产后早期接触低剂量十溴联苯醚(BDE-209)对雄性小鼠血清代谢物的影响。

A. Eguchi, H. Miyaso, C. Mori
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引用次数: 7

摘要

十溴联苯醚(BDE-209)的毒性已在几项研究中得到报道。然而,关于BDE-209暴露的毒理学生物标志物的了解并不多。在本研究中,我们在小鼠出生后第1 ~ 5天皮下注射0.025 mg/kg/天的BDE-209,并在12周龄(第84天)处死小鼠。采用流动注射分析和亲水相互作用色谱-三重四极杆质谱法测定小鼠血清代谢组,以表征BDE-209暴露对小鼠的影响。数据分析显示,对照小鼠和暴露小鼠之间存在良好的分离(R(2) = 0.953, Q(2) = 0.728,交叉验证残差(CV - ANOVA)的方差分析(P值= 0.0317)和54种代谢物在暴露小鼠中被鉴定为改变。使用可变重要性(VIP)和负荷进行选择,并通过相关系数标准和正交偏最小二乘判别分析(OPLS - DA)进行缩放。暴露于BDE - 209的小鼠显示出较低水平的长链酰基肉碱和柠檬酸循环相关代谢物,以及较高水平的某些氨基酸、长链磷脂和短链酰基肉碱。在血清代谢组中观察到的脂肪酸、碳水化合物和氨基酸代谢的破坏可能与先前观察到的产后早期暴露于低剂量BDE-209的小鼠精子发生受损有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The effects of early postnatal exposure to a low dose of decabromodiphenyl ether (BDE-209) on serum metabolites in male mice.
The toxicity of decabromodiphenyl ether (BDE-209) has been reported in several studies. However, there is not much known about the toxicological biomarkers that characterize BDE-209 exposure. In this study, we subcutaneously exposed mice to 0.025 mg/kg/day BDE-209 on postnatal days 1‑5 and sacrificed the animals at 12 weeks of age (day 84). Flow injection analysis and hydrophilic interaction chromatography-triple quadrupole mass spectrometry were used to determine the serum metabolomes of these mice in order to characterize the effects of BDE-209 exposure. Data analysis showed a good separation between control and exposed mice (R(2) = 0.953, Q(2) = 0.728, and ANOVA of the cross‑validated residuals (CV‑ANOVA): P‑value = 0.0317) and 54 metabolites were identified as altered in the exposed animals. These were selected using variable importance (VIP) and loadings scaled by a correlation coefficient criteria and orthogonal partial least squares discriminant analysis (OPLS‑DA). BDE‑209‑exposed mice showed lower levels of long-chain acylcarnitines and citrate cycle-related metabolites, and higher levels of some amino acids, long-chain phospholipids, and short-chain acylcarnitines. The disruption of fatty acid, carbohydrate, and amino acid metabolism observed in the serum metabolome might be related to the previously observed impaired spermatogenesis in mice with early postnatal exposure to a low dose of BDE-209.
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