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Prenatal Exposure to Phenanthrene Impairs Spermatogenesis and Fertility by Elevating Apoptosis, Altering Gene Expression, and Disrupting Steroidogenesis in Adult Male Mice Across Two Generations Publisher Pubmed



Afshar A1 ; Nazarian H1 ; Fadaefathabadi F1 ; Masteryfarahani R1 ; Aghajanpour F1 ; Soltani R1 ; Salimi M1 ; Nourozian M1 ; Hassanzadeh G2
Authors
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Authors Affiliations
  1. 1. Department of Biology and Anatomical Sciences, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  2. 2. Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Source: Reproductive Toxicology Published:2025


Abstract

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. © 2025 Elsevier Inc.