scholarly journals Participation of intraluteal progesterone and prostaglandin F2 alpha in LH-induced luteolysis in pregnant rat

1998 ◽  
Vol 156 (2) ◽  
pp. 253-259 ◽  
Author(s):  
CO Stocco ◽  
RP Deis

We examined the participation of the intraluteal levels of progesterone (P4) and prostaglandin F2 alpha (PGF2 alpha) in the induction of luteolysis by LH and its relationship with the induction of the 20 alpha-hydroxysteroid dehydrogenase activity (20 alpha-HSD). Subcutaneous administration of four doses of 10 microgram ovine LH (oLH) at 0800, 0900, 1000 and 1100 h on day 19 of pregnancy induced a decrease in the activity of the enzyme 3 beta-HSD 24 and 48 h after treatment and an increase in luteal 20 alpha-HSD activity 48 h after oLH treatment when compared with control rats. Intraluteal and serum P4 levels were lower than control values 24 and 48 h after oLH treatment, with a significant increase in luteal PGF2 alpha content and a decrease in corpus luteum (CL) weight 48 h after oLH treatment. Intrabursal ovarian (i.b.) treatment with an inhibitor of PG's biosynthesis (diclofenac) (70 microgram/ovary) or P4 (3 microgram/ovary) on day 20 of pregnancy, prevented the increase in 20 alpha-HSD activity observed 48 h after oLH treatment, without any effect on 3 beta-HSD activity. The i.b. administration of P4 prevented the increase in intraluteal PGF2 alpha content induced by oLH treatment and the increases in 20 alpha-HSD activity and intraluteal PGF2 alpha content observed in control animals on day 21 of pregnancy. The inhibition of PG biosynthesis also prevents the decrease in intraluteal and serum P4 level induced by oLH. These results provide good evidence of the important participation of intraluteal P4 and PGF2 alpha on the oLH-induced luteolysis in pregnant rats. We also found the P4 produced by the CL is involved, in part, in the regulation of luteal PG synthesis. Thus, the early decline in 3 beta-HSD activity and the consequent fall in intraluteal P4 content, may trigger the synthesis of PGs and thereafter the increase in luteal 20 alpha-HSD activity to establish luteolysis.

1983 ◽  
Vol 210 (3) ◽  
pp. 761-767 ◽  
Author(s):  
G E Bunce ◽  
G R Wilson ◽  
C F Mills ◽  
A Klopper

1. Pregnant rats were fed either low (less than 1 p.p.m.) Zn or control (40 p.p.m. Zn) diets from day 10 of gestation. They were killed at intervals during the last 96 h preceding the normal time for onset of parturition, and differences in plasma progesterone, oestradiol-17 beta and ovarian 20 alpha-hydroxysteroid dehydrogenase were assessed. 2. Gestation was prolonged in Zn-deficient rats. 3. Although the preparturient decline in plasma progesterone began at the same time in all groups, at term, plasma progesterone concentration in Zn-deficient rats remained significantly higher than in normal females. 4. Induction of ovarian 20 alpha-hydroxysteroid dehydrogenase activity was delayed by about 8 h by Zn deficiency. This delay was not observed if prostaglandin F2 alpha was injected previously. 5. The results suggest a Zn-dependent step(s) in uterine synthesis and/or release of prostanoids.


1996 ◽  
Vol 150 (3) ◽  
pp. 423-429 ◽  
Author(s):  
C O Stocco ◽  
R P Deis

Abstract The mechanisms associated with the onset of luteolysis in the pregnant rat are not well known. The effect of a specific rat LH antiserum (AS-rLH) and of ovine LH (oLH) on luteal steroidogenesis on day 19 of pregnancy was examined. Rat LH antiserum administered intrabursally at 1000–1100 h on day 19 of pregnancy prevented the physiological decrease in 3β-hydroxysteroid dehydrogenase (3β-HSD) activity, the increase in 20α-hydroxysteroid dehydrogenase (20α-HSD) activity and the fall in serum progesterone (P4) level observed at 1800 h on day 21 of pregnancy. To see if oLH has a direct effect on luteal steroidogenesis, the gonadotrophin was injected into the periovarian bursa. The intrabursa treatment with 1 μg oLH on day 19 of pregnancy at 0800–0900 h did not modify corpus luteal function 36 h after treatment, but treatment with 4 μg oLH per ovary induced a significant progressive decrease in luteal 3β-HSD activity starting 12 h after treatment, while a significant increase in 20α-HSD activity, concomitant with a decrease in serum P4 level, occurred 48 h after treatment. Luteal P4 content decreased with respect to control groups 36 and 48 h after intrabursal treatment with 4 μg oLH. The intrabursal administration of 8 μg oLH induced an increase in 20α-HSD activity and a decrease in 3β-HSD activity 36 h after treatment. Administration of 4 μg oLH per ovary on day 8 of pregnancy induced a significant increase in serum P4 levels without modifying 3β-HSD activity. In rats treated with oLH on day 19 of pregnancy the decrease in 3β-HSD activity occurred 36 h before the significant increase in 20α-HSD activity and serum P4 level. In conclusion, the luteal enzymatic activity changes and the significant decrease in the intraluteal P4 concentration induced by the intrabursal administration of oLH and the clear effect of AS-rLH preventing the physiological luteal changes preceding parturition provide good evidence of an intraovarian action of LH during the normal progression of luteolysis in late pregnant rats. Journal of Endocrinology (1996) 150, 423–429


1984 ◽  
Vol 101 (3) ◽  
pp. 285-288
Author(s):  
F. Miyauchi ◽  
H. Kato ◽  
H. Yamashita ◽  
K. Ueda ◽  
H. Tamura ◽  
...  

ABSTRACT The effects of a conceptus-derived substance on the activity of 3β-hydroxysteroid dehydrogenase (3β-HSD) and 20α-HSD in the ovary were studied in the rat. On day 7 of pregnancy (day 1 = insemination), rats were laparotomized and the desired number of conceptuses was aspirated from the uterus; thus, rats carrying one, two, three, four, five to seven or eight to ten conceptuses were prepared. They were autopsied on day 15 and 3β-HSD and 20α-HSD activity in the corpus luteum (CL) or non-luteal ovarian tissue (NLO) was determined. Conceptus number was directly related to 3β-HSD and inversely related to 20α-HSD activity in the CL. The serum progesterone level and CL weight were also directly related to conceptus number. Neither 3β-HSD nor 20α-HSD activity in the NLO was affected by conceptus number. These results indicated that 3β-HSD and 20α-HSD in the CL are probably regulated by placental hormone secreted in proportion to the number of conceptuses; in the NLO these enzymes may be controlled by a different mechanism. J. Endocr. (1984) 101, 285–288


1964 ◽  
Vol 12 (9) ◽  
pp. 670-673 ◽  
Author(s):  
KÁROLY BALOGH

20α-Hydroxysteroid dehydrogenase activity was localized histochemically in the corpus luteum of the rat by using Nitro-BT as an indicator. Intensive enzyme activity was obseryed in the corpus luteum cells, especially during involution. The placenta and corpora lutea of pregnancy failed to reveal enzyme activity during the last week of gravidity. Other tissues, including endocrine glands, liver and kidneys were also negative. The Present method offers a possibility to identify the sites of progesterone metabolism in the rat ovary at the microscopic level.


1981 ◽  
Vol 98 (1) ◽  
pp. 133-136 ◽  
Author(s):  
K. Loewit ◽  
R. Kofler ◽  
M. Tabarelli ◽  
S. Schwarz

Abstract. Pregnant Sprague Dawley rats were passively immunized with antiserum to bovine luteinizing hormone (anti-LH) on day 10 of pregnancy, and treated with 1 mg/day or 1.5 mg/day of the prolactin (Prl) inhibitor bromocryptine (BEC) between days 10 to 12 or 9 to 12, respectively. On day 12 a laparotomy was performed to assess the state of pregnancy and to remove the ovaries for histochemical detection of 20α-hydroxysteroiddehydrogenase (20α-OHSD) in the corpora lutea of pregnancy. In a second experiment pregnant rats were treated with 1.5mg BEC/day from days 17 to 22, checked for foetal state and ovariectomized on day 22 before giving birth. Treatment with BEC in effective doses did not interfere with anti-LH-induced termination of pregnancy and consequent reappearance of 20α-OHSD activity on day 12, or with spontanenous recurrence of enzyme activity at the end of gestation. It is concluded that Prl has no direct and immediate role in 20α-OHSD regulation, at least on day 12, although substitution by endogenous rat placental lactogen at the end of pregnancy cannot be excluded.


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