma Prolactin

Orexin immunoreactive fibres are abundant in the hypothalamus suggesting a neuroendocrine regulatory role. Intracerebroventricular (ICV) administration of orexin A suppressed plasma prolactin in male rats by 71% at 20 min post-injection and 83% at 90 min post-injection (P < 0.005 vs saline at both time points). To investigate whether this effect was through the tuberoinfundibular dopaminergic (TIDA) system, a supra-maximal dose of domperidone, a dopamine receptor antagonist, was injected intraperitoneally (i.p.) prior to ICV injection of orexin A. ICV orexin A significantly suppressed domperidone (9 mg/kg)-stimulated plasma prolactin levels, by up to 40% (i.p. domperidone + ICV orexin A 3 nmol 34.5 +/- 7.4 ng/ml and i.p. domperidone + ICV orexin A 20 nmol 43.5 +/- 4.3 ng/ml, both P < 0.005 vs i.p. domperidone + ICV saline 57.9 +/- 2.7 ng/ml). Orexin A, 100 nM, significantly stimulated release of neurotensin, vasoactive intestinal polypeptide, somatostatin, corticotropin releasing factor and luteinizing hormone releasing hormone, but had no effect on release of dopamine, thyrotropin releasing hormone (TRH), vasopressin or melanin-concentrating hormone from hypothalamic explants in vitro. Orexin A did not alter basal or TRH stimulated prolactin release in dispersed pituitary cells harvested from male rats. The data suggest that ICV administration of orexin A suppresses plasma prolactin in part through a pathway independent of the dopaminergic system.

Regulation of testosterone secretion by prolactin in male rats

Regulation of testosterone secretion by prolactin in male rats

Regulation of testosterone secretion by prolactin in male rats

The goal of this study was to characterize the mechanism by which hyperprolactinemia alters testosterone production in rat testicular interstitial cells (TICs). Hyperprolactinemia was induced by grafting 2 anterior pituitary (AP) glands under the subcapsular space of the kidney in experimental rats. Control rats were grafted with brain cortex (CX). Six weeks post-grafting, rats were challenged with human chorionic gonadotropin (hCG) then, the changes in either plasma testosterone or luteinizing hormone was measured. Additionally, TICs were isolated and challenged in vitro with hCG or prolactin, and the testosterone release measured by radioimmunoassay. Further investigation in signal transduction as intracellular 3':5' cyclic adenosine monophosphate (cAMP) production was observed under a regulation of forskolin or SQ22536. After the challenge of hCG or GnRH, the AP-grafted rats showed a suppressed response in testosterone release as compared to those in the CX-grafted group. The in vitro data from the AP-grafted rats compared to the CX-grafted animals showed a diminished response in testosterone release upon hCG stimulation. Administration of forskolin or SQ22536 disclosed dysfunction of adenylate cyclase in TICs from the AP-grafted rats. When 8-Br-cAMP was incubated with TICs, the testosterone production was lower in the AP-grafted compared to the CX-grafted group. These results suggest that in addition to adenylate cyclase dysfunction, inefficiency of post-cAMP pathways are also involved in the hypogonadism elicited by hyperprolactinemia in rats.

Effects of Chronic Alternating Cadmium Exposure on the Episodic Secretion of Prolactin in Male Rats

Cadmium increases or decreases prolactin secretion depending on the dose and duration of the exposure to the metal. However, whether there are cadmium effects on the episodic prolactin secretion is less well known. This study was undertaken to address whether chronic alternating exposure to two different doses of cadmium affects the episodic pattern of prolactin and to what extent the effects of cadmium are age-dependent. Male rats were treated s.c. with cadmium chloride (0.5 or 1.0 mg/kg) from day 30 to 60, or from day 60 to 90 of age, with alteration of the doses every 4 days, starting with the smaller dose. Controls received vehicle every 4 days. The last dose of cadmium was given 48 h prior to the pulsatility study. Prolactin secretion in the 4 experimental groups studied was episodic and changed significantly after cadmium exposure. Cadmium administration from day 30 to 60 of life significantly decreased the mean half-life of prolactin. On the other hand, when administered from day 60 to 90 cadmium significantly decreased the mean as well as serum prolactin levels and the absolute amplitude of the prolactin pulses, their duration, the relative amplitude or the mean half-life of the hormone. The frequency of prolactin peaks was not changed by cadmium administration. The results indicate that low intermittent doses of cadmium chronically administered change the episodic secretion pattern of prolactin in rats. The effects of cadmium on prolactin secretion were age dependent.

Hypothalamic histamine, growth rate, plasma prolactin and growth hormone levels in rats with long-term portacaval anastomosis.

Histamine can modulate feeding behaviour and hormone release; therefore we examined the hypothalamic histamine system, the growth pattern and the serum levels of prolactin and growth hormone in rats with portacaval anastomosis (PCA). The growth rate of 30 PCA- and 30 sham-operated male Han:Wistar rats was monitored for 6 months. Thirteen sham and 9 PCA rats were used for biochemical studies. Histamine was assayed by HPLC, tele-methylhistamine by GC-MS, prolactin and growth hormone by RIA. Student's t-test was used to compare the groups. Six months after surgery, the PCA rats exhibited marked growth retardation (weight gain of 20 g vs. 140 g for the sham rats; p < 0.001), increased plasma levels of prolactin (9.7 +/- 2.4 vs. 3.6 +/- 0.6; p<0.01) and unaltered growth hormone levels (6.2 +/- 0.5 vs. 8.1 +/- 1.0). A six-fold elevation of histamine concentration (29.5 +/- 3.9 vs. 4.8 +/- 0.4; p<0.001) and a two-fold increase of tele-methylhistamine levels (1.8 +/- 0.1 vs. 0.8 +/- 0.02; p<0.001) were found in hypothalamus. We suggest that increased histaminergic activity in the hypothalamus may be involved in the development of growth retardation and in the enhanced basal secretion of prolactin in male rats with long-term PCA.

Possible interactions of cyclosporine and hyperprolactinemia modulating the episodic secretion of prolactin.

The interrelationship between the effects of prolactin and cyclosporine (CsA) appears to be very complex and until now poorly understood. The aim of the present work was to analyze whether chronic treatment with CsA could modify the episodic secretion of prolactin in male rats and whether the presence of an ectopic pituitary could counteract the effects of the drug on the pulsatile secretion pattern of this hormone. At 30 days of age, male rats were implanted with one anterior pituitary under the kidney capsule or where sham-operated. Both pituitary-grafted and sham-operated rats were injected sc for 30 days with the vehicle or CsA (5 mg/kg/day), beginning on the day of surgery. Pituitary grafting and/or CsA administration changed the pulsatile secretion pattern of prolactin. In pituitary-grafted male rats, mean serum prolactin levels, absolute pulse amplitude, and half-life of the hormone increased, while the pulse frequency decreased, compared with the values found in sham-operated rats. CsA administration to sham-operated rats increased the relative amplitude of prolactin peaks and diminished the half-life of the hormone, compared with rats of the same group treated with vehicle. However, CsA treatment in pituitary grafted rats led to lower mean serum prolactin levels and absolute amplitude, while the frequency, duration, and relative amplitude of prolactin pulses were not modified. Plasma prolactin levels did not change in control animals, whereas a reduction in circulating values of the hormone was found in pituitary grafted animals. These data suggest that CsA modifies the pulsatile secretory pattern of prolactin in pituitary-grafted male rats. The different effects observed in the control and pituitary-grafted animals might be due to a direct effect of the drug on the ectopic lactotrophs that are submitted to local regulatory influences different from those of the in situ pituitary which are submitted to the regulatory influence of the hypothalamus.

Effects of intraventricular taurine, homotaurine and GABA on serum prolactin and thyrotropin levels in female and in male rats.

Serum prolactin and thyrotropin levels of conscious, unrestrained male and female rats were compared after intracerebroventricular (i.c.v.) administration of taurine, gamma-aminobutyric acid (GABA) and homotaurine. The amino acids studied had no clear effect on serum basal thyrotropin levels in male or female rats. All amino acids elevated serum prolactin levels in female rats at the dose of 5 mumol/rat; homotaurine by about 18-fold, taurine and GABA by 3-fold. Only homotaurine elevated serum prolactin of male rats at this dose, but its effect was less pronounced (p < 0.01) in male than in female rats. Although homotaurine was clearly more potent than the two other amino acids, at the dose of 10 mumol/rat taurine and GABA also elevated serum prolactin in male rats. These findings show that there are gender-related differences in the responses of serum prolactin levels to homotaurine, taurine and GABA in rats. The tuberoinfundibular dopaminergic pathway, which exerts tonic inhibitory influence on prolactin secretion, is sexually differentiated. Hence the gender-related differences in the effects of the amino acids on prolactin secretion suggest that they might inhibit dopamine release from the median eminence. In case of homotaurine, the gender effect was most pronounced. The less clear dependence of GABA's effect on the gender is in accordance with the suggestions that GABA influences the secretion of serum prolactin by more than one mechanism.

A GABA B-receptor mechanism is involved in the prolactin release in both male and female rats

In order to evaluate the possible involvement of a GABA B-receptor mechanism in the control of prolactin release, the effect of baclofen, a GABA B-receptor agonist, on prolactin release was studied in male and female rats. Baclofen at a dose of 2–12 mg/kg was injected i.v. and blood samples were collected through an intraatrial cannula in freely moving rats. Baclofen caused an immediate increase in the prolactin concentration in serum, peaking at 6 min, in female rats. The injection also caused an increase in prolactin in male rats, the increase being smaller than in female rats. Together with the previous finding that the pituitary gland does not have GABA B receptors, the results support the concept that GABA plays a role in the central stimulation of prolactin release, mediated by GABA B receptors.

Effect of serotonin 5-HT1, 5-HT2, and 5-HT3 receptor antagonists on the prolactin response to restraint and ether stress.

Serotonin (5-HT) appears to be involved in the central control of the prolactin (PRL) response to suckling and estrogen. Furthermore, 5-HT may participate in the mediation of stress-induced PRL release. In order further to elucidate the role of 5-HT and the type of 5-HT receptor(s) involved in the PRL response to stress, we investigated the effect of blockade of 5-HT1, 5-HT2 or 5-HT3 receptors on the restraint or ether stress-induced release of PRL in male rats. Pretreatment with the 5-HT1 + 2 receptor antagonist methysergide (0.5 or 2.5 mg/kg i.p.) inhibited or prevented the PRL response to restraint or ether stress. Pretreatment with the 5-HT2 receptor antagonists ketanserin or LY 53857 (0.5 or 2.5 mg/kg i.p.) inhibited the response to restraint or ether stress approximately 30 or 60%, respectively. Higher doses of both 5-HT2 receptor antagonists (10 mg/kg i.p.) had a minor inhibitory effect (5-30% for ketanserin and 50% for LY 53857). Prior intraperitoneal administration of the 5-HT3 receptor antagonists ICS 205-930 or GR 38032F (0.05-2.5 mg/kg i.p.) inhibited the restraint stress-induced PRL release dose-dependently. Both compounds inhibited the PRL response to ether stress, but only the effect of GR was dose-related. The maximal inhibitory effect (70% inhibition of the PRL response to restraint or ether stress) was obtained for both compounds at a dose of 0.1 mg/kg. We conclude that serotonergic neurons are involved in the mediation of the stress-induced PRL release by activation of 5-HT1, 5-HT2 as well as 5-HT3 receptors.

Multiple, but not acute, infusions of cocaine alter the release of prolactin in male rats

Hypothalamic dopamine tonically inhibits the release of prolactin (PRL) from the anterior pituitary gland. Cocaine, in turn, alters dopaminergic transmission. We compared the effects of acute and repeated injections of cocaine on the release of PRL in male rats to assess whether cocaine could affect dopaminergically mediated hormonal responses. We found that the concentration of PRL in plasma was not affected by single i.v. injections of 1, 3 or 10 mg/kg of cocaine. However, in rats infused repeatedly with 1 mg/kg of cocaine for 5 s every 12 min for 2 h over 10 days, the pre-infusion concentrations of PRL increased in a time-dependent manner whereas cocaine uniformly decreased post-infusion levels of PRL. Repeated administration of cocaine may produce long-term changes in either the tuberoinfundibular dopaminergic neurons of the adenohypophysial dopamine D 2-receptors, or both. Changes in the peripheral concentration of PRL after multiple injections of cocaine and during cocaine withdrawal may reflect dopaminergic activity in the hypothalamus. In contrast, single injections of cocaine increased adrenocorticotropin (ACTH) in a dose-dependent manner whereas repeated infusions did not increase peripheral concentrations of ACTH or corticosterone. It seems that repeated injections of cocaine do not result in persistant changes in the hypothalamo-pituitary-adrenal axis.

Daily illuminance levels affect pituitary prolactin in male rats

The 24-h patterns of melatonin, PRL, and gonadotropins in male rats maintained under natural lighting conditions have been found to differ from the patterns in rats kept under artificial lighting. In the present experiments we studied the role of different daily illuminances as a possible causative factor for the variation of the hormonal patterns. Three groups of male rats were kept under artificial lighting conditions (12 h on/12 h off), where the daily illuminance was 550, 110 or 25 lux. After a 7-day adaptation period the pineal content of melatonin, the serum levels of LH, FSH and PRL, and the pituitary content of these hormones were measured by RIAs in samples taken at 10.00, 13.00, 22.00 and 01.00 h. The patterns of pineal melatonin were equal in all three groups. The variation of daily illuminance did not change the serum levels of LH, FSH and PRL or the pituitary content of the gonadotropins. However, the pituitary content of PRL during the light phase was inversely related to the illuminance. The results suggest that the intensity of daily lighting in the studied range does not affect the patterns of melatonin or gonadotropins, but the synthesis of prolactin may be significantly regulated by the daily illuminance level.

Histaminergic mediation of the stress-induced release of prolactin in male rats.

Histamine (HA) is likely to participate in the neuroendocrine regulation of prolactin (PRL) secretion. We, therefore, studied the possible involvement of HA in the stress-induced release of PRL in conscious male rats. HA (30 micrograms) infused intracerebroventricularly 15 min before decapitation elevated PRL plasma levels from 5 +/- 1 to 54 +/- 6 ng/ml (p less than 0.01). Intracerebroventricular infusion of the H2 receptor antagonists cimetidine (CIM: 100 micrograms) or ranitidine (RAN: 125 micrograms) abolished the PRL response to HA (p less than 0.01), while intracerebroventricular infusion of the H1 receptor antagonist mepyramine (MEP; 100 micrograms) inhibited the response only 40% (p less than 0.05). Intra-arterial infusion of CIM (2,000 micrograms) or RAN (2,500 micrograms) inhibited the HA-stimulated PRL secretion 52% (p less than 0.01) or 63% (p less than 0.01), respectively. The H1 receptor antagonists MEP (1,000 micrograms) and SKF-93944 (1,500 micrograms) had no effect following intra-arterial administration. Restraint stress increased the PRL level to 84 +/- 6 ng/ml (p less than 0.01 vs. control). This effect was prevented by intracerebroventricular infusion of CIM or RAN (p less than 0.01) and inhibited 75% by MEP (p less than 0.01). Intra-arterial infusion of CIM, MEP, and SKF-93944 inhibited the stress response about 50% (p less than 0.01), while RAN decreased the response only 25% (p less than 0.05). Ether stress elevated the plasma PRL concentration to 46 +/- 5 ng/ml (p less than 0.01 vs. control). When infused intracerebroventricularly CIM or RAN prevented the response (p less than 0.01), while MEP had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of the cholecystokinin antagonist, proglumide, on prolactin secretion in the rat

Since cholecystokinin produced important effects on prolactin secretion following its intraventricular injection in ovariectomized rats, we have evaluated the effects of the cholecystokinin antagonist, proglumide, to assess the physiologic significance of CCK in the control of prolactin release. Conscious rats of either sex were used following implantation of third ventricular and/or intravenous cannulae for the administration of proglumide. Blood samples were drawn from conscious animals at various times after injection of the compound. Intraventricular injection of 1 or 10 μg of proglumide produced a dramatic decline in plasma prolactin levels in either castrate or intact male rats. Similar results were found following the intravenous injection of 10 or 100 μg of the drug. These results contrasted sharply with the findings in ovariectomized females in which the intraventricular injection of the same two doses of proglumide used in males produced a dose-related elevation of prolactin which was opposite to the delayed lowering of prolactin following the intravenous injection of the same doses of the compound used in males. These results indicate that proglumide can lower prolactin in male rats and suggests a physiologically significant role of CCK in the control of prolactin secretion in the male. There appears to be a sex difference in the response since the results contrasted sharply in ovariectomized female rats. The results in the females are puzzling and it is apparent that further studies are needed to determine whether or not CCK has a physiologically significant role to play in prolactin secretion in the female. Since previous results have shown that CCK has no effect on the release of prolactin by the pituitary directly these interactions are presumably taking place in the hypothalamus.

Effects of thyroidectomy and thyroxine replacement on the responsiveness of the anterior pituitaries from male rats to thyrotropin-releasing hormone in vitro

Thyroidectomy decreased prolactin concentrations in the anterior pituitary (AP) and serum of the male rat. The amount of basal and thyrotropin-releasing hormone (TRH)-stimulated release of prolactin by AP in vitro was lower in thyroidectomized (Tx) rats than in sham Tx rats. These results suggest that the inhibitory effects of thyroidectomy on pituitary and serum prolactin in male rats are mediated in part by the reduction of the production and spontaneous release of prolactin and the responsiveness of prolactin to TRH.

Involvement of prostate in the regulation of serum levels of FSH, LH, and prolactin in male rats.

Circulatory levels of LH and FSH were measured in serum of male rats (28, 35, 42, 63, 70, 77, and 207 days of age) 7 days following sham operation, castration (C), prostatectomy (P), and castration + prostatectomy (C + P). In C + P rats that were 49, 63, 70, 77, and 207 days of age, the plasma FSH was significantly elevated as compared to the C group. Administration of aqueous prostatic extract restored the circulatory FSH level in C + P animals to that observed in C animals, whereas in C animals FSH levels were suppressed, indicating inhibinlike activity. In rats 49 and 77 days of age, circulatory LH levels were significantly suppressed in C + P animals as compared to the C group. Both castration and prostatectomy alone suppressed circulatory prolactin levels. Administration of prostatic extract to castrated animals restored the prolactin levels to that of the sham-operated control animals. Results of the present study suggest a role of the prostate in feedback regulation of FSH and prolactin.

Recent studies on the role of brain peptides in control of anterior pituitary hormone secretion

Recent work in our laboratory on the role of peptides to influence release of pituitary hormones by direct action on the gland and also some of the interactions of these peptides at the hypothalamic level to alter release of pituitary hormones will be reviewed. Considerable evidence from hypothalamic stimulation and lesion studies suggests the existence of a separate FSH-releasing factor (FSHRF). We have been able to purify a bioactive FSHRF which appears to be distinct from LHRH. Consequently, we believe that a distinct FSHRF will ultimately be isolated. With regard to prolactin, it is now clear that it is under dual control by both prolactin-inhibiting (PI) and prolactin-releasing factors (PRF). Although dopamine acts as a PIF, our recent fractionation studies indicate the existence of a peptidic PIF in hypothalamic extracts which can be separated from dopamine and GABA. The peptidic PIF is eluted from Sephadex in the same position originally described by us a number of years ago. Thus, inhibitory control is probably mediated by a combination of factors which would include dopamine, possibly GABA and a peptidic PIF. A number of peptides have been shown to have PRF activity which include TRF and also VIP. In recent studies, we have shown a prolactin-releasing action of oxytocin on male hemipituitaries or dispersed pituitary cells. Furthermore, high doses of oxytocin given intravenously released prolactin in male rats. There is a correlation between estrogen-induced prolactin release and an increase in plasma oxytocin and a correlation between suckling-induced oxytocin and prolactin release. These results suggest that oxytocin may be an important PRF. Control of growth hormone (GH) secretion is similarly under dual control via panhibin (somatostatin) and GRF. We have recently shown that motilin can stimulate release of GH from hemipituitaries or dispersed pituitary cells in vitro and that large doses are also effective in vivo. Furthermore, antisera raised against motilin were capable of lowering plasma GH. Motilin has been found in the median eminence and also in somatotrophs. Therefore, these results suggest that motilin may be a physiologically important GRF. In the meantime, a tumor (t) GRF has been synthesized by two laboratories and is extremely potent to release GH in vivo and in vitro. This peptide is much more potent than motilin and has an additive effect with motilin to increase GH release in vitro. We also have evidence for an important interplay amongst the various releasing and inhibiting factors at the hypothalamic level. For example, somatostatin injected into the ventricle will elevate GH instead of lowering it. This action is probably due to an ultrashort loop feedback to suppress somatostatin release and/or also stimulate GRF release. Similarly, peptides which stimulate prolactin release via direct action on the pituitary tend to inhibit it when given intraventricularly. Motilin, which stimulates GH release when given systemically, inhibits it when given intraventricularly and we have found similar results with synthetic GRF, low doses of which given intraventricularly suppress instead of stimulating GH release.

249. Dietary influences on plasma levels of testosterone, 5 α-dihydro-testosterone and prolactin in male rats

249. Dietary influences on plasma levels of testosterone, 5 α-dihydro-testosterone and prolactin in male rats