Gestational exposure to phenanthrene induces follicular atresia and endocrine dyscrasia in F1 adult female

Epidemiological investigations and animal studies demonstrate a significantly positive relationship between polycyclic aromatic hydrocarbons (PAHs) exposure and reproductive disorders. However, few researches are focused on the reproductive toxicity of low-molecular-weight PAHs (number of benzene ring <= 3) which occupy a large part of PAHs. Phenanthrene (Phe), a typical low-molecular-weight PAH, is one of the most abundant PAHs detected in foods. In the present study, oral treatment with Phe at a human exposure related level during gestation (60 mu g/kg body weight every three days, six times in total) induced reproductive disorders in F1 adult female mice: the number of antral follicles (an immature stage of follicular development) were significantly increased, while the maturation of oocytes was inhibited and aggravated follicular atresia was observed; the serum levels of luteinizing hormone (LH), testosterone and estradiol were significantly reduced; the receptor of follicle-stimulating hormone (FSHR) and aromatase in the ovary were significantly upregulated; transcriptome analysis demonstrated that the phosphatidylinositol 3-kinase and protein kinase B (PI3K/Akt) signal pathway was upregulated, and the calcium signal pathway was disturbed, which probably accounts for the exacerbated atresia of the growing follicles and the excessive consumption of follicles. The reproductive toxicity of low molecular-weight PAHs could not be neglected.

Automated summary

Epidemiological investigations and animal studies have shown a positive relationship between exposure to polycyclic aromatic hydrocarbons (PAHs) and reproductive disorders. However, little research has been conducted on the reproductive toxicity of low-molecular-weight PAHs (with 3 or fewer benzene rings) which make up a large portion of PAHs. This study focused on phenanthrene (Phe), a typical low-molecular-weight PAH, and found that oral treatment with Phe during gestation induced reproductive disorders in adult female mice, including inhibited oocyte maturation, increased follicular atresia, and reduced hormone levels.