Reproductive toxicology (Elmsford, N.Y.) · 2025
Prenatal exposure to phenanthrene impairs spermatogenesis and fertility by elevating apoptosis, altering gene expression, and disrupting steroidogenesis in adult male mice across two generations.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Afshar Azar, Nazarian Hamid, Fadaefathabadi Fatemeh, Mastery-Farahani Reza, Aghajanpour Fakhroddin, Soltani Reza, Salimi Maryam, Nourozian Mohsen, Hassanzadeh Gholamreza
Аннотация
BACKGROUND: Phenanthrene, a polycyclic aromatic hydrocarbon, can enter the human body via various routes and affect reproductive health. Its low molecular weight enables its transfer from the mother to the fetus. However, comprehensive research on its effects on reproductive system development is lacking. This study aimed to examine the impacts of prenatal phenanthrene exposure on the reproductive systems of both the immediate offspring and their progeny.
METHODS: Pregnant mice were divided into three groups: control, sham, and phenanthrene. From the detection of the vaginal plug until pregnancy day 18, mice in the phenanthrene group were administered phenanthrene solution (60 μg/kg), while sham mice received corn oil on alternate days. Following birth, male offspring were maintained without intervention until PND56. After puberty, a portion of these males were bred, while others were euthanized for histological and molecular analyses. The subsequent generation was born and developed under standard conditions without intervention, and underwent procedures similar to those of the first generation.
RESULTS: The study revealed that exposure to phenanthrene during fetal development, across two consecutive generations, led to a reduction in the expression of genes associated with mitosis and meiosis, while simultaneously increasing the rate of cell death. Additionally, the research found that a decline in Leydig cells resulted in decreased serum testosterone levels, which subsequently led to diminished quality and quantity of sperm.
CONCLUSION: Prenatal phenanthrene exposure, by disrupting gene expression and steroidogenesis, causes impaired testicular tissue function, reduced spermatogenesis, and ultimately reduced male fertility rates in the F1 and F2.
METHODS: Pregnant mice were divided into three groups: control, sham, and phenanthrene. From the detection of the vaginal plug until pregnancy day 18, mice in the phenanthrene group were administered phenanthrene solution (60 μg/kg), while sham mice received corn oil on alternate days. Following birth, male offspring were maintained without intervention until PND56. After puberty, a portion of these males were bred, while others were euthanized for histological and molecular analyses. The subsequent generation was born and developed under standard conditions without intervention, and underwent procedures similar to those of the first generation.
RESULTS: The study revealed that exposure to phenanthrene during fetal development, across two consecutive generations, led to a reduction in the expression of genes associated with mitosis and meiosis, while simultaneously increasing the rate of cell death. Additionally, the research found that a decline in Leydig cells resulted in decreased serum testosterone levels, which subsequently led to diminished quality and quantity of sperm.
CONCLUSION: Prenatal phenanthrene exposure, by disrupting gene expression and steroidogenesis, causes impaired testicular tissue function, reduced spermatogenesis, and ultimately reduced male fertility rates in the F1 and F2.