Benzo(a)pyrene (BaP) is an ubiquitous environmental pollutant which can lead to adverse effects on male reproduction. However, the persistence of these changes on a multigenerational scale has not been sufficiently explored. This study evaluated if peripubertal exposure to BaP in male rats can induce reproductive impairment in offspring. Male rats received BaP at environmentally relevant doses (0, 0.1, 1, or 10 μg/kg/day) orally from post-natal (PND) 23–53. On PND 90, treated males were mated with non-treated females for obtaining the next generation (F1). The paternal exposure to BaP decreased the body weight of offspring on PND 1, 13 and 22, as well as it provoked a reduction in the relative anogenital distance of the males. This exposure also brought forward the onset of puberty, evidenced by an earlier vaginal opening and first estrous in females of the lowest dose group and by a delay in the testicular descent and preputial separation ages in males. The males presented a decrease in the daily sperm production and a disrupted sperm morphology. Furthermore, the testicular histology was altered, evidenced by a reduction in the Leydig cell numbers and in the seminiferous tubules diameter, as well as a disrupted seminiferous tubules staging. The estrous cyclicity and some fertility parameters were changed in the females, as well as alterations in the ovary and uterus histology were observed. BaP compromised several reproductive parameters of the F1 generation, suggesting that peripubertal exposure to this compound provokes permanent modifications in male germ line of F0 generation.

苯并 (a) 芘 (BaP) 是一种普遍存在的环境污染物，可对雄性生殖产生不利影响。然而，这些变化在多代规模上的持久性尚未得到充分探索。该研究评估了雄性大鼠青春期周围暴露于 BaP 是否会导致后代的生殖障碍。从出生后 (PND) 23-53 开始，雄性大鼠口服接受环境相关剂量（0、0.1、1 或 10 μg/kg/天）的 BaP。在 PND 90 时，经过处理的雄性与未经处理的雌性交配以获得下一代 (F1)。父系暴露于 BaP 降低了 PND 1、13 和 22 时后代的体重，并引起了雄性相对肛门生殖器距离的减少。这种暴露也提前了青春期的开始，最低剂量组女性的阴道开口较早和第一次发情以及男性睾丸下降和包皮分离年龄的延迟都证明了这一点。雄性表现出每日精子产量减少和精子形态破坏。此外，睾丸组织学发生了改变，这可以通过 Leydig 细胞数量和生精小管直径的减少以及生精小管分期中断来证明。雌性的发情周期和一些生育参数发生了变化，并且观察到了卵巢和子宫组织学的改变。BaP 损害了 F1 代的几个生殖参数，表明青春期暴露于这种化合物会引起 F0 代雄性生殖系的永久性改变。