Depression is one of the most prevalent disorders in the world and may occur during pregnancy and postpartum periods. Fluoxetine (FLX) has been widely prescribed for use during depression in pregnancy and lactation. This study aimed to investigate if in utero and lactational exposure to FLX could compromise reproductive parameters in female offspring. Wistar rats received, by daily gavage, FLX 5mg/kg or 0.3ml of water (control group) from the first gestational day until weaning (21 days). Assessments in the female offspring included: body weight, anogenital distance, vaginal opening, first estrus, estrous cycle, reproductive organs weight, uterine morphometric analyses, ovarian follicle and corpora lutea counting, estradiol plasmatic concentration, sexual behavior, maternal behavior and fertility test. Exposure to FLX delayed the puberty onset in female pups. The present study demonstrated that developmental exposure to FLX can deregulate the neuroendocrine hormonal control of female offspring during prepubertal and pubertal periods.

Psychotropics are among the most prescribed medications. There are indications in the literature that fluoxetine (FLX; selective serotonin reuptake inhibitor [SSRI] antidepressant) and methylphenidate (MPH) could have a hormonal mode of action. This study was designed to evaluate the immature rat uterotrophic assay Substitute by (1) if sertraline (SER) and escitalopram (ESC) 2 other SSRI antidepressants would share the estrogenicity described for FLX and (2) MPH for estrogenicity and antiestrogenicity. The 18-day-old Wistar rats with were divided into olive oil, estradiol (0.3 mg/kg), estradiol + tamoxifen (10 mg/kg), SER (5, 15, or 45 mg/kg), ESC (2, 6, or 18 mg/kg), MPH (2.5 or 5 mg/kg), and estradiol + MPH groups. As expected, estradiol increased the weight of uterus, and this effect was counterbalanced by concomitant treatment with tamoxifen. The SER, ESC, and MPH had no effect on the uterus weight. The results suggest that ESC and SER do not share the estrogenicity described for FLX and that MPH does not disrupt estrogenic signaling.

No abstract

No abstract