Desensitization to follicle-stimulating hormone in cumulus cells is coincident with hormone induction of oocyte maturation in the rat follicle

Pellicer, A.; Tg, Parmer; Jm, Stoane; Hr, Behrman

doi:10.1016/0303-7207(89)90144-5

Cited by 15 publications

(6 citation statements)

References 34 publications

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“…After incubation, OCC were scored for oocyte maturation by using a squash technique that enables visualization of the oocyte with its surrounding investment of cumulus cells, as described earlier (13). Briefly, the OCC were placed on slides pretreated with Sigmacote (Sigma Chemical) that were rinsed and dried.…”

Section: Methodsmentioning

confidence: 99%

Eicosatetraynoic and eicosatriynoic acids, lipoxygenase inhibitors, block meiosis via antioxidant action

Takami

Preston

Behrman

2000

American Journal of Physiology-Cell Physiology

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We previously showed that nordihydroguaiaretic acid (NDGA) and other antioxidants inhibit the resumption of meiosis in oocyte-cumulus complexes (OCC) and denuded oocytes (DO). Because NDGA is well known to be an inhibitor of lipoxygenases (LOX), we assessed whether other LOX inhibitors influence spontaneous germinal vesicle breakdown (GVBD) in OCC and DO. Spontaneous GVBD in rat OCC obtained from preovulatory follicles was significantly and reversibly inhibited by the minimum effective doses of 80 and 100 microM 5,8,11, 14-eicosatetraynoic acid (ETYA) and 5,8,11-eicosatriynoic acid (ETI), respectively. In DO, GVBD was significantly inhibited by 100 microM ETYA or ETI. The minimum effective concentrations of ETYA and ETI for inhibition of GVBD in either OCC or DO are approximately 30- to 50-fold higher than the concentrations necessary to inhibit LOX activity by 50% in intact cells. Because we previously showed that NDGA and other antioxidants inhibit the spontaneous resumption of meiosis, we assessed whether ETYA and ETI may act similarly as scavengers of reactive oxygen species (ROS). Luminol-amplified chemiluminescence showed that 50 microM of either ETYA or ETI markedly and significantly reduced ROS generated with 10 mM 2, 2'-azobis(2-amidinopropane)dihydrochloride (AAPH). Moreover, incubation of DO with 30 mM AAPH reversed the inhibition of GVBD produced by 100 microM ETYA or ETI. These findings support the conclusion that ETYA and ETI inhibit oocyte maturation by acting as antioxidants rather than by inhibiting LOX.

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Section: Methodsmentioning

confidence: 99%

Eicosatetraynoic and eicosatriynoic acids, lipoxygenase inhibitors, block meiosis via antioxidant action

Takami

Preston

Behrman

2000

American Journal of Physiology-Cell Physiology

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“…In animals, FSH clearly drives many events at mid-cycle, such as oocyte maturation (Pellicer et al, 1989), luteinization, corpus luteum formation and follicular rupture (Galway et al, 1990;Montgomery-Rice et al, 1993;Zelinski-Wooten et al, 1998). However, in humans, the concept that FSH might function in the same way as LH or hCG in mid-cycle events is far from orthodox.…”

Section: Prevention Of Vegf Overexpressionmentioning

confidence: 99%

Targeting the vascular endothelial growth factor system to prevent ovarian hyperstimulation syndrome

Soares¹,

Gómez²,

Simón³

et al. 2008

Human Reproduction Update

186

131

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“…Low-dose LH prevents OHSS in superovulated rats 487 oocyte maturation (Pellicer et al 1989), luteinization, corpus luteum formation and follicular rupture (Galway et al 1990, Montgomeri-Rice et al 1993, Zelinski-Wooten et al 1998. We have shown here that a dose of 10 IU rFSH has a biological activity similar to that of 10 IU hCG in inducing follicular rupture and increasing VP and VEGF expression.…”

Section: Discussionmentioning

confidence: 99%

Administration of low-dose LH induces ovulation and prevents vascular hyperpermeability and vascular endothelial growth factor expression in superovulated rats

Gómez¹,

Lima²,

Simón³

et al. 2004

Reproduction

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The administration, to rats, of a combination of pregnant mares serum gonadotrophin (PMSG) and human chorionic gonadotrophin (hCG) in high doses induces the ovarian hyperstimulation syndrome (OHSS) which is characterized by increased vascular permeability (VP) and simultaneous overexpression of vascular endothelial growth factor (VEGF) in ovarian cells. hCG has a longer half-life than LH and a greater biological activity, expressed in a higher incidence of complications such as OHSS. Similarly, FSH may also be related to the ovulatory changes within the follicle as there is a simultaneous surge in spontaneous cycles. The aim of this study was to compare the capacity of hCG, FSH and LH to induce ovulation and simultaneously prevent OHSS in the animal model. Immature female rats were treated with 10 IU PMSG for 4 days, and ovulation was triggered with saline, 10 IU hCG, 10 IU FSH, 10 IU LH or 60 IU LH. The number of oocytes ovulated into the tubes, VP and mRNA VEGF expression were evaluated and compared. All the hormones employed were as effective at triggering ovulation, with similar significant P values when compared with the control for which saline was used. The use of 10 IU LH resulted in significantly lower VP and VEGF expression than that seen in the groups treated with 10 IU hCG, 10 IU FSH or 60 IU LH. In conclusion, FSH and hCG, as well as a sixfold increase in LH, displayed similar biological activities, including increased VP due to excessive VEGF expression. The use of lower doses of LH produced similar rates of ovulation, while preventing the undesired changes in permeability. These experiments should therefore encourage clinicians to determine the optimal dose of LH to be employed in women in order to trigger ovulation and, at the same time, avoid the risk of OHSS.

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Desensitization to follicle-stimulating hormone in cumulus cells is coincident with hormone induction of oocyte maturation in the rat follicle

Cited by 15 publications

References 34 publications

Eicosatetraynoic and eicosatriynoic acids, lipoxygenase inhibitors, block meiosis via antioxidant action

Eicosatetraynoic and eicosatriynoic acids, lipoxygenase inhibitors, block meiosis via antioxidant action

Targeting the vascular endothelial growth factor system to prevent ovarian hyperstimulation syndrome

Administration of low-dose LH induces ovulation and prevents vascular hyperpermeability and vascular endothelial growth factor expression in superovulated rats

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