EFFECTS OF MATERNAL SLEEP DEPRIVATION ON REPRODUCTIVE FUNCTIONS OF MALE OFFSPRINGS IN WISTRAR RATS

Abstract

Maternal Sleep Deprivation (MSD) has been reported to alter sexual performance in offsprings of rats. There is paucity of information on the critical period during gestation at which MSD affects reproductive functions. This study was designed to investigate the effects of MSD at different gestation periods on reproductive functions of male offsprings in Wistar rats. Sixty pregnant rats were assigned into six (Control = C; Sleep Deprived = SD) groups (n=10) at different Gestation Days (GD) as follows: GD1-7C, GD1-7SD, GD8-14C, GD8-14SD, GD15-21C and GD15-21SD. The MSD was induced using the modified multiple platform method. Caesarean section was performed on five animals from each group on GD 8, 15 and 21 for placental morphometric and biochemical analyses. The remaining five dams from each group littered naturally and only their male offsprings were studied. The offsprings were weighed on post-natal day 1 on a digital electronic balance. Reproductive functions of male offsprings were determined by assessing; testes descent, fertility index, sperm count and motility, testosterone, corticosterone, melatonin and reproductive organ histology. The testes descent day was determined by daily palpation of the scrotal sac for the presence of testes. Fertility index was determined on post-natal week 17 after mating, as percentage of female rats (of proven fertility) impregnated by the male offsprings according to the standard technique. Epididymal fluid was analysed by microscopy to determine the sperm motility and sperm count. Serum testosterone, corticosterone and melatonin were quantitated by ELISA. Histological assessment of the testes and epididymes was done using paraffin section processing and microscopy for tissue microscopic examination. Placental malondialdehyde, superoxide dismutase (SOD) and glutathione peroxidase (GPx) were assayed by spectrophotometry to determine the redox status. Immunohistochemistry of placental Bcl2 and p53 was done to determine apoptotic status. Data were subjected to descriptive statistics and analysed using Student’s t-test at α0.05. Birth weight reduced in GD15-21SD (5.3±0.1 vs 5.7±0.2 g). Testes descent occurred late in GD15-21SD (25.8±0.4 vs 23.0±0.8 days). Fertility index of GD15-21SD was 0 %. Sperm motility and count decreased in GD15-21SD (72.0±4.9 vs 89.0±2.9 %; 64.4±14.9 vs 114.5±3.0 million/mL). Offspring’s testosterone reduced in GD15-21SD (2.9±1.1 vs 7.0±1.3 ng/mL). Offspring’s corticosterone increased in GD1-7SD, GD8-14SD and GD15-21SD (106.0±3.0, 115.0±8.2, and 131.6 ± 6.6 nmol/L) compared with their controls (57.2±19.5, 65.8±5.9, 96.6±9.3 nmol/L), respectively. Melatonin increased in GD1-7SD (482.1±33.5 vs 355.3±19.21 iii nmol/L) and decreased in GD8-14SD (237.3±15.1. vs 353.6±20.5 nmol/L). The testicular and epididymal sections of GD15-21SD showed aberrant seminiferous tubules and atrophic ducts respectively. Dam’s testosterone reduced in GD15-21SD (216.0±5.8 vs 370.0±38.2 pg/mL). Placental malondialdehyde increased in GD1-7SD (0.1±0.0 vs 0.0±0.0 nmol/mg) and GD15-21SD (0.2 ± 0.0 vs 0.1 ± 0.0 nmol/mg). Placental SOD decreased and GPx increased in GD15-21SD (62.9±5.6 vs 103.0±11.7; 53.0±5.7 vs 35.3±4.7 U/mg), respectively. Bcl2 and p53 decreased in GD15-21SD decidua (7.8±0.7 vs 16.4±0.2; 0.4±0.1 vs 9.4±0.3 %), respectively. Reproductive functions were adversely affected during the fifteenth to twenty-first days of gestation.