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Prenatally administered dexamethasone impairs folliculogenesis in spiny mouse offspring
Monika Hułas-Stasiak1, Piotr Dobrowolski1, Ewa Tomaszewska2
1Department of Comparative Anatomy and Anthropology, Maria Curie-Sklodowska University, Akademicka St.19, 20-033 Lublin, Poland.
Abstract:
This study was designed to determine whether prenatal dexamethasone treatment has an effect on follicular development and atresia in the ovary of spiny mouse (Acomys cahirinus) offspring. Dexamethasone (125µg kg-1 bodyweight per day) was administered to pregnant spiny mice from Day 20 of gestation to parturition. The processes of follicle loss were analysed using classical markers of apoptosis (terminal deoxynucleotidyl transferase-mediated dUTP nick end-labelling reaction, active caspase-3) and autophagy (Lamp1). The present study indicated that dexamethasone reduced the pool of healthy primordial follicles. Moreover, the oocytes from these follicles showed intensive caspase-3 and Lamp1 staining. Surprisingly, dexamethasone caused an increase in the number of secondary follicles; however, most of these follicles were characterised by extensive degeneration of the oocyte and caspase-3 and Lamp1 labelling. Western-blot analysis indicated that the glucocorticoid receptor as well as apoptosis and autophagy markers were more strongly expressed in the DEX-treated group than in the control. On the basis of these findings, we have concluded that dexamethasone impairs spiny mouse folliculogenesis and enhances follicular atresia through induction of autophagy or combined autophagy and apoptosis.
Insights
Prenatal dexamethasone exposure in spiny mice reduces healthy primordial follicles and increases degenerating secondary follicles. This impairs ovarian development and enhances follicular atresia via apoptosis and autophagy.
Area of Science:
- Reproductive biology
- Developmental toxicology
- Ovarian physiology
Background:
- Prenatal exposure to synthetic glucocorticoids can impact reproductive health.
- Understanding the effects of dexamethasone on ovarian development is crucial for reproductive toxicology.
Purpose of the Study:
- To investigate the effects of prenatal dexamethasone treatment on follicular development and atresia in spiny mouse offspring.
- To determine the role of apoptosis and autophagy in dexamethasone-induced ovarian changes.
Main Methods:
- Pregnant spiny mice received daily dexamethasone injections from Day 20 of gestation to parturition.
- Follicular atresia was assessed using markers for apoptosis (TUNEL, caspase-3) and autophagy (Lamp1).
- Western blotting was used to analyze protein expression of glucocorticoid receptor, apoptosis, and autophagy markers.
Main Results:
- Dexamethasone treatment reduced the number of healthy primordial follicles.
- An increase in secondary follicles was observed, but these showed oocyte degeneration and positive staining for caspase-3 and Lamp1.
- Enhanced expression of glucocorticoid receptor, apoptosis, and autophagy markers was detected in the dexamethasone-treated group.
Conclusions:
- Prenatal dexamethasone exposure impairs folliculogenesis in spiny mice.
- Dexamethasone enhances follicular atresia by inducing autophagy or a combination of autophagy and apoptosis.
- The study highlights the potential adverse effects of prenatal glucocorticoid exposure on ovarian development.
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