Eicosanoids and ovulation

Priddy, A.R.; Killick, S.R.

doi:10.1016/0952-3278(93)90204-a

Cited by 42 publications

(15 citation statements)

References 48 publications

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“…Considering that prostaglandins are involved in the paracrine regulation of the rupture of ovarian follicles associated with ovulation (Priddy & Killick 1993) and that PGE has been reported to have immunomodulatory properties by modulating cytokine production (Kuroda & Yamashita 2003, Lakier Smith 2003, Yang et al 2003, we also evaluated whether the ovarian concentration of PGE was modified by DHEA-induced hyperandrogenization. The fact that the treatment with DHEA reduced ovarian PGE production was an expected result since DHEAhyperandrogenized animals not only did not start to cycle but also showed increased levels of TNF-a when compared with controls.…”

Section: Discussionmentioning

confidence: 99%

Role of the N, N′-dimethylbiguanide metformin in the treatment of female prepuberal BALB/c mice hyperandrogenized with dehydroepiandrosterone

Sander¹,

Luchetti²,

Solano³

et al. 2006

Reproduction

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The present study investigated the role of the N, N{ 0 }-dimethylbiguanide metformin (50 mg/100 g body weight in 0.05 ml water, given orally with a canulla) in the prevention of endocrine and immune disorders provoked by the hyperandrogenization with dehydroepiandrosterone (DHEA) in prepuberal BALB/c mice. The treatment with DHEA (6 mg/100 g body weight in 0.1 ml oil) for 20 consecutive days, recreates a mouse model that resembles some aspects of the human polycystic ovary syndrome (PCOS). The treatment with DHEA did not modify either body mass index (BMI) or blood glucose levels, but did increase fasting insulin levels when compared with controls. Markers of ovarian function -serum estradiol (E), progesterone (P) and ovarian prostaglandin E (PGE) -were evaluated. The treatment with DHEA increased serum E and P levels while ovarian PGE diminished. When metformin was administered together with DHEA, serum insulin, E and P levels, and ovarian PGE values did not differ when compared with controls. Using flow cytometry assays we found that the treatment with DHEA diminished the percentage of the CD4 1 T lymphocyte population and increased the percentage of the CD8 1 T lymphocyte population from both ovarian tissue and retroperitoneal lymph nodes. However, when metformin was administered together with DHEA, the percentages of CD4 1 and CD8 1 T lymphocyte populations from both ovarian tissue and retroperitoneal lymph nodes were similar to those observed in controls. Finally, when DHEA was administered alone it increased the serum tumor necrosis factor-alpha (TNF-a) levels when compared with controls; however, when metformin was administered together with DHEA, serum TNF-a levels were similar to controls. These results indicate that metformin is able, directly or indirectly, to avoid the endocrine and immune alterations produced when mice are hyperandrogenized with DHEA.

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Section: Discussionmentioning

confidence: 99%

Role of the N, N′-dimethylbiguanide metformin in the treatment of female prepuberal BALB/c mice hyperandrogenized with dehydroepiandrosterone

Sander¹,

Luchetti²,

Solano³

et al. 2006

Reproduction

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“…However, the results herein suggest that (1) the role of each receptor subtype in the process of ovulation and (2) the effectiveness of these commonly used peptide-based antagonists on analysis of the ovulatory cascade, need to be re-evaluated. Furthermore, the role of alternative contractile factors such as prostaglandins (Priddy and Killick 1993), histamines (Schmidt et al 1987) and bradykinin (Smith and Perks 1984) should be considered inclusive to the process of ovulation. Palanisamy et al (2006) reported that a dose of 10 mg per kg bodyweight of the EDNRB antagonist, BQ788, administered intra-peritoneally to immature gonadotrophin-primed mice resulted in a dramatic decrease in ovulation.…”

Section: Discussionmentioning

confidence: 99%

Production and binding of endothelin-2 (EDN2) in the rat ovary: endothelin receptor subtype A (EDNRA)-mediated contraction

Bridges

Alem

et al. 2010

Reprod. Fertil. Dev.

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Abstract. Endothelin-2 (EDN2)-mediated contraction has been proposed as a final mechanical signal facilitating ovulation. The objectives herein were to determine (1) whether ovarian endothelins were increased before ovulation; (2) whether a specific endothelin-converting enzyme (ECE) was mediating their production; (3) which receptor was facilitating ovarian contraction; and (4) whether receptor-specific antagonism affected ovulation. Follicular development was induced in immature rats with 10 IU pregnant mare serum gonadotrophin (PMSG) and the ovulatory cascade was initiated 48 h later with 10 IU human chorionic gonadotrophin (hCG). In Experiment 1, an immunoassay revealed that the ovarian concentration of endothelin peptide was increased 7-fold 12 h after hCG when compared with 48 h after PMSG (P < 0.05). In Experiment 2, real-time PCR indicated that mRNA for Ece1, but not Ece2, was increased in granulosa cells collected 12 h after hCG when compared with those collected before the ovulatory stimulus (P < 0.05). In Experiment 3, isometric tension analysis revealed that the contractile effect of EDN2 was mediated by endothelin receptor A (EDNRA), not B (EDNRB). In Experiment 4, no effect was observed on the rate of ovulation when rats were treated with an antagonist specific to EDNRA (BQ123) or EDNRB (BQ788), or when mice were treated with BQ123, BQ788 or BQ123 + BQ788. In conclusion, endothelin peptide is produced before ovulation and the contractile action of EDN2 within the ovary is facilitated via EDNRA. In addition, findings of this study indicate synergistic interactions among contractile factors affect ovulatory outcome, while the role of EDNRB alone in the process of ovulation requires further investigation.

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“…Eicosanoids have several actions in reproductive biology of vertebrates (Murdoch et al 1993, Priddy and Killick 1993, Funk 2001, which have encouraged many research groups to study their relevance in insect reproduction. The first report on the biosynthesis of eicosanoids in the insect reproductive system was in the house cricket Acheta domesticus by Destephano and Brady (1977).…”

Section: Eicosanoids As Local Regulators Of Oogenesismentioning

confidence: 99%

Oogenesis and egg development in triatomines: a biochemical approach

Atella

Gondim

Machado

et al. 2005

An. Acad. Bras. Ciênc.

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In triatomines, as well as in other insects, accumulation of yolk is a process in which an extra-ovarian tissue, the fat body, produces yolk proteins that are packed in the egg. The main protein, synthesized by the fat body, which is accumulated inside the oocyte, is vitellogenin. This process is also known as vitellogenesis. There are growing evidences in triatomines that besides fat body the ovary also produces yolk proteins. The way these yolk proteins enter the oocyte will be discussed. Yolk is a complex material composed of proteins, lipids, carbohydrates and other minor components which are packed inside the oocyte in an organized manner. Fertilization triggers embryogenesis, a process where an embryo will develop. During embryogenesis the yolk will be used for the construction of a new individual, the first instar nymph. The challenge for the next decade is to understand how and where these egg proteins are used up together with their non-protein components, in pace with the genetic program of the embryo, which enables cell differentiation (early phase of embryogenesis) and embryo differentiation (late phase) inside the egg.

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Eicosanoids and ovulation

Cited by 42 publications

References 48 publications

Role of the N, N′-dimethylbiguanide metformin in the treatment of female prepuberal BALB/c mice hyperandrogenized with dehydroepiandrosterone

Role of the N, N′-dimethylbiguanide metformin in the treatment of female prepuberal BALB/c mice hyperandrogenized with dehydroepiandrosterone

Production and binding of endothelin-2 (EDN2) in the rat ovary: endothelin receptor subtype A (EDNRA)-mediated contraction

Oogenesis and egg development in triatomines: a biochemical approach

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