Comparative effects of some steroidal and nonsteroidal antifertility agents in rats and hamsters

Giannina, T.; Butler, M. C.; Popick, F.; Steinetz, Bernard G.

doi:10.1016/0010-7824(71)90073-4

Cited by 27 publications

(12 citation statements)

References 15 publications

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“…The hamster uterus is very sensitive to P 4 , and treatment of 500 g of P 4 daily is reported to be sufficient to maintain pregnancy in ovariectomized pregnant hamsters (33). In contrast, sensitivity of the hamster uterus to E 2 is poor (40), and single injection of 1 g of E 2 is required to induce genes in the ovariectomized hamster uterus (37).…”

Section: Analysis Of Blastocyst Implantation After Treatment Of Ptgs mentioning

confidence: 99%

Prostaglandin E2 Is a Product of Induced Prostaglandin-endoperoxide Synthase 2 and Microsomal-type Prostaglandin E Synthase at the Implantation Site of the Hamster

Wang¹,

Su²,

Deb³

et al. 2004

Journal of Biological Chemistry

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Certain uterine prostaglandins (PGs) are elevated at implantation sites and are needed to trigger the events of blastocyst implantation that include blastocyst-uterine attachment and stromal decidualization with vascular permeability changes. Several decades of investigations showed that treatment with PG synthesis inhibitors, prior to or during the time of implantation, resulted in either complete inhibition or a delay in implantation or reduction in the number of implantation sites with diminished decidual tissue. Consistent with these findings, we observed that whereas a selective PG endoperoxide synthase (Ptgs) 1 inhibitor SC-560 failed to inhibit implantation, a selective Ptgs2 inhibitor SC-236 showed significantly reduced number and size of implantation sites in progesterone-treated ovariectomized pregnant hamsters. It is known that Ptgs2 expression and Ptgs2-derived prostacyclin (PGI 2 ) synthesis at implantation sites are needed for implantation in the mouse (a rodent that needs ovarian estrogen for implantation). However, it is unknown which Ptgs and PG synthases produce which PGs at implantation sites of the hamster (a rodent that does not need ovarian estrogen for implantation). Here we demonstrate that as blastocyst implantation proceeds, a reduction in Ptgs1 expression from uterine luminal epithelial cells and a gradual induction in Ptgs2 expression exclusively in luminal epithelial and adjacent decidual cells occurred at implantation sites of hamsters. Results also reveal that PGE 2 , but not PGI 2 , is the major PG at implantation sites where Ptgs2 and microsomal type PGE synthases but not PGI synthases are co-expressed. This elevated uterine PGE 2 at implantation sites may serve to initiate or amplify physiological signals required for specific aspects of the implantation process in hamsters.

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Section: Analysis Of Blastocyst Implantation After Treatment Of Ptgs mentioning

confidence: 99%

Prostaglandin E2 Is a Product of Induced Prostaglandin-endoperoxide Synthase 2 and Microsomal-type Prostaglandin E Synthase at the Implantation Site of the Hamster

Wang¹,

Su²,

Deb³

et al. 2004

Journal of Biological Chemistry

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“…The choice of the higher dose level of estrogen, was carefully considered. The hamster is indeed, refractive uterotrophically to low exogenous doses of estrogen [5] and since the uteri of these animals were being examined for various morphological and histochemical changes it was considered necessary to use a higher dosage than used in rat studies. Our results also indicate that progesterone at our dose levels are much more stimulatory than reported by others [17].…”

Section: Discussionmentioning

confidence: 99%

The effect of an intrauterine device on mast cell numbers and distribution in the hamster uterus

1979

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The effect of an IUD on mast cell numbers and distribution in the uterus was studied in castrated, castrated hormone-treated and cycling hamsters. The device had a stimulatory effect on total mast cell numbers in those animals that received no treatment, peanut oil, or estrogen therapy and in all cycling animals. The device also apparently causes mast cells to be redistributed in the different areas of the uterus. The results indicate that the IUD alters the uterine mast cell response to exogenous hormones and cycle times.

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“…A comparison of these data indicates that some in-vivo factor (s) and/or mechanism(s) reduce the uptake of oestradiol by the hamster uteri. Giannina et al (1971) have shown that seventeen and twenty times more oes¬ tradiol is required by the hamster to give uterotrophic and contraceptive activities equivalent to those observed for the rat. Thus, it appears that the differences between the hamster's and the rat's requirements in vivo for oestra¬ diol are not solely confined to the uterus and its ability to take up oestradiol as shown by the in-vitro data.…”

mentioning

confidence: 88%

“…The target tissues in the hamster are less sensitive to oestrogens and respond less to anti-oestrogens than those in the rat (Giannina, Butler, Popick & Steinetz, 1971). These investigators suggest that differences in metabolism or oestrogen affinity may explain their observations.…”

mentioning

confidence: 97%

“…Giannina et al (1971) reported that the effects of oestradiol can be completely antagonized by These data strongly indicate that the differences in the effects of oestrogens and anti-oestrogens in vivo on the uterotrophic, anti-uterotrophic and contra¬ ceptive activities between rats and hamsters may be due either to one or to a combination of the following: (a) non-target tissue metabolism, (b) action on target tissues other than the uterus, (c) uterine oestrogen receptor affinities and/or concentration, and possibly (d) assay sensitivities.…”

mentioning

confidence: 99%

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Uptake of Oestradiol by Rat and Hamster Uteri in Vitro: Effects of Ethynyl Oestradiol and an Anti-Oestrogen

Perry¹,

Ferguson²

1974

Reproduction

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Oestrogenic and anti-oestrogenic compounds that are effective antifertility agents for rats do not necessarily behave in a similar way for hamsters. The target tissues in the hamster are less sensitive to oestrogens and respond less to anti-oestrogens than those in the rat (Giannina, Butler, Popick & Steinetz, 1971). These investigators suggest that differences in metabolism or oestrogen affinity may explain their observations. Experiments in vivo show that hamster uteri retain significantly less tritiated oestradiol than is retained by rat uteri under identical experimental conditions (Ciaccio & Lisk, 1972). Prasad, Orsini & Meyer (1960) have shown that, unlike the rat, oestrogen is not required for implantation in the hamster.In the present investigation, the uptake in vitro of tritiated oestradiol and the effects of ethynyl oestradiol or the anti-oestrogen, (1-[2-(p-{\g=a\\x=req-\ (p-methoxyphenyl)-\g=b\-nitrostyryl}-phenoxy)ethyl]pyrrolidine monocitrate), on this uptake were compared in rat and hamster uterine tissue.A tritiated oestrogen ([6,7-3H]oestradiol-17\g=b\; 40 Ci/mmole; New England Nuclear Corp., Boston, Mass.) with radiochemical purity \m=ge\96\m=.\8% and radi oisotopic purity > 99% was used in these in-vitro studies. Benzene : ethanol (9:1) was used to dilute the tritiated oestradiol so that 0\m=.\16 ml of the diluted isotope in 400 ml incubation medium gave a final oestradiol concentration of 10\ m=-\ 10m.The in-vitro system used for the uptake of tritiated oestradiol by uterine tissue was described by Jensen, De Sombre, Hurst, Kawashima & Jungblut (1967). Uteri were obtained from immature (40 to 50 g) Sprague-Dawley derived rats and outbred Lak : LVG golden hamsters. The slit uterine horns were stirred in beakers containing Krebs-Ringer-Henseleit glucose buffer (pH 7-3) at 37°C. Each beaker contained twenty uterine horns in 400 ml buffer with 10-10 M-tritiated oestradiol. The effects of the oestrogen and anti-oestrogen on the uptake in vitro of the tritiated oestradiol were determined by adding unlabelled ethynyl oestradiol (10-9 m) or CN-55945-27 (20 µg|ml or 3-14 -5 m) to the incubation medium. Five uterine horns were removed from each beaker at the end of each specific time period, frozen in a dry ice-acetone bath * Present address :

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Comparative effects of some steroidal and nonsteroidal antifertility agents in rats and hamsters

Cited by 27 publications

References 15 publications

Prostaglandin E2 Is a Product of Induced Prostaglandin-endoperoxide Synthase 2 and Microsomal-type Prostaglandin E Synthase at the Implantation Site of the Hamster

Prostaglandin E2 Is a Product of Induced Prostaglandin-endoperoxide Synthase 2 and Microsomal-type Prostaglandin E Synthase at the Implantation Site of the Hamster

The effect of an intrauterine device on mast cell numbers and distribution in the hamster uterus

Uptake of Oestradiol by Rat and Hamster Uteri in Vitro: Effects of Ethynyl Oestradiol and an Anti-Oestrogen

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