活性氧
壬基酚
过氧化氢酶
氧化应激
超氧化物歧化酶
间质细胞
细胞凋亡
下调和上调
内科学
内分泌学
化学
男科
生物
分子生物学
基因
生物化学
医学
遗传学
促黄体激素
激素
作者
Shanhui Tao,Zhiang Yao,Huitao Li,Li Wang,Xinyi Qiao,Yang Yu,Yang Li,Ning Yi,Ren‐Shan Ge,Shijun Li
标识
DOI:10.1016/j.ecoenv.2023.115612
摘要
Exposure to 4-nonyl phenol (4-NP) on Leydig cell (LC) development and function remains poorly understood. We explored the effects of 4-NP on LC development and elucidate the underlying mechanisms. Male (28-day-old) mice received orally 4-NP (0.125, 0.25, and 0.5 mg/kg/day) for 28 days. We found that 4-NP at ≥ 0.125 mg/kg markedly compromised serum testosterone levels and LC numbers. Gene and protein expression analysis demonstrated downregulation of key genes and their proteins involved in LC steroidogenesis, including Star, Cyp11a1, Cyp17a1, Hsd17b3, Hsd3b6, and Scarb1. Furthermore, exposure to 4-NP induced oxidative stress, as evidenced by elevated reactive oxygen species (ROS) and malondialdehyde (MDA), as well as reduced superoxide dismutase 1/2 and catalase (CAT). Apoptosis was also observed in LCs following exposure to 4-NP, as shown by an increased BAX/BCL2 ratio and caspase-3. A TM3 mouse LC line further confirmed that 4-NP induced ROS and the expression of apoptosis-related genes and proteins. In conclusion, this study demonstrates that 4-NP exposure compromises LC development through multiple mechanisms.
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