Abstract

ObjectiveDexamethasone is a widely used glucocorticoid, which has been prescribed increasingly in recent years. The effects of Dexamethasone on the ovary and uterus was investigated in present study.MethodsTwenty (20) adult female Wistar rats, weighing 130-170 g were assigned to four (4) groups of five (5) animals each. The rats in the control group received saline, while the rats in the experimental group was subjected to oral treatment of dexamethasone of 12 mg/kg, 10 mg/kg, and 7 mg/kg doses daily for a period of 10 days, respectively. The rats were slaughtered after 24 hours of the last administration, and the uterus and ovaries were harvested following abdominal incision. Histological and biochemical investigations were carried out and the results were analyzed using ANOVA with the Graph-Pad prism software package 6.ResultsThere was a significant decrease in the activities of the carbohydrate metabolic enzymes of the uterus in the dexamethasone-treated groups compared to the control group (p<0.05). Vacuolation, atrophy, thick epithelium, enlarged cells, inactive interstitial glands and follicular cyst, characterized the histological observation in the dexamethasone-treated groups in a dose-dependent manner.ConclusionThis present study revealed that high-dose dexamethasone causes multiple changes in the histological features of the ovary and uterus, exerting type I and type II anti-oestrogenic effects on the female reproductive compartment.

Highlights

  • The female reproductive system consists of three major components, the ovary, uterine tube and uterus, which function synchronously under strict hormonal control, in a graded continuum, from fully competent menstrual cycles to the complete absence of cyclic ovarian activity (Agarwal et al, 2005; Tsigos & Chrousos, 1994)

  • This study has demonstrated a decrease in bodyweight and Glucose-6-phosphate dehydrogenase (G-6-PDH) enzyme activities by the administration of dexamethasone in a dose-dependent manner, with the highest significant reduction observed at 12 mg/ kg (p

  • As expressed in type I anti-oestrogenic morphological responses associated with endocrine disruption, thin, atrophic endometrial and glandular epithelium consisting of low columnar cells and sparse endometrial glands and atrophic myometrium (Yuan, 1991; Goldman et al, 2000) as well as in the ovary, endocrine disruption cause atrophy with inactive interstitial glands; glandular cells are small and spindle-shaped and associated cystic anovulatory follicle present

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Summary

Introduction

The female reproductive system consists of three major components, the ovary, uterine tube and uterus, which function synchronously under strict hormonal control, in a graded continuum, from fully competent menstrual cycles (eumenorrhoea) to the complete absence of cyclic ovarian activity (amenorrhea) (Agarwal et al, 2005; Tsigos & Chrousos, 1994). Glucocorticoids (GCs) classified as corticosteroids are an example of steroid hormones. GCs have been reported to interfere with abnormal cell division that take place in the cancer cell formation mechanism; high doses of GCs are used in the treatment of cancer (Pelt, 2011). This includes inhibitory effects on lymphocyte proliferation, as in the treatment of lymphomas and leukemia; and the mitigation of side effects of anticancer drugs (Provan et al, 2010)

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