The mechanism of immunosuppression by perfluorooctanoic acid in BALB/c mice
The mechanism of immunosuppression by perfluorooctanoic acid in BALB/c mice
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全氟辛酸对BALB/c小鼠免疫抑制的机制
DOI：
10.1039/c3tx50096a
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发表时间：
2014-04
影响因子：
2.1
通讯作者：
Jiang, Guibin
中科院分区：
文献类型：
--
作者：
Ji, Huan;Zhang, Jie;Zhou, Qunfang;Jiang, Guibin
全氟辛酸（PFOA）可降低小鼠的免疫功能，但其免疫毒性机制尚不清楚。为了确定PFOA的免疫毒性是否与脂质代谢有关，雄性BALB/c小鼠被喂食常规（RD）或高脂肪（HFD）饮食，并以每天0、5、10和20 mg kg−1的剂量暴露于PFOA，持续14天。暴露后，用PFOA处理的RD喂养小鼠的体重显著下降，免疫系统器官出现严重萎缩。组织学和超微结构的变化也被发现。同时，胸腺和脾脏过氧化物酶体增殖物激活受体（peroxisome proliferator-activated receptor，PPAR）α和γ基因表达也上调。凋亡细胞的百分比随着PFOA剂量的增加而增加，并且胸腺内的淋巴细胞比脾脏内的淋巴细胞发生凋亡的数量更多。在HFD暴露组中，仍观察到类似的现象。HFD喂养引起PFOA组胸腺内PPARγ而非PPARα表达上调。这些结果表明，过量的膳食脂质并不能阻止PFOA诱导的过氧化物酶体增殖物引起的免疫抑制，PFOA的免疫调节是通过过氧化物酶体增殖物激活受体途径，以及诱导线粒体损伤和淋巴细胞凋亡途径。
Perfluorooctanoic acid (PFOA) has been demonstrated to decrease immunity of mice, but little is known about the mechanisms of its immunotoxicity. In order to determine whether the immunotoxicity of PFOA is associated with lipid metabolism, male BALB/c mice were fed with either a regular (RD) or high fat (HFD) diet, and exposed to PFOA at doses of 0, 5, 10, and 20 mg kg−1 per day for 14 days. Following exposure, the body weights of RD-fed mice treated with PFOA were significantly decreased, and the immune system organs showed serious atrophy. Histopathological and ultrastructural changes were also detected. At the same time, the gene expressions of peroxisome proliferator-activated receptor (PPAR) α and γ were also up-regulated in the thymus and the spleen. The percentage of apoptotic cells increased with increasing doses of PFOA, and a larger number of lymphocytes underwent apoptosis within the thymus than the spleen. In the HFD exposure groups, similar phenomena were still observed. HFD feeding caused up-regulation of PPARγ but not PPARα within the thymus of PFOA groups. These results suggest that an excess of dietary lipids does not prevent PFOA-induced immune suppression caused by peroxisome proliferators, and immunomodulation by PFOA is via the PPAR pathway, and the induction of mitochondrial damage and lymphocyte apoptosis pathway.
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成年雄性 C57BL/6 小鼠口服全氟辛烷磺酸 (PFOS) 7 天后发生的免疫毒性变化
影响因子：
6.1
作者：
Dong, Guang-Hui;Zheng, Li;Jin, Yi-He;He, Qin-Cheng
通讯作者：
He, Qin-Cheng
影响因子：
5.8
作者：
Yang, Q;Xie, Y;DePierre, JW
通讯作者：
DePierre, JW
影响因子：
4.4
作者：
Yanhong Wei;L. Chan;Dazhi Wang;Hongxia Zhang;Jianshe Wang;Jiayin Dai
通讯作者：
Yanhong Wei;L. Chan;Dazhi Wang;Hongxia Zhang;Jianshe Wang;Jiayin Dai
DOI：
--
发表时间：
2006-12
期刊：
Biomedical and environmental sciences : BES
影响因子：
--
作者：
Hongbin Deng;Chun-lei Cheng;D. Cui;Dian-dong Li;L. Cui;N. Cai
通讯作者：
Hongbin Deng;Chun-lei Cheng;D. Cui;Dian-dong Li;L. Cui;N. Cai
DOI：
--
发表时间：
2007
期刊：
Toxicological sciences : an official journal of the Society of Toxicology
影响因子：
--
作者：
K. Fairley;R. Purdy;S. Kearns;S. Anderson;B. Meade
通讯作者：
K. Fairley;R. Purdy;S. Kearns;S. Anderson;B. Meade