Melatonin reduces LH, 17 beta-estradiol and induces differential regulation of sex steroid receptors in reproductive tissues during rat ovulation.

BACKGROUND: Melatonin is associated with direct or indirect actions upon female reproductive function. However, its effects on sex hormones and steroid receptors during ovulation are not clearly defined. This study aimed to verify whether exposure to long-term melatonin is able to cause reproductive hormonal disturbances as well as their role on sex steroid receptors in the rat ovary, oviduct and uterus during ovulation. METHODS: Twenty-four adult Wistar rats, 60 days old (+/-250 g) were randomly divided into two groups. Control group (Co): received 0.9% NaCl 0.3 mL+95% ethanol 0.04 mL as vehicle; Melatonin-treated group (MEL): received vehicle+melatonin [100 µg/100 g BW/day] both intraperitoneally during 60 days. All animals were euthanized by decapitation during the morning estrus at 4 a.m. RESULTS: Melatonin significantly reduced the plasma levels of LH and 17 beta-estradiol, while urinary 6-sulfatoximelatonin (STM) was increased at the morning estrus. In addition, melatonin promoted differential regulation of the estrogen receptor (ER), progesterone receptor (PR), androgen receptor (AR) and melatonin receptor (MTR) along the reproductive tissues. In ovary, melatonin induced a down-regulation of ER-alpha and PRB levels. Conversely, it was observed that PRA and MT1R were up-regulated. In oviduct, AR and ER-alpha levels were down-regulated, in contrast to high expression of both PRA and PRB. Finally, the ER-beta and PRB levels were down-regulated in uterus tissue and only MT1R was up-regulated. CONCLUSIONS: We suggest that melatonin partially suppress the hypothalamus-pituitary-ovarian axis, in addition, it induces differential regulation of sex steroid receptors in the ovary, oviduct and uterus during ovulation.

Reproductive development and function of female rats exposed to di-eta-butyl-phthalate (DBP) in utero and during lactation.

Phthalates are environmental contaminants used in the production of plastics, cosmetics and medical devices. Studies on the effects of phthalates on female reproductive health are particularly sparse and mostly restricted to high-dose exposure in rats. In the present study, pregnant rats were treated with 100mg/kg-d of di-eta-butyl-phthalate (DBP) or only the vehicle (control group), from GD 12 to GD 20 for evaluation of reproductive outcomes and fetal gonads analysis (F0), and from GD 12 to PND 21 to evaluate reproductive development and function on F1 female offspring. Results showed that all parameters were comparable between groups, although there was a significant increase in the fetal weight after DBP exposure. However, the body weight at birth was normal. Based on these data we can conclude that, in these experimental conditions, DBP did not disturb the reproductive development or function of female rats.

Alterations in the central vasopressin and oxytocin axis after lesion of a brain osmotic sensory region.

The anteroventral region of the third ventricle (AV3V) is critical in mediating osmotic sensitivity. AV3V lesions increase plasma osmolality and block osmotic-induced vasopressin (VP) and oxytocin (OT) secretion. The aim was to evaluate the effects of AV3V lesions on neurosecretion under control/water replete conditions and after 48 h dehydration. The focus was on central peptidergic changes with measurement of OT and VP content in the hypothalamic paraventricular (PVN) and supraoptic (OT) regions and the posterior pituitary. AV3V-lesioned rats exhibited an elevated plasma osmolality and higher OT content in SON and PVN. There was an increase in VP content in PVN, but no change in SON. As predicted, the plasma peptide response to dehydration was absent in lesioned animals. However, dehydration produced depletion in posterior pituitary VP in lesioned animals with no change in OT. No changes in nuclear VP and OT levels were seen after dehydration. These results demonstrate that AV3V lesions alter the VP and OT neurosecretory system, seen as a blockade of osmotic-induced release and an increase in basal nuclear peptide content. The data indicate that interruption of the osmotic sensory system affects the central neurosecretory axis, resulting in a backup in content and likely changes in synthesis and processing.