Differences In Prolactin Levels Research Articles

Effectiveness of prophylactic mastectomy in the prevention of breast tumors in C3H mice.

The effectiveness of prophylactic mastectomy in the prevention of breast tumors was studied in spontaneous breast-tumor-forming C3H mice. Prolactin levels were assayed to determine if this hormone was related to the incidence of mammary tumors. Two-hundred and fifty-six 1-month-old C3H mice were divided into four groups (control, 1; sham surgery, 2; mammectomy 50 percent, 3; and mammectomy 100 percent, 4). At the time of sacrifice (0 to 1 year postoperatively) estrus cycles were determined, ventral skin (breast) and ovaries were removed for histology, and serum was collected for prolactin assays. Prolactin levels 24 hours postoperatively were significantly elevated (p less than 0.01) in groups 2 to 4 when compared with group 1. Six months postoperatively, prolactin levels were significantly higher (p less than 0.05) in mice with tumors compared with those without tumors in groups 3 and 4. There were no differences in tumor incidence between the four groups. At 12 months postoperatively, no differences in prolactin levels were noted, but group 2 animals had the highest incidence of mammary tumors (89 percent; p less than 0.01) when compared to groups 3 and 4. Mammary tumor incidence was not decreased by 50 percent or 100 percent mammectomy in C3H mice. Prolactin levels rose in response to surgery and/or anesthesia and remained elevated only in tumor-bearing mice who underwent mammectomy, an occurrence similar to that reported in humans.

Prolactin in patients with major depressive disorder and in healthy subjects: III. Investigation of basal and Post-TRH prolactin during different forms of acute and chronic psychological stress

Prolactin (PRL) levels after thyrotropin-releasing hormone (TRH) (ΔPRL) were determined 4 times and basal prolactin levels 6 times in 10 healthy medical students before, during, and after a major examination in medicine. No significant differences in basal or ΔPRL levels occurred during the examination period. Basal PRL was also measured in 14 doctors of medicine after delivering a paper at a clinical conference and a further 9 doctors both before and after delivering a paper. PRL was measured serially at 20-min intervals in 4 doctors on the day on which they presented the paper. No significant differences in PRL levels were found in any of the tests conducted during this kind of stress as compared with the corresponding values obtained under nonstressful conditions. Increases in PRL before delivering the paper were seen in 3 subjects, but such increases also occurred completely independently of stress. An 18-hr fast did not influence PRL secretion in 11 healthy volunteers. Both the information obtained from a review of the literature on the influence of stress on PRL secretion and our own results strongly suggest that contrary to common opinion, there is no evidence at all that psychological stress affects PRL secretion in man.

Changes in serum prolactin after electroconvulsive and epileptic seizures.

Serial serum prolactin (PRL) concentrations were measured after epileptic seizures and seizures following electroconvulsive therapy (ECT). There was a large and rapid rise in PRL after ECT seizures but a much more variable PRL response after spontaneous seizures. Only epileptic seizures of longer duration and of grand mal character resulted in a more substantial rise in PRL. In ECT seizures there was a significant positive correlation between the duration of seizures and the rise in postictal PRL. The postictal PRL curves over 24 h were similar in both spontaneous seizures and ECT seizures. Interictally there were no difference in PRL levels between epileptic patients compared to patients with other neurological diseases or healthy volunteers. Chronic treatment with drugs affecting dopamine transmission had a profound effect on PRL secretion, and a dose-dependent significant increase in PRL with neuroleptics was observed.

Preovulatory secretion of progesterone, luteinizing hormone, and prolactin in 4-day and 5-day cycling rats.

Timing of ovulation and changes in plasma progesterone, luteinizing hormone (LH), and prolactin (PRL) during periovulatory stages were determined in Holtzman rats exhibiting regular 4- or 5-day cycles under a daily artificial illumination from 0500 to 1900 h. The 5-day cycling rats ovulated between 0130 and 0930 h on estrus, whereas some of the 4-day cycling animals ovulated as early as about 0130 h and others as late as 1130 h on estrus. Onset time of preovulatory LH and progesterone surges was about 1500 h on proestrus in both the 4- and the 5-day cycling rats. Peak levels of plasma LH and progesterone were measured at 1700 to 1900 h on proestrus, while the first rises and peak values of plasma PRL were evident a few hours earlier than those of plasma LH in the rats with two cycle lengths. Plasma LH levels at 1900 h on proestrus as well as plasma progesterone levels at 1600 and 2300 h on proestrus and at 0130 and 0330 h on estrus were significantly lower in the 5-day cycling rats than in the 4-day cycling animals (p less than 0.05). In contrast, PRL levels from 1500 through 2300 h on proestrus remained consistently higher in 5-day cycling rats than in 4-day cycling rats, and significant differences in PRL levels between these rats were apparent at 1500, 1600, and 2100 h (p less than 0.05-0.01). Thus, these results demonstrate that the 5-day cycling rats exhibit the attenuated magnitude of LH surge accompanied by the augmented preovulatory PRL release, and that plasma progesterone levels reflect the magnitude of LH surge. A tentative working hypothesis concerning the etiology of the 5-day cycle has been proposed.

Changes in LH and prolactin levels in diabetic male rats and the role of the opiate system in the control of their secretion

Diabetic male rat has low serum levels of luteinizing hormone (LH) and testosterone (T), which are accompanied by atrophy of the testes and accessory glands. The present study investigated changes in the serum levels of LH, prolactin (PRL) and glucose, following diabetes induction by streptozotocin. In addition, involvement of the opiate system in the control of LH and PRL secretion was evaluated. There was no difference in PRL levels between diabetic and control animals, except at 8 hours after streptozotocin injection. In contrast, the diabetic animals had consistently lower levels of LH, starting on the second day of diabetes. Blockade of the opiate system by naltrexone caused a sharp increase of LH levels in normoglycemic rats, while only a gradual decrease was observed in hyperglycemic animals. PRL secretion was inhibited by naltrexone, both in diabetic and control groups. It is concluded that, unlike normoglycemic rats, inhibition of LH secretion in diabetes is not under the control of the opiate system, probably as a result of T deficiency. In contrast, PRL secretion in diabetic rats, as in the control group, is under the influence of endogenous opiates.

Effects of Benztropine Mesylate on Haloperidol-Induced Prolactin Secretion and Serum Haloperidol Levels in Rats

The effects of benztropine mesylate on haloperidol-induced prolactin secretion and serum haloperidol levels were investigated in 240 rats. Animals were pretreated with benztropine mesylate or saline 20min prior to receiving haloperidol or saline. Serum prolactin and haloperidol levels were analyzed at six time periods over 150min. There was no significant difference in prolactin levels of control animals, i.e., saline pretreated/saline treated rats compared to benztropine mesylate pretreated/saline treated rats. Haloperidol caused a significant rise (p < 0.0001) in serum prolactin compared with controls. The prolactin concentration for the 30–150-min sampling period was significantly higher when the rats received benztropine mesylate prior to haloperidol (p < 0.05). There was a significant correlation (r = 0.57, p < 0.001) between serum haloperidol levels and serum prolactin levels in haloperidol-treated animals pretreated with either saline or benztropine mesylate. Additionally, serum haloperidol levels were not significantly different in animals pretreated with benztropine mesylate compared with those pretreated with saline. Thus, the enhancement of prolactin levels by benztropine mesylate was independent of any effect of haloperidol metabolism. This study appears to indicate that in the rat, cholinergic mechanisms exert a weak inhibitory effect on prolactin secretion under conditions of dopamine blockade.

Evidence for an inhibitory influence of rat placental lactogen on prolactin release in vitro.

Incubation of placental tissue from Day 11 pregnant rats for increasing periods of time resulted in proportionately more rat placental lactogen (rPL) release. The amount of placental tissue incubated correlated directly with the amount of rPL released into the medium. When placentas were coincubated with anterior pituitaries from ovariectomized rats, prolactin release was significantly inhibited. When media from incubations which had contained varying numbers of Day 11 placentas for 24 h were added to vials containing anterior pituitaries, prolactin release was inhibited, proportionate to the amount of rPL in the media. Media from incubations of Day 9 placentas, which contained very little rPL, had no effect on prolactin release. When medium containing anterior pituitary tissue was incubated for 24 h, pituitaries removed, and the medium incubated with placental tissue for an additional 24 h, there was no difference in prolactin levels compared to incubation medium not containing placental tissue. Addition of a trypsin inhibitor to the medium containing placental tissue did not augment the amount of prolactin remaining after a 24-h incubation. Thus it would appear that the placenta does not release a substance into the medium that destroys prolactin. This suggests that secretions from the placenta, presumably rPL, can exert a negative feedback on prolactin secretion at the level of the anterior pituitary.

Plasma prolactin levels and breast cancer: relation to parity, weight and height, and age at first birth.

Plasma prolactin has been measured in over 3,500 women volunteers from a normal population. In premenopausal women there was a significant decrease in prolactin levels with increasing parity. However, this effect was transitory since plasma prolactin concentration rose with increasing time after the birth of the last child. There were no significant differences in prolactin levels with respect to height and weight, although overweight compared to underweight women had approximately 15% more plasma prolactin. If prolactin is a carcinogen, then these results are in keeping with the epidemiological findings that multiparity affords protection and that age at last delivery is a risk factor in the development of breast cancer.

Effects of season, lactation and plane of nutrition on prolactin concentrations in ovine plasma and the role of prolactin in the control of ewe fertility.

Plasma prolactin concentrations during the first 2 months after lambing, at oestrus, and during early pregnancy were investigated in 2 experiments in which Finn x Dorset Horn ewes were mated at an induced oestrus approximately 9 weeks after lambing. Mean prolactin concentrations between lambing and mating were dependent on seasons, being greater than 260 ng/ml plasma in lactating ewes mated in July and less than 150 ng/ml in those mated in October. Within 8 days of weaning of the lambs at 50 days post partum values declined to 122 and 30 ng/ml respectively. Plane of nutrition had little effect on prolactin levels. Higher prolactin values were recorded during oestrus in ewes mated in March or July, the normal period of anoestrus, than in December, the normal breeding season, mean values being approximately 200 ng/ml and 35 ng/ml respectively. The mean increases in the concentrations of prolactin during oestrus were smaller in lactating than non-lactating ewes. It is suggested that these differences in prolactin levels may be responsible for the effects of season and lactation on ewe fertility.

Prolactin release in parent ring doves after brief exposure to their young.

A pigeon crop sac radioreceptor assay was used to measure changes in pituitary prolactin levels in parent ring doves of both sexes on the third day after hatching of their young. After a deprivation of 17 h from the squabs, exposure to a 3-day-old squab for 1 h resulted in a significant decrease in the prolactin content of the pituitary gland as compared with levels obtained in control birds deprived of their young for 18 h. No significant sex differences in prolactin levels were observed in either group. Because exposure to the young also promotes prolactin-induced crop sac growth, it appears probable that the squab-induced decrease in prolactin content of the pituitary gland reflects the release of prolactin into the circulation. Accordingly, the environmental regulation of prolactin secretion in parent ring doves appears similar to that observed in lactating mammals.

Plasma levels of fractionated estrogens and pituitary hormones in endometrial carcinoma

Plasma levels of estrone (E1), estradiol-17β (E2), and estriol (E3), as well as follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin were measured in 30 control subjects and in 20 postmenopausal patients with adenocarcinoma of the endometrium. Within the sensitivity of the assay (5 to 10 pg.), no E3 was found. Mean levels of E1 and E2 in the patients with carcinoma (42.64 ± 3.8 (S.E.M.) and 17.3 ± 1.7 (S.E.M.) pg. per milliliter) were significantly higher than those measured in the control subjects (E1 = 26.97 ± 2.4 (S.E.M.) pg. per milliliter, p < 0.001; E2 = 12.08 ± 1.2 (S.E.M.) pg. per milliliter, p < 0.02). Effects of age, diabetic status, and obesity were taken into consideration. Significant differences in FSH and marginally significant differences in prolactin levels were observed between the two groups. Mean levels of FSH, LH, and prolactin in the control group and the group with adenocarcinoma, respectively, were as follows: FSH = 152.3 ± 7.0 (S.E.M.) versus 98.1 ± 8.9 (S.E.M.) ml.U. per milliliter, p < 0.001; LH = 64.7 ± 3.1 (S.E.M.) versus 66.5 ± 5.2 ml.U. per milliliter, difference not significant; and prolactin = 14.3 ± 0.9 (S.E.M.) versus 17.8 ± 1.7 (S.E.M.) ng. per milliliter, p < 0.06. These results, as well as previously reported alterations in human growth hormone secretion, suggest aberrations in hypothalamic function in endometrial carcinoma.

Basal and Stimulated Prolactin Levels in Childhood

Basal serum prolactin concentrations have been measured in 50 normal prepubertal children. There was no significant difference in prolactin levels between males and females and all concentrations were within the normal range for adult females (3-15 mug/l). Prolactin concentrations before and during insulin hypoglycaemia and intravenous thyrotrophin releasing hormone (TRH) have been measured in normal children of short stature, in children with isolated growth hormone (GH) deficiency and in those with hypothalamo-pituitary disease. There was no difference in either basal or stimulated prolactin levels in the normal group compared with the isolated GH-deficient group. In most of the children with hypothalamo-pituitary disease basal prolactin concentrations were within the normal range but there was an impaired response to both hypoglycaemia and TRH. Basal and stimulated levels of prolactin are compared in the same subjects with those of GH, thyroid stimulating hormone and the gonadotrophins and the clinical value of the dynamic tests described is discussed.

Prolactin in hypertensive pregnancy.

Plasma prolactin levels were measured in 68 pregnant women with hypertension at 32 weeks gestation. They were raised in pregnancies with pre-eclamptic features, most significantly in women with a rising plasma urate level. No correlation was found between the level of the untreated blood pressure and prolactin. Proteinuria did not influence prolactin levels independently of changes in the plasma urate. The differences in prolactin levels could not be ascribed to the drugs administered.