Gestational exposure to continuous light impairs the development of the female reproductive system in adult Wistar rat offspring.

INTRODUCTION: It has been suggested that maternal exposure to constant light during the gestational period could be considered as a chronic stressor, impairing offspring development by interfering in neuroendocrine and behavior responses. OBJECTIVE: This study aimed to evaluate whether maternal exposure to continuous light during pregnancy affects the adult reproductive system in the female offspring. MATERIALS AND METHODS: Pregnant Wistar rats were allocated into light-dark (LD) group, exposed to light and dark photoperiod during gestation, and the light-light (LL) group, exposed to a photoperiod of constant light during gestation. After birth, pups were maintained under normal light-dark photoperiod until adulthood. At postnatal day 90, blood was collected from the female offspring, to analyze plasma luteinizing hormone (LH) and progesterone levels, and the uterus and ovaries were harvested for morphometric, histological, and oxidative stress evaluations. RESULTS AND DISCUSSION: Female exposure to continuous light during the intrauterine period resulted in the adult reduction of LH and increased progesterone plasma levels, and uterine injuries a higher number of endometrial glands and reduced levels of antioxidant enzymes, such as glutathione reductase and glutathione S-transferase. In these experimental conditions, gestational continuous light exposure disturbs sex hormone balance and reduces the antioxidant enzymatic activity in the uterus of female offspring in adult life.

Extended light period in the maternal circadian cycle impairs the reproductive system of the rat male offspring.

Alterations in the circadian cycle are known to cause physiological disorders in the hypothalamic-pituitary-adrenal and the hypothalamic-pituitary-gonadal axes in adult individuals. Therefore, the present study aimed to evaluate whether exposure of pregnant rats to constant light can alter the reproductive system development of male offspring. The dams were divided into two groups: a light-dark group (LD), in which pregnant rats were exposed to an LD photoperiod (12 h/12 h) and a light-light (LL) group, in which pregnant rats were exposed to a photoperiod of constant light during the gestation period. After birth, offspring from both groups remained in the normal LD photoperiod (12 h/12 h) until adulthood. One male of each litter was selected and, at adulthood (postnatal day (PND) 90), the trunk blood was collected to measure plasma testosterone levels, testes and epididymis for sperm count, oxidative stress and histopathological analyses, and the spermatozoa from the vas deferens to perform the morphological and motility analyses. Results showed that a photoperiod of constant light caused a decrease in testosterone levels, epididymal weight and sperm count in the epididymis, seminiferous tubule diameter, Sertoli cell number, and normal spermatozoa number. Histopathological damage was also observed in the testes, and stereological alterations, in the LL group. In conclusion, exposure to constant light during the gestational period impairs the reproductive system of male offspring in adulthood.

Correction to: Impairment of testicular development in rats exposed to acephate during maternal gestation and lactation.

The original publication of this paper contains a mistake.

Impairment of testicular development in rats exposed to acephate during maternal gestation and lactation.

Acephate is an organophosphate insecticide that disrupts the endocrine system and impairs the male reproductive system. Thus, the aim of the present study was to evaluate whether exposure to acephate during maternal gestation and lactation histologically damages the testes of male Wistar rats in adulthood. For this study, adult Wistar rats were divided into the following groups: ACE-mother, (2.5 mg/kg/bw, gestational day (GD) 7 to postnatal day (PND) 21) and oil-mother (corn oil (control), GD 7 to PND 21). The male offspring (PND 90) were euthanized, and the prostates and testes were collected and weighed. The testes were utilized for histopathological analyses and to determine the sperm count. A spermatogenesis kinetic analysis revealed an increased number of seminiferous tubules in stages I-VI in the ACE-mother group. Additionally, we observed a decrease in the epithelium and the diameters of the evaluated seminiferous tubules and in the number of Sertoli cells in the group exposed to acephate. The sperm count analysis showed no difference between the groups. We conclude that maternal exposure to the pesticide acephate did not affect testicular function, but led to the impairment of testicular development and morphology of the tissue in adulthood.