UPTAKE OF 125I-LABELLED HUMAN PLACENTAL LACTOGEN AND HUMAN PLACENTAL LACTOGEN BY THE TISSUES OF NORMAL AND LACTATING RATS

1975 ◽  
Vol 65 (2) ◽  
pp. 183-NP ◽  
Author(s):  
S. REDDY ◽  
W. B. WATKINS

SUMMARY The rate of clearance from the circulation and uptake into tissues of radioactive label was studied after i.v. injection of 125I-labelled human placental lactogen (HPL) into rats at various stages of pregnancy. The half-life was obtained for the disappearance of the trichloroacetic acid-precipitable material from the plasma. The half-life, t½(S), calculated over the first 5 min after injection of the hormone was 5·4 ± 1·1 (s.d.) min, while a half-life, t½(L), of 27·9 ± 2·3 min was obtained from the decay period of 15–35 min. In the non-pregnant and pregnant rat the highest ratio of the radioactivity in an organ to that in the blood was 12–14:1 in the kidney. That the kidney is mainly involved in the uptake of exogenous HPL is further confirmed by the application of the histochemical immunoperoxidase technique. Human placental lactogen was localized in the cells of the proximal tubules of the cortex and to a lesser extent in the tubular lumen and the tubules of the medulla region. Uptake of HPL in vivo also occurs in the mammary gland tissue of the post-partum rat and reaches a maximum uptake between 15 and 30 min after injection of the hormone. Furthermore, specific uptake of HPL was observed on the alveolar cell membranes after the incubation of paraffin-embedded sections of formalin-fixed mammary gland and subsequent treatment by the peroxidase-labelled antibody method. These findings support the work of others who have demonstrated the presence of specific membrane receptors in the mammary gland for hormones with prolactin-like activity.

1991 ◽  
Vol 58 (4) ◽  
pp. 401-409 ◽  
Author(s):  
Thomas J. Hayden ◽  
Denise Brennan ◽  
Katherine Quirke ◽  
Paddie Murphy

SummaryXanthine oxidase/dehydrogenase (XO/XDH) increases at mid gestation in mammary gland but not in liver of the mouse and remains elevated until the pups are weaned at 20 d post partum. The increase in enzyme activity is due neither to alteration in activators or inhibitors nor to a production of a variant enzyme with altered catalytic properties. The increase is preceded in vivo by a surge of prolactin-like activity (placental lactogen) in plasma, and prolactin is required for induction of XO/XDH in explant culture in vitro. Induction of XO/XDH in vivo and in vitro precedes the full histological differentiation of the gland. In addition, induction of XO/XDH in vitro occurs more rapidly and at lower concentrations of prolactin than does histological differentiation. Thus although XO/XDH is present in milk, increased XO/XDH activity is an early event in mammogenesis in vivo and in vitro rather than a terminal component of differentiation.


1966 ◽  
Vol 34 (4) ◽  
pp. 491-496 ◽  
Author(s):  
D. Y. WANG ◽  
STRETTON YOUNG ◽  
R. D. BULBROOK

SUMMARY (1) The incorporation of [1,2-3H]testosterone in vivo into various tissues of virgin, pregnant, post-partum and tumour-bearing female rats was studied. (2) In virgin female rats the clearance of radioactivity from mesenteric fat, mammary gland, uterus, spleen, lung and blood was similar. This similarity in the rates of clearance of radioactivity for all the tissues examined was also found for the tissues of pregnant, post-partum, and tumour-bearing rats. (3) After the administration of [1,2-3H]testosterone different amounts of radioactivity were found in each of the tissues examined. In virgin rats the levels of incorporation were fat > uterus ≥ mammary gland > lung > blood ≥ spleen. This pattern was also obtained in post-partum and tumour-bearing animals; the tumours in the latter behaved in a similar way to normal mammary glands. In the pregnant rat, the foetus incorporated the least amount of radioactivity.


1988 ◽  
Vol 24 (6) ◽  
pp. 663-667 ◽  
Author(s):  
James W Collins ◽  
Sandra L Finley ◽  
Daniel Merrick ◽  
Edward S Ogata

1972 ◽  
Vol 55 (2) ◽  
pp. 323-NP ◽  
Author(s):  
MARGARET BIRKINSHAW ◽  
I. R. FALCONER

SUMMARY Study of the removal of 125I-labelled prolactin from the blood of virgin oestrous, pseudopregnant, lactating, weaned and post-partum oestrous rabbits gave a mean half-life of 16·0 ± 1·54 min. No conclusions could be drawn from the results on the influence of physiological condition on half-life. Tissue distribution of 125I-labelled prolactin 60 min after i.v. injection showed that the highest uptake ratio of tissue: plasma was in the kidney, which was confirmed with a concentration of 125I in the urine 6·43 times higher than in the plasma. However, approximately 90% of the 125I in the urine was in the form of labelled products of prolactin degradation. The uptake ratio of mammary tissue: plasma was 2·40 ± 0·09:1 during lactation but was only 0·41 ± 0·04:1 in oestrous rabbits. Of other tissues liver showed the highest ratio of 0·85 ± 0·03:1. The half-life of both 125I- and 131I-labelled prolactin was investigated in vivo in mammary tissue, after i.v. or intraductal injection. No significant differences were seen between methods of administration or differences of isotope, and the average half-life was 52·4 ± 5·9 h. Autoradiographic studies of the tissue localization of 125I- and 131I-labelled prolactin were carried out, the hormone being administered by i.v. or intraductal injection to 15-day pseudopregnant rabbits, or by incubation with 0·5 mm slices of lactating mammary tissue from rabbits. Samples of tissue were obtained from 10 min to 50 h after administration of labelled hormone. Irrespective of method of administration, isotope or time interval, a selective localization of radioactivity was observed on or near to the alveolar secretory cell membrane, on the side adjacent to the vascular supply. It was concluded that specific sites for labelled prolactin occur in this location, since the opposite side of the alveolar cell membrane adjacent to the duct lumen did not show radioactivity localized on or near it, even when the hormone was administered into the teat ducts.


1978 ◽  
Vol 26 (4) ◽  
pp. 288-292 ◽  
Author(s):  
W B Watkins

The recent claim by Gau and Chard (Br J Obstet Gynaecol 83:876, 1976) that, on theoretical grounds, it may be impossible to demonstrate the presence of human placental lactogen in placental tissue using the immunoperoxidase technique, has been reinvestigated. Placental tissue fragments fixed in Carnoy's fluid retained their morphologic identity compared with tissue fixed in formalin. Using these nonformalin fixed tissues, human placental lactogen was successfully localized within the cytoplasm of the syncytial layer of the placental villus. It is concluded that placental villi at term do in fact contain sufficient human placental lactogen to be demonstrated using the immunoperoxidase technique in contrast to the observation of Gau and Chard.


1974 ◽  
Vol 76 (2) ◽  
pp. 369-376 ◽  
Author(s):  
P. Gæde ◽  
B. Nørgaard-Pedersen

ABSTRACT By a simple rocket immunoelectrophoretic method the 90 % normal range of serum human placental lactogen hormone (HPL) in the second half of pregnancy was determined in 436 normal pregnant women. The mean half life of HPL after delivery of normal infants determined in 5 patients was found to be 14.6 min (range 13.2–16.4 min). A close correlation was found between serum HPL and serum progesterone (r = 0.75). No circadian rhythm was found.


1993 ◽  
Vol 128 (1) ◽  
pp. 65-68 ◽  
Author(s):  
Mimi H Chiang ◽  
Kevin M Kelley ◽  
Charles S Nicoll

We have recently reported that human placental lactogen inhibits the growth of young female rats without changing the serum levels of insulin like growth factor-I. Accordingly, experiments were conducted to determine whether human placental lactogen could directly inhibit cartilage growth processes in vivo and in vitro. Osmotic minipumps with attached polyethylene catheters were used to infuse the hormone for seven days into the left hindlimb of three-month-old female rats via the common iliac artery. The right hindlimb of each animal served as an internal control. Infusion of the placental lactogen at 10 μg/rat/day caused a slight (10%) but significant decrease in the width of the tibial epiphysial cartilage plate and a higher dose (100 μg/rat/day) caused a greater degree of inhibition (25%). However, the higher dose also inhibited the tibial cartilage plate of the contralateral (non-infused) limb. The possibility that human placental lactogen could directly inhibit cartilage anabolic activity in vitro was evaluated by measuring the incorporation of 35SO4 into costal cartilage explants from three to four-month-old female rats. The placental hormone inhibited the incorporation of 35SO4 in a dose-related manner at concentrations ranging from 1.0 to 100 μg/l. As a test of the specificity of this inhibition the effect of the hormone on the incorporation of 35SO4 into cartilage explants from Coho salmon was determined. The placental lactogen did not affect incorporation of the sulfate into the fish cartilage over a range of doses from 1.0 to 1000 μg/l. These results indicate that at least some of the inhibitory effects of human placental lactogen on the growth of rats is direct on peripheral tissues, such as cartilage. This effect may be mediated by the well-established anti-insulin action of the placental hormone.


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