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Valproic acid during pregnancy decrease the number of spermatogenic cells and testicular volume in the offspring of
Daniel Conei1,2,3, Mariana Rojas2, Luis Santamaría4
1Doctoral Program in Morphological Sciences, Faculty of Medicine, Universidad de La Frontera, Temuco, Chile.
Histology and Histopathology
|October 19, 2021
Summary
Prenatal exposure to valproic acid (VPA) significantly impacts male offspring testicular development. This antiepileptic drug exposure led to reduced testicular volume and fewer essential reproductive cells from embryonic stages through postnatal development.
Area of Science:
- Reproductive Biology
- Developmental Toxicology
- Pharmacology
Background:
- Valproic acid (VPA) is an antiepileptic drug with known secondary effects on male reproductive health.
- Previous studies indicate VPA can decrease androgens and gonadotropins, causing testicular defects.
- The effects of prenatal VPA exposure on offspring testicular development remained unevaluated.
Purpose of the Study:
- To investigate the morphological effects of VPA exposure during male mouse testicular development.
- To assess VPA's impact from embryonic stages to postnatal maturation.
Main Methods:
- Pregnant BALB/c mice received either 600 mg/kg VPA or a saline control orally throughout gestation.
- Male offspring were analyzed at 12.5 days post coitum (dpc), 17.5 dpc, and 6 weeks postnatal.
- Morpho-quantitative analysis of testicular development was performed.
Main Results:
- VPA-exposed offspring exhibited reduced testicular volume at all studied ages.
- Embryonic stages (12.5 dpc) showed underdeveloped sex cords with fewer gonocytes and somatic cells.
- Fetal (17.5 dpc) and postnatal (6 weeks) stages revealed decreased interstitial space and fewer key reproductive cells (spermatogonia, Sertoli, Leydig cells).
Conclusions:
- Prenatal VPA exposure induces significant histopathological alterations in male offspring testicular development.
- These effects are evident from embryonic development through early postnatal life.
- VPA poses a risk to male reproductive organogenesis.
