Temporal window in which exposure to estradiol permanently modifies ovarian function causing polycystic ovary morphology in rats

Cruz, Gonzalo; Barra, Rafael; González, Diego López; Sotomayor‐Zárate, Ramón; Lara, Hernán E.

doi:10.1016/j.fertnstert.2012.07.1060

Cited by 43 publications

(36 citation statements)

References 39 publications

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“…It has been shown in other studies that the ovarian noradrenaline content decreases as a response to SON section in prepubertal animals [30, 61]. Our results support the idea that the neonatal period in rats (1–5 days after birth) is the critical window [62, 63] of steroid hormone action on central or peripheral structures producing ovarian function alterations and, in this particular experimental model, the reduced ovary sympathetic tone does not enable the reestablishment of ovary functions.…”

Section: Discussionsupporting

confidence: 90%

Polycystic ovary syndrome induced by exposure to testosterone propionate and effects of sympathectomy on the persistence of the syndrome

Morales‐Ledesma¹,

Ramos²,

Hernández

2017

Reprod Biol Endocrinol

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BackgroundPolycystic ovary syndrome is a complex disorder affecting 6 to 10% of women of reproductive age. In recent years, the cause of the syndrome has been associated with increased androgen serum levels, as well as sympathetic nervous system hyperactivity. The present study analyzed the effects at birth of a single testosterone propionate dose in rats, as well as the role of the superior ovarian nerve in polycystic ovary syndrome persistence.MethodsNewborn female rats of the CIIZV strain were injected with a single dose of 100 μg testosterone propionate, or corn oil as a vehicle. At 24 days of age, rats were subjected to superior ovarian nerve unilateral or bilateral section. A group of animals was sacrificed on their first vaginal estrus, and a second group was sacrificed at 90 days of age, when they presented an estrus preceded by a proestrus.ResultsTestosterone propionate administration at birth blocked ovulation both in adult animals and in animals sacrificed on the first vaginal estrus. Histological analysis of testosterone propionate-treated adult rat ovaries revealed the development of follicular cysts. Ovulation could not be restored by unilateral or bilateral section, and ovaries presented follicular cyst and absence of corpora lutea.ConclusionsOur results suggest that testosterone propionate treatment at birth results in the development of polycystic ovary syndrome, and that this outcome is not due to superior ovarian nerve noradrenergic innervation hyperactivity.

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Section: Discussionsupporting

confidence: 90%

Polycystic ovary syndrome induced by exposure to testosterone propionate and effects of sympathectomy on the persistence of the syndrome

Morales‐Ledesma¹,

Ramos²,

Hernández

2017

Reprod Biol Endocrinol

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“…The presence of secondary, antral, type III and cystic follicles was analyzed according to the work presented in Acuna et al (2009), Cruz et al (2012, Fernandois et al (2012) and Lara et al (2000). All of the slices were analyzed.…”

Section: Ovarian Morphologymentioning

confidence: 99%

Kisspeptin is involved in ovarian follicular development during aging in rats

Fernandois¹,

Na²,

Cuevas³

et al. 2015

Journal of Endocrinology

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We have previously reported that kisspeptin (KP) may be under the control of the sympathetic innervation of the ovary. Considering that the sympathetic activity of the ovary increases with aging, it is possible that ovarian KP also increases during this period and participates in follicular development. To evaluate this possibility, we determined ovarian KP expression and its action on follicular development during reproductive aging in rats. We measured ovarian KP mRNA and protein levels in 6-, 8-, 10-and 12-month-old rats. To evaluate follicular developmental changes, intraovarian administration of KP or its antagonist, peptide 234 (P234), was performed using a mini-osmotic pump, and to evaluate FSH receptor (FSHR) changes in the senescent ovary, we stimulated cultured ovaries with KP, P234 and isoproterenol (ISO). Our results shows that KP expression in the ovary was increased in 10-and 12-month-old rats compared with 6-month-old rats, and this increase in KP was strongly correlated with the increase in ovarian norepinephrine observed with aging. The administration of KP produced an increase in corpora lutea and type III follicles in 6-and 10-month-old rats, which was reversed by P234 administration at 10 months. In addition, KP decreased the number and size of antral follicles in 6-and 10-month-old rats, while P234 administration produced an increase in these structures at the same ages. In ovarian cultures KP prevented the induction of FSHR by ISO. These results suggest that intraovarian KP negatively participates in the acquisition of FSHR, indicating a local role in the regulation of follicular development and ovulation during reproductive aging.

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“…After females reach puberty, groups of follicles are recruited in cohorts to grow up until the early antral stage, independently of central control. Neonatal exposure to oestrogenic chemicals, such as BPA , MXC and oestradiol valerate , has been linked to reduced growth and development of primary, secondary and antral follicles. Because the early stages of follicular development do not depend upon the influence of gonadotrophin; the ovary could be a direct target of disruption by oestrogenic compounds.…”

Section: Introductionmentioning

confidence: 99%

Long‐Term Effects of Early‐Life Exposure to Environmental Oestrogens on Ovarian Function: Role of Epigenetics

Cruz

Foster

Paredes

et al. 2014

J Neuroendocrinology

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Estrogens play an important role in development and function of the brain and reproductive tract. Accordingly, it is thought that developmental exposure to environmental estrogens can disrupt neural and reproductive tract development potentially resulting in long-term alterations in neurobehavior and reproductive function. Many chemicals have been shown to have estrogenic activity whereas others affect estrogen production and turnover resulting in disruption of estrogen signaling pathways. However, these mechanisms and the concentrations required to induce these effects cannot account for the myriad adverse effects of environmental toxicants on estrogen sensitive target tissues. Hence, alternative mechanisms are thought to underlie the adverse effects documented in experimental animal models and thus could be important to human health. In this review, the epigenetic regulation of gene expression is explored as a potential target of environmental toxicants including estrogenic chemicals. We suggest that toxicant-induced changes in epigenetic signatures are important mechanisms underlying disruption of ovarian follicular development. In addition, we discuss how exposure to environmental estrogens during early life can alter gene expression through effects on epigenetic control potentially leading to permanent changes in ovarian physiology.

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Temporal window in which exposure to estradiol permanently modifies ovarian function causing polycystic ovary morphology in rats

Cited by 43 publications

References 39 publications

Polycystic ovary syndrome induced by exposure to testosterone propionate and effects of sympathectomy on the persistence of the syndrome

Polycystic ovary syndrome induced by exposure to testosterone propionate and effects of sympathectomy on the persistence of the syndrome

Kisspeptin is involved in ovarian follicular development during aging in rats

Long‐Term Effects of Early‐Life Exposure to Environmental Oestrogens on Ovarian Function: Role of Epigenetics

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