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PubMed1986

A possible role of arachidonate metabolism in the mechanism of prolactin release.

The cleavage of arachidonate from pituitary phospholipids may contribute to the process that regulates the release of prolactin. To test this hypothesis, primary cultures of anterior pituitary cells from female rats were preincubated with [3H]arachidonate to label their phospholipid-containing components. The cells were then washed and incubated with vehicle or test agents and the release into the medium of prolactin and [3H]arachidonate cleaved from the phospholipids was measured. Thyrotropin-releasing hormone (TRH) and neurotensin significantly increased the release of both [3H]arachidonate and prolactin. Although basal [3H]arachidonate release was not affected by dopamine or somatostatin, both of these agents reduced [3H]arachidonate release induced by TRH. The relationship between calcium mobilization and arachidonate release was investigated by exposing the cells to agents that modify calcium balance. Maitotoxin, a calcium channel activator, stimulated prolactin and arachidonate release. In contrast cobalt, a calcium channel blocker, penfluridol, a calcium-binding protein inhibitor, and low-calcium medium decreased basal and TRH-induced prolactin release and diminished the TRH-induced release of arachidonate. RHC 80267, an inhibitor of diacylglycerol lipase, decreased TRH-induced prolactin and arachidonate release. BW755c, an inhibitor of the conversion of arachidonate to its metabolites, decreased TRH-induced prolactin release but predictably increased arachidonate release. These findings support the hypothesis that arachidonate metabolites may be involved in the process regulating prolactin release.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1990

In vivo studies on paracrine actions of pituitary angiotensin II in stimulating prolactin release in rats.

The present experiments were performed to test the hypothesis that, in vivo, intrapituitary angiotensin II (ANG II) mediates the effect of luteinizing hormone-releasing hormone (LHRH) on prolactin release. After intravenous administration of LHRH (100 ng/100 microliters saline), plasma levels of both luteinizing hormone (LH) and prolactin were increased in ovariectomized rats pretreated with estradiol and progesterone. Intravenous administration of saralasin or sarthran (ANG II receptor blockers) reduced or abolished, respectively, the LHRH-induced increase in prolactin without affecting the rise in LH. In other ovariectomized steroid-treated rats, saralasin did not affect the increase in LH or prolactin induced by 10 min of restraint stress. Finally, in intact female rats on the day of proestrus, neither saralasin nor sarthran affected the mid-cycle prolactin surge. Taken together, these results show that in vivo exogenous LHRH stimulates prolactin release via a paracrine action of pituitary ANG II. However, under other conditions in which both LH and prolactin (and presumably endogenous LHRH) are elevated, pituitary ANG II does not appear to be involved in the prolactin rise.

Angiotensin II↗
PubMed1993

Mechanism of the prolactin rebound after dopamine withdrawal in rat pituitary cells.

To study the mechanism underlying the effect of dopamine withdrawal on prolactin release, continuous perfusion experiments were performed on rat lactotroph-enriched primary cultures. Removal of dopamine (10(-7) M) after a short-term application (15 min) produced a rebound of prolactin secretion, which was enhanced by pretreatment of the cell culture with 17 beta-estradiol (10(-8) M for 48 h). Ca2+ channel blockade by Co2+ (1 mM) abolished the rebound in prolactin release. An increase in intracellular adenosine 3',5'-cyclic monophosphate by either forskolin (5 microM) or 3-isobutyl-1-methylxanthine (100 microM) enhanced the prolactin rebound after dopamine withdrawal. Application of thyrotropin-releasing hormone (10(-7) M) increased the prolactin rebound after dopamine withdrawal with a maximum effect obtained by commencing treatment immediately after removal of dopamine. Pretreatment of cell cultures with pertussis toxin (100 ng/ml, for 10 h) totally abolished the effects of dopamine on prolactin secretion. The dopamine agonist bromocriptine (10(-9) M) significantly decreased prolactin secretion, but no rebound effect was observed after its removal. We conclude that the rebound of prolactin release after dopamine treatment involves the influx of Ca2+.

Animals↗
PubMed1992

Micropuncture study of avian kidney: effect of prolactin.

Renal function was studied in anesthetized European starlings (Sturnis vulgaris) by micropuncture and clearance techniques. A previous study had shown some changes in the renal function of birds in molt. Endogenous prolactin levels have been shown to be elevated at this time. In the present study, renal function was studied during the infusion of an isotonic sodium chloride solution and then when ovine prolactin was added to the infusion. Ovine prolactin resulted in an elevation of plasma urate concentration but had no significant effects on other plasma parameters or on the concentration of the various ions in tubular fluid samples. Urine flow rate was significantly higher during prolactin infusion, although whole animal glomerular filtration rate, single nephron glomerular filtration rate, and the percentage fluid reabsorption in the proximal tubule (up to the point of micropuncture) were unaltered. The whole animal fractional excretions of sodium and chloride were significantly higher, those of magnesium and potassium were significantly lower, and the fractional excretion of phosphate tended to be lower during prolactin infusion. At the level of the proximal tubules of the reptilian-type nephrons, prolactin infusion caused a slight reduction in the net reabsorption of sodium and chloride. Therefore the main effects of prolactin on renal function are occurring in the distal nephron of the reptilian-type nephrons or in the mammalian-type nephrons. It appears that prolactin may affect renal function in avian species and that these actions may be modulated by a range of factors as has been demonstrated in mammals.

Absorption↗
PubMed2006

Effects of raloxifene on circulating prolactin and estradiol levels in premenopausal women at high risk for developing breast cancer.

BACKGROUND: Prolactin is a peptide hormone necessary for normal breast development that may contribute to breast tumorigenesis. Estrogen is a significant positive regulator of prolactin synthesis; therefore, raloxifene, a selective estrogen receptor modulator under study as a breast cancer prevention agent, may modulate both estradiol and prolactin levels by inhibiting estradiol from binding to its receptor. METHODS: Premenopausal women at increased risk for invasive breast cancer participated in a pilot chemoprevention trial and were given 60 mg raloxifene daily for 24 months. Fasting serum samples collected at baseline and after 12 months on drug were used to measure circulating prolactin, estradiol, and sex hormone binding globulin (SHBG) levels. RESULTS: Of the 27 subjects who completed 12 months of raloxifene, 23 had paired prolactin samples, and 20 had paired estradiol and SHBG samples. Prolactin levels did not significantly change with raloxifene treatment, but SHBG levels increased (mean change = 7.3 nmol/L; P = 0.0001; 95% confidence interval, 3.9-10.7). Estradiol (mean change = 42 pg/mL; P = 0.048; 95% confidence interval, 1-84 pg/mL) levels were elevated when comparing 15 of the 20 women with paired estradiol measurements who also had both of these samples taken during the early follicular phase of the menstrual cycle. CONCLUSIONS: This report is the first to examine the long-term effects of raloxifene on prolactin, estradiol, and SHBG levels in premenopausal women who are also at increased risk for developing invasive breast cancer. Raloxifene had no significant effect on prolactin levels but did increase estradiol and SHBG measurements.

Adult↗
PubMed1980

Lack of evidence that the central serotoninergic system plays a role in the activation of prolactin secretion following inhibition of dopamine synthesis or blockade of dopamine receptors in the male rat.

Administration of alpha MT to inhibit catecholamine synthesis or dopamine (DA) receptor blockade with spiroperidol had no effect on the hypothalamic concentration of 5HT or 5HIAA. Fluoxetine to block serotonin uptake had no influence on the elevation of serum prolactin levels induced by alpha MT or DA receptor blockers and conversely alpha MT did not influence the prolactin-releasing action of 5HTP alone or in combination with fluoxetine. Depletion of brain serotonin stores with p-chlorophenylalanine did not affect the prolactin-releasing action of alpha MT or DA receptor blockers. In contrast, the serotonin blocker methysergide, but not cyproheptadine, inhibited the prolactin-releasing effect of alpha MT or alpha-flupentixol, a DA receptor blocker, but not of spiroperidol, another DA receptor blocker. The intensity of the inhibition induced by methysergide paralleled the intensity of inhibition induced by apomorphine. Methysergide conspicuously lowered serum prolactin in animals with electrolytic destruction of the median eminence, whereas cyproheptadine had only a slight effect. The prolactin-inhibiting effect of methysergide could be prevented by pretreatment of the lesioned rats with spiroperidol. It is concluded (1) that elimination of the influence of the DA system does not activate the central serotoninergic system; (2) that activity of the serotoninergic system has no role in the activation of prolactin secretion induced by suppression of the inhibitory dopaminergic influence, and (3) that the inhibiting action of methysergide on the prolactin-releasing effect of alpha MT or alpha-flupentixol is due to its dopamine receptor agonist activity rather than to blockade of serotonin receptors.

5-Hydroxytryptophan↗
PubMed1980

Effect of antiestrogens on pituitary prolactin production in normal and pituitary tumor-bearing rats.

Administration of the antiestrogen tamoxifen to normal Buffalo female rats caused a 45% reduction (p less than 0.01) in 3H-prolactin synthesis and release in vitro. Radioimmunoassayable prolactin in incubated glands and medium also decreased significantly. Similar results were observed in Wistar-Furth animals except for in vitro radioimmunoassayable prolactin, which decreased less markedly (by 33%, p less than 0.01). Serum prolactin concentration in treated rats was unchanged. Tamoxifen did not affect the extremely high serum prolactin concentration in rats bearing mammotropic tumors. It further reduced in vitro synthesis of radioactive prolactin but not of the radioimmunoassayable hormone. No interaction between antiestrogens and the dopamine agonist bromocriptine was observed. These observations suggest that the nonsteroidal antiestrogens decrease the synthesis of prolactin but have little effect on release of the hormone. Tamoxifen inhibits growth of transplantable mammotropic tumors MtTW15 and 7315a potently without altering tumor prolactin production. In vivo treatment of adult female rats with tamoxifen did not affect in vitro synthesis and release of radioactive growth hormone, but reversed the elevated growth hormone production of rats bearing 7315a tumors.

Animals↗
PubMed1982

Effect of alpha-melanocyte-stimulating hormone on basal and stimulated release of prolactin: evidence for dopaminergic mediation.

The effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on basal and stimulated of prolactin were studied. Intraventricular (i.v.t.) injection of 2 microgram of alpha-MSH in ovariectomized (OVX) rats produced a 50% depression of plasma prolactin levels within 10 min, whereas 100 ng of alpha-MSH or saline had no effect. 2 microgram of alpha-MSH (i.v.t.) produced a more dramatic and sustained depression of prolactin levels if initial prolactin concentrations were elevated. This dose of alpha-MSH was also effective in lowering plasma prolactin levels in OVX rats, primed 72 h earlier with 50 microgram of estradiol benzoate (s.c.), although this depression was of lower relative magnitude than in the unprimed OVX animals. The intravenous injection of a dopamine receptor blocker, spiroperidol (0.1 mg/kg), prior to (i.v.t.) alpha-MSH blocked the inhibitory effect of alpha-MSH on prolactin release. In vitro, alpha-MSH in doses ranging from 0.5 to 5 microgram did not alter prolactin release from hemipituitaries of male or OVX female rates and from dispersed pituitary cells from female rats. These results suggest that alpha-MSH can modulate prolactin release possibly via the hypothalamic dopaminergic system, and that this modulation may be of greater significance during stress.

Animals↗
PubMed1983

Histamine-induced prolactin release: pharmacological characterization of receptors in male rats.

Studies were undertaken to investigate the nature of receptors involved in the prolactin-releasing action of histamine in male rats. The increase of plasma prolactin levels induced by third-ventricle injection of histamine was blocked by intraventricular injection of ranitidine, an H2-antagonist, but not by systemic administration of mepyramine, an H1-antagonist. The H2-histamine agonists 4-methylhistamine and Dimaprit, given intraventricularly in unrestrained and ether-anesthetized rats, enhanced prolactin release. The effect of 4-methylhistamine was dose-dependent, whereas Dimaprit had opposite effects depending on the dose. In low doses, Dimaprit decreased whereas in higher doses it increased plasma prolactin levels. The stimulatory effects of both agonists, similar to those produced by histamine itself, were blocked by metiamide (H2-antagonist), but not by intraventricular mepyramine. High doses of mepyramine only partially decreased the effects of 4-methylhistamine. Ranitidine was able to prevent the prolactin response to 4-methylhistamine. The selective H1-histamine agonist 2,2-pyridylethylamine had no action on prolactin release. 2-Methylhistamine, which exhibits predominantly H1-mediated actions, increased the release of prolactin. Its effect, however, was blocked by low doses of metiamide and was obtained at higher concentrations than 4-methylhistamine. Mepyramine prevented 2-methylhistamine action only at high doses. It is concluded that the increased release of prolactin evoked by histamine in male rats is mainly due to its action on H2-receptors. In addition, the results altogether indicate that H1-receptors have not a significant participation.

Anesthesia↗
PubMed1983

Arachidonic acid metabolism and prolactin secretion in vitro: a possible role for the lipoxygenase products.

This study was designed to investigate basal and thyrotropin-releasing hormone (TRH)-stimulated prolactin release in the presence of agents that influence arachidonic acid metabolism. Agents that decrease its production by blocking phospholipase A2 activity, i.e., quinacrine and 4-bromophenacylbromide, significantly decreased prolactin secretion from anterior pituitary glands in vitro and from dispersed pituitary cells in a perifusion column. Phospholipase A2 and phorbol myristate acetate, substances that increase intracellular concentrations of arachidonic acid, markedly stimulated prolactin release by dispersed pituitary cells and by anterior pituitary glands incubated in vitro. The involvement in prolactin secretion of arachidonic acid metabolic products produced via the lipoxygenase pathway was investigated indirectly using nordihydroguaiaretic acid (NDGA), a specific inhibitor of this enzyme. NDGA progressively (dose-related) inhibited the release of prolactin in vitro and blocked the stimulating effect of 50 nM TRH on prolactin release from hemipituitary glands. Indomethacin, a specific inhibitor of the cycloxygenase pathway, had no significant effect on basal and TRH-stimulated prolactin release. The results suggest that arachidonic acid metabolism is involved in basal and TRH-stimulated prolactin secretion and that lipoxygenase pathway products are at least partially responsible for these effects.

Animals↗
PubMed1988

Axons containing a prolactin-like peptide project into the perivascular layer of the median eminence: an immunocytochemical light and electron microscope study in adult and infant rats.

A light and electron microscopic immunocytochemical study was undertaken to explore the fine structural organization of prolactin-immunoreactive axons in the rat median eminence. In adult intact males and females and in hypophysectomized females, light microscopic immunocytochemical labeling of the mediobasal hypothalamus revealed a marked concentration of prolactin-like immunoreactive fibers in the perivascular layer throughout the median eminence and the hypophysial stalk. At the electron microscopic level, immunostaining was associated with typical neurosecretory axons located either in the palisade layer where they displayed numerous contacts with tanycyte processes, or in the perivascular layer where they frequently contacted the perivascular space. Within the labeled axonal profiles, immunostaining was essentially located on secretory granules, 90-120 nm in diameter, whereas the microvesicles accumulated in some perivascular profiles constantly remained unlabeled. These data strongly suggest that most prolactin-immunoreactive axons of the median eminence release their content into the hypophysial portal vessels. In 1-day-old infant rats, intensely prolactin-like immunoreactive fibers were similarly localized in the most external layer of the median eminence, in which, contrary to adult animals, very slight if any tyrosine-hydroxylase-immunoreactive fibers were detected. Since earlier studies have provided evidence for a nondopaminergic prolactin-release-inhibiting factor in the hypothalamus of infant rats, and for an inhibitory effect of prolactin on pituitary mammotrophs, we propose that hypothalamic prolactin may contribute, as an additional prolactin-release-inhibiting factor, to the multifactorial control of pituitary mammotrophs.

Aging↗
PubMed1992

In vitro glucoregulation of prolactin secretion.

In this study we have examined the direct glucoregulation of prolactin secretion from normal anterior pituitary cells in vitro and have found that changes in medium glucose concentration regulate the amount of prolactin released. Nature and/or degree of this response to glucose was influenced by some effect, long-lived in vitro, which was correlatable to serum insulin levels. When the cells were derived from animals with mean low-normal serum insulin levels, there was a stimulation of prolactin secretion by hypoglycemia, the response was rapid, transient, dose-dependent, and could be duplicated by 2-deoxyglucose. When the cells were derived from animals with a higher mean serum insulin level, the prolactin secretion from the cells was slowly, adversely affected by hypoglycemia. Conversely, elevated glucose caused a depression in prolactin secretion in the first group and a stimulation of prolactin secretion in the second. We conclude (1) that modulation of glucose levels in vitro regulates prolactin release from pituitary mammotrophs and (2) that this glucose regulation of prolactin release is in turn coregulated with or regulated by insulin.

Animals↗
PubMed1995

Does melatonin act on dopaminergic pathways in the mediobasal hypothalamus to mediate effects of photoperiod on prolactin secretion in the ram?

Previous studies have shown that the chronic administration of melatonin in the mediobasal hypothalamus (MBH) using micro-implants in Soay rams housed under long days causes a sustained decrease in the secretion of prolactin as occurs in response to short days. The purpose of this study was to investigate whether hypothalamic dopaminergic (DA) systems acting through D2 receptors may be involved in this melatonin-induced effect. Groups of Soay rams living under long days were treated in the MBH with micro-implants containing bromocriptine (BROM, DA D2 receptor agonist), or sulpiride (SULP, DA D2 receptor antagonist), given alone or in combination with melatonin (MEL), to establish whether the DA drugs would mimic or negate the effects of melatonin. A control group (C) received empty micro-implants or no treatment. The micro-implants were bilateral and were left in place for 14 weeks; the trial continued for a total of 28 weeks (14-week implant period and 14-week post-implant period) while the animals remained under long days. The ability of the micro-implants to release BROM and SULP for 14 weeks was confirmed by incubating implants in vitro and testing for the presence of the compounds using a pituitary cell bioassay. MEL in the MBH induced a marked decrease in the blood plasma concentrations of prolactin during the implant period and an increase during the postimplant period (MEL vs. C, p < 0.001). BROM given alone induced a sustained decrease in the plasma concentrations of prolactin (less marked than MEL), while SULP caused an increase (BROM and SULP vs. C, p < 0.001); the effects were restricted to the implant period. BROM given in combination with MEL produced the same effect as MEL alone during both the implant and postimplant periods, while SULP given with MEL produced the same effect as MEL during the implant period, but impaired the increase in plasma concentrations of prolactin during the postimplant period (MEL + SULP vs. MEL, p < 0.001). There were changes in growth and moulting of the pelage correlated with the marked changes in the secretion of prolactin induced by MEL, but not related to the lesser effects of BROM and SULP. In conclusion, the long-term effects of the D2 agonist and antagonist are consistent with the inhibitory role of hypothalamic DA pathways in the homeostatic regulation of prolactin secretion. The inhibitory effect of the D2 agonist did not mimic that of MEL in the MBH, thus it is unlikely that the short day MEL signal operates primarily through a hypothalamic DA system to inhibit the secretion of prolactin. However, since the administration of the D2 antagonist in the MBH did influence the response to MEL, it is probable that DA pathways are involved in relaying the effects of MEL on the long-term cycle in the secretion of prolactin in the ram.

Analysis of Variance↗
PubMed1996

Different serotonin receptor types participate in 5-hydroxytryptophan-induced gonadotropins and prolactin release in the female infantile rat.

Serotonin (5-HT) receptors can be classified into at least three, possibly up to seven, classes of receptors. They comprise the 5-HT1, 5-HT2, and 5-HT3 classes, the "uncloned' 5-HT4 receptor and the recombinant receptors 5-ht5, 5-ht6 and 5-ht7. We investigated the role of different serotonin receptor types in a neuroendocrine response to the activation of the serotonergic system. Female immature rats were chosen as an experimental model as it has been shown that during the 3rd week of life, and not at later developmental stages, 5-hydroxytryptophan (5-HTP, a serotonin precursor) induces gonadotropin release in females and not in males. Besides, at this age, serotonin releases prolactin in both sexes. 5-HTP (50 mg/kg) released prolactin, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) as expected. Ketanserin (5-HT2A antagonist) and methysergide (5-HT2C antagonist) blocked 5-HTP-induced prolactin release, but did not block the LH or FSH responses. Ondansetron (5-HT3 receptor antagonist) did not modify prolactin response to 5-HTP, whereas it blocked 5-HTP-induced LH and FSH release. Propranolol (5-HT1 and beta-adrenergic antagonist) blocked prolactin, LH and FSH release induced by 5-HTP. The 5-HT2C agonist 1-(3-chlorophenyl)piperazine dihydrochloride released prolactin, without modifying LH or FSH release. Methyl-quipazine and phenylbiguanide (5-HT3 agonists) increased both LH and FSH levels, without altering prolactin secretion. The present experiments indicate that serotonin acting at the 5-HT3 receptor mediates LH and FSH release in infantile female rats, whereas 5-HT2C or 2A receptor types participate in the release of prolactin at this age. 5-HT1 receptor type may be involved in the release of the three hormones, though a beta-adrenergic component of the response cannot be discarded.

5-Hydroxytryptophan↗
PubMed1976

Prolactin and testicular lipids.

The effects of prolactin and prolactin plus progesterone (P-P) on the testes of adult rats were investigated. The weight of testes, seminal vesicles and the lipid composition of testes were studied 24 h after the administration of hormones. Prolactin treatment increased the weight of seminal vesicles but did not affect testicular weight, whereas P-P treatment had markedly reduced the weights of testes and seminal vesicles. Progesterone did not have any effect on the weight of testes and seminal vesicles. Both treatments had significantly reduced the total testicular lipids, which was more pronounced in the P-P treated group (28, 50%, respectively). The esterified cholesterol was increased by the administration of prolactin and P-P with a concurrent fall in the free cholesterol. The total cholesterol was depleted only by prolactin treatment. Testicular phospholipids, particularly the phosphatidylcholine and phosphatidylethanolamine were markedly depleted by these hormones. This action of prolactin is more significant in the presence of progesterone. The depletion of phospholipids appears to be mainly due to enhanced flow of testicular tubular fluid carrying away phospholipids from testis rather than a shift in the biosynthetic pathway favouring glyceride formation. In our previous study, it has been shown that progesterone favours accumulation of esterified cholesterol by depleting the available free cholesterol. Prolactin on the other hand depletes phospholipids and total cholesterol, increases esterified cholesterol. Thus, prolactin appears to have a role in steroidogensis as well as in the secretory processes of the testis.

Animals↗
PubMed1976

Antidiuretic action of prolactin in the rat with diabetes insipidus.

Rats with hereditary hypothalamic diabetes insipidus, devoid of endogenous ADH, exhibited a prompt antidiuresis when injected subcutaneously or intraarterially with ovine prolactin. The antidiuresis was accompanied by a decrease in free water clearance and an increase in urine osmolality without a change in osmolal clearance or creatinine excretion. Measurement of PAH and insulin clearances indicated that prolactin had no effect on renal plasma flow or glomerular filtration rate. Prolactin injection caused a transient decrease in urinary sodium excretion, but proximal tubular sodium reabsorption, estimated by lissamine green transit time, was unaffected. The antidiuretic effect of prolactin could not be attributed to ADH contamination of the ovine prolactin preparation. Kidney cyclic AMP content was increased significantly 5 min after injection of prolactin. Thus, prolactin has an antidiuretic effect similar to that which occurs as a result of ADH action on the kidney and does not require either the release or the presence of ADH in order to cause the antidiuresis. Further, the impaired water excretion cannot be attributed to an increase in proximal tubular sodium reabsorption or to alteration of renal hemodynamics. It is suggested that prolactin has a direct ADH-like action on the kidney resulting in antidiuresis.

Animals↗
PubMed1988

[Comparative studies of prolactin, estrogen, progesterone and androgen receptor levels in human breast cancers].

A receptor for lactogenic hormones (prolactin of several species and human growth hormone) was characterized in crude plasma membrane preparations of adult female rat liver. The binding of 125J-labeled prolactin to receptors was specific, saturable, reversible, and of high affinity (Kd = 0.23 x 10(-10)M). The maximum amount of prolactin specifically bound to liver of untreated female rats was 45 fmol/mg protein, whereas no specific prolactin binding was detected in plasma membrane preparations of adult male or immature rats. With this assay, a specific and reversible binding of ovine prolactin was detected in plasma membrane preparations of 25 human breast cancers, ranging from 2-29% of total activity. The estrogen-, progesterone- and androgen receptor content was determined in the breast cancer specimens using the dextran-coated charcoal method. Specimens with the highest specific prolactin binding showed the lowest steroid receptor concentrations, but no significant correlation between estrogen-, progesterone-, androgen-, and prolactin receptor content and other prognostic factors was observed in our series. We conclude, that steroid and prolactin receptors are expressed independently in human breast cancer.

Adult↗
PubMed1987

Effect of prolactin on galactose cataractogenesis.

Prolactin has been known to affect the water and electrolyte balance. Because increased lens hydration has been shown to be a common phenomenon in most, if not all types of cataracts, we have been interested in investigating a possible role of prolactin in sugar cataract induction and progression. For this study, we have used morphological and biochemical approaches. The prolactin delivery method involved intraperitoneal implantation of one or more pellets in Sprague-Dawley female rats. Following implantation of the desired number of prolactin or control (nonprolactin) pellets, animals were either fed galactose and lab chow, or lab chow diet. Gross morphological observations of whole lenses, slit-lamp examination of lenses and light microscopic analysis of lens sections showed that in the galactose-fed prolactin group, galactose associated alteration progressed faster and total opacification (mature cataract development) was achieved earlier than in the nonprolactin group. The levels of galactose and dulcitol were higher in the lenses of galactose-fed prolactin treated rats as compared to lenses from nonprolactin (control) rats. No significant difference in lens Na+-K+ ATPase activity between the prolactin and nonprolactin group was observed. Our results indicate that prolactin accelerates galactose-induced cataractogenesis in rats.

Animals↗