Institute of Marine Research, Bergen, Norway; Department of Nutritional Sciences, School of Life Course Sciences, King's College London, UK.
Department of Nutritional Sciences, School of Life Course Sciences, King's College London, UK.
Reprod Toxicol. 2018 Sep;80:105-116. doi: 10.1016/j.reprotox.2018.06.010. Epub 2018 Jun 20.
Developmental health risks of chronical exposure to low doses of foodborne persistent organic pollutants (POP) are recognized but still largely uncharacterized. Juvenile female BALB/c mice exposed to either HBCD, CB-153 or TCDD at doses relevant to human dietary exposures (49.5 μg, 1.35 μg and 0.90 ng kg bw day, respectively) for 28 days displayed histopathological changes in liver (HBCD, CB-153, TCDD), thymus (HBCD, CB-153) and uterus (HBCD), reduced serum oestradiol 17β (E2) levels (HBCD), increased serum testosterone (T) levels (CB-153) and an increased T/E2 ratio (HBCD). Proteomics analysis of brain provided molecular support for the HBCD-induced reduction in E2. Neural gene expression analysis, confirmed effects on 18 out of 30 genes previously found to be affected after exposure to higher doses to the same pollutants. Our findings indicate that exposure to POP at low doses is associated with subtle, but toxicological relevant effects on post-natal development in female mice.
慢性暴露于低剂量食源性持久性有机污染物 (POP) 对发育健康的危害已得到认识，但仍在很大程度上未得到充分描述。暴露于与人类饮食暴露相关剂量的六溴环十二烷 (HBCD)、CB-153 或 TCDD（分别为 49.5μg、1.35μg 和 0.90ng kg bw day）28 天的幼年雌性 BALB/c 小鼠表现出肝（HBCD、CB-153、TCDD）、胸腺（HBCD、CB-153）和子宫（HBCD）的组织病理学变化，血清雌二醇 17β（E2）水平降低（HBCD），血清睾酮（T）水平升高（CB-153），T/E2 比值升高（HBCD）。大脑的蛋白质组学分析为 HBCD 诱导的 E2 减少提供了分子支持。神经基因表达分析证实了暴露于相同污染物高剂量后 30 个基因中 18 个基因受到影响。我们的研究结果表明，低剂量接触 POP 会导致雌性小鼠产后发育出现细微但具有毒理学相关性的影响。
