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膳食脂肪对暴露于全氟辛烷磺酸的 BALB/c 小鼠胸腺和脾脏毒理学效应的调节作用。

Modulation of dietary fat on the toxicological effects in thymus and spleen in BALB/c mice exposed to perfluorooctane sulfonate.

机构信息

Key Laboratory of Subtropical Agriculture and Environment, Ministry of Agriculture, Huazhong Agricultural University, Wuhan 430070, PR China.

出版信息

Toxicol Lett. 2011 Jul 28;204(2-3):174-82. doi: 10.1016/j.toxlet.2011.04.029. Epub 2011 May 6.

DOI:10.1016/j.toxlet.2011.04.029
PMID:21571052
Abstract

Perfluorooctane sulfonate (PFOS) can cause atrophy of the immune organs in rodents, but the mechanism underlying this action is not completely understood. In this study, BALB/c mice were fed a regular (RD) or high-fat diet (HFD). They were then exposed to PFOS (0, 5, and 20mg/kg/day) for 14 days. In the RD-exposure group, body weight significantly decreased and the immune organs showed considerable atrophy. Histopathological analyses showed that the corticomedullary junction of the thymus was indistinguishable, and sinus expansion in the spleen was observed. Transmission electron microscopy (TEM) results showed that lipofuscin granules and vacuoles appeared in the thymus and spleen. Increased apoptosis of thymocytes was observed. In the HFD group, all of these phenomena were not eliminated. More serious atrophy was seen in the immune organs under TEM. Even more adipocytes were in the lobules of the thymus in the HFD 20mg/kg/day PFOS groups. Expression of the proliferator-activated receptor-alpha and interleukin-1 beta were upregulated in the thymus and spleen in all exposure groups. These results suggest that PFOS may indirectly attack the immune organs by interfering with lipid metabolism, leading to co-senescence of the thymus and spleen. These data may aid understanding of how PFOS affects the immune system.

摘要

全氟辛烷磺酸 (PFOS) 可导致啮齿动物免疫器官萎缩,但这种作用的机制尚不完全清楚。在本研究中,BALB/c 小鼠喂食常规(RD)或高脂肪饮食(HFD)。然后,它们暴露于 PFOS(0、5 和 20mg/kg/天)14 天。在 RD 暴露组中,体重明显下降,免疫器官明显萎缩。组织病理学分析表明,胸腺的皮质髓质交界处难以区分,脾脏出现窦扩张。透射电子显微镜(TEM)结果显示,胸腺和脾脏中出现脂褐素颗粒和空泡。胸腺细胞凋亡增加。在 HFD 组中,这些现象并未消除。TEM 下观察到免疫器官更严重的萎缩。在 HFD 20mg/kg/天 PFOS 组中,胸腺小叶中甚至有更多的脂肪细胞。在所有暴露组中,胸腺和脾脏中增殖物激活受体-α和白细胞介素-1β的表达均上调。这些结果表明,PFOS 可能通过干扰脂质代谢间接攻击免疫器官,导致胸腺和脾脏的共衰老。这些数据可能有助于理解 PFOS 如何影响免疫系统。

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Modulation of dietary fat on the toxicological effects in thymus and spleen in BALB/c mice exposed to perfluorooctane sulfonate.膳食脂肪对暴露于全氟辛烷磺酸的 BALB/c 小鼠胸腺和脾脏毒理学效应的调节作用。
Toxicol Lett. 2011 Jul 28;204(2-3):174-82. doi: 10.1016/j.toxlet.2011.04.029. Epub 2011 May 6.
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The atrophy and changes in the cellular compositions of the thymus and spleen observed in mice subjected to short-term exposure to perfluorooctanesulfonate are high-dose phenomena mediated in part by peroxisome proliferator-activated receptor-alpha (PPARalpha).在短期接触全氟辛烷磺酸的小鼠中观察到的胸腺和脾脏萎缩及细胞组成变化是高剂量现象,部分由过氧化物酶体增殖物激活受体α(PPARα)介导。
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In vivo immunotoxicity of perfluorooctane sulfonate in BALB/c mice: Identification of T-cell receptor and calcium-mediated signaling pathway disruption through gene expression profiling of the spleen.体内研究全氟辛烷磺酸对 BALB/c 小鼠的免疫毒性:通过脾脏基因表达谱分析鉴定 T 细胞受体和钙介导信号通路的破坏。
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