dc.description | A THESIS SUBMITTED TO THE DEPARTMENT OF PHYSIOLOGY,
FACULTY OF BASIC MEDICAL SCIENCES, COLLEGE OF MEDICINE,
UNIVERSITY OF IBADAN, IBADAN, NIGERIA
IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE AWARD OF
DOCTOR OF PHILOSOPHY, UNIVERSITY OF IBADAN, IBADAN,
NIGERIA. | en_US |
dc.description.abstract | Maternal treatment with dexamethasone in threatening preterm delivery leads to high basal corticosterone
level. This level may interfere with hormones of hypothalamic-pituitary-gonadal axis in the offspring.
However, there is paucity of information on the effects of maternal dexamethasone administration on
reproductive functions of offsprings. This study was designed to investigate the effects of maternal
treatment with dexamethasone on male reproductive functions in the F1 and F2 offsprings.
Forty-five pregnant Wistar rats (180-200 g) were divided into 9 groups (n=5). Groups 1 and 6 were
administered 0.02 mL/100g/day normal saline (control) throughout pregnancy and lactation respectively.
Groups 2, 3, 4 and 5 were administered 100 μg/kg/day dexamethasone at different gestational days 1-7, 8-
14, 15-21 and 1-21 respectively. Groups 7, 8 and 9 were administered 100 μg/kg/day dexamethasone at
lactation days 1-7, 1-14 and 1-21 respectively. All the treatments were administered subcutaneously. The
F2 offsprings were generated by cross-breeding each of the F1 treatment groups with their control females.
The male offsprings (F1 and F2) were sacrificed at 12 weeks of age. Serum Gonadotropin Releasing
Hormone (GnRH), Follicle Stimulating Hormone (FSH), Luetinizing Hormone (LH), testosterone and
corticosterone were measured using enzyme linked immunosorbent assay. Testicular Superoxide
Dismutase (SOD) activity was estimated using spectrophotometry while sperm counts, motility and
morphology were assessed by light microscopy. Data were analysed using ANOVA and Tukey’s post hoc
test at p=0.05.
Serum corticosterone, testosterone, FSH, LH and GnRH in control offsprings were 5.2±1.2 ng/mL,
10.0±1.1 nmoL/L, 5.9±0.4 mLU/mL, 5.7±0.4 mLU/mL, and 3.0±0.2 pg/mL respectively in F1 and
14.9±2.1 ng/mL, 4.9±0.3 nmoL/L, 9.0±1.4 mLU/mL, 5.9±0.9 and 7.0±0.3 pg/mL respectively in F2.
Dexamethasone exposure during prenatal days 15-21 and 1-21 significantly raised serum corticosterone
(33.7±4.2, 38.6±4.0 ng/mL), GnRH (10.2±2.1, 10.9±1.9 pg/mL), and FSH (6.5±0.2, 7.9±0.3 mLU/mL)
respectively but reduced serum testosterone (4.1±1.1, 4.3±1.0 nmoL/L) and LH (3.9±0.1, 3.5±0.1
mLU/mL) respectively when compared with F1 control. However, in the F2 offsprings, dexamethasone
reduced serum corticosterone (3.5±0.9, 5.9±0.8 ng/mL), testosterone (2.3±0.2, 2.2±0.4 nmoL/L), FSH
(3.9±0.5, 2.4±0.5 mLU/mL) and GnRH (1.2±0.1, 1.5±0.2 pg/mL) respectively when compared with the
F2 control. Treatment with dexamethasone at lactation days 1-7, 1-14 and 1-21 also significantly raised
the serum corticosterone (15.6±2.1, 18.8±1.9, 19.3±2.1 ng/mL) but reduced serum testosterone (4.5±1.3,
3.4±1.1, 2.5±0.2 nmoL/L), FSH (4.9±0.1, 3.3±0.2, 2.3±0.0 mLU/mL) and LH (2.2±0.1, 1.3±0.1, 0.8±0.1
mLU/mL) respectively when compared with the F1 control. There was a significant reduction in SOD
level in dexamethasone-treated groups at prenatal days 1-7, 8-14, 15-21 and 1-21 (13.0±2.0, 10.9±1.0,
8.0±1.4, 4.8±2.3 U/mg/mL respectively) as well as in lactation days 1-7, 1-14 and 1-21 (18.3±1.0,
10.5±0.7, 2.4±0.0 U/mg/mL respectively) when compared with the F1 control (30.7±4.2 U/mg/mL).
Dexamethasone treatment at prenatal days 15-21 and 1-21 significantly reduced sperm motility in the F1
and F2 offsprings, but increased the value of abnormal sperm in the F1 and F2 offsprings when compared
with respective control groups.
Maternal dexamethasone treatment in rats during late gestation and through lactation may disrupt
reproductive functions by altering the activity at hypothalamic-pituitary-gonadal axis. These effects may
be transferred to the F2 offsprings. | en_US |