Research Institute of the McGill University Health Centre, Montréal, Québec, Canada.
Department of Medicine, McGill University, Montréal, Québec, Canada.
Sci Rep. 2017 Sep 11;7(1):11072. doi: 10.1038/s41598-017-11325-7.
In 2002, the plasticizer 1,2-cyclohexane dicarboxylic acid diisononyl ester (DINCH) was introduced in the European market as a substitute for endocrine-disrupting phthalates. We found that in utero exposure of rats to DINCH from gestational day 14 until parturition affected reproductive organ physiology and reduced circulating testosterone levels at post-natal day 60, indicating a long-term effect on Leydig cells of the testis. Metabolically, animals exhibited randomly increased serum glucose concentrations not associated with impaired glucose utilization. Analysis of liver markers in the serum showed a hepatic effect; e.g. reduced bilirubin levels and albumin/globulin ratio. At post-natal day 200, random appearance of testicular atrophy was noted in exposed offspring, and limited changes in other reproductive parameters were observed. In conclusion, DINCH exposure appears to directly affect Leydig cell function, likely causing premature aging of the testes and impaired liver metabolic capacity. These effects might be attenuated with physiologic aging.
2002 年，增塑剂 1,2-环己烷二羧酸二异壬酯（DINCH）作为一种内分泌干扰物邻苯二甲酸酯的替代品被引入欧洲市场。我们发现，妊娠第 14 天至分娩期间，大鼠子宫内接触 DINCH 会影响生殖器官的生理功能，并降低产后 60 天的循环睾丸酮水平，表明其对睾丸的莱迪希细胞具有长期影响。在代谢方面，动物的血清葡萄糖浓度随机升高，而葡萄糖利用并未受损。血清中肝脏标志物的分析表明存在肝效应；例如，胆红素水平和白蛋白/球蛋白比值降低。在产后 200 天，暴露组的后代出现睾丸萎缩的随机表现，其他生殖参数的变化有限。总之，DINCH 暴露似乎直接影响莱迪希细胞的功能，可能导致睾丸早衰和肝脏代谢能力受损。这些影响可能会随着生理老化而减弱。
