Pyridostigmine bromide, chlorpyrifos, and DEET combined Gulf War exposure insult depresses mitochondrial function in neuroblastoma cells.
Pyridostigmine bromide, chlorpyrifos, and DEET combined Gulf War exposure insult depresses mitochondrial function in neuroblastoma cells.
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DOI：
10.1002/jbt.22913
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发表时间：
2021-12
影响因子：
3.6
通讯作者：
Citron BA
中科院分区：
文献类型：
--
作者：
Delic V;Karp J;Klein J;Stalnaker KJ;Murray KE;Ratliff WA;Myers CE;Beck KD;Citron BA
海湾战争疾病（GWI）由疾病控制和预防中心（CDC）定义为一种多症状疾病，具有三种因素中的两种至少一种症状，包括：疲劳，情绪认知问题和肌肉骨骼疾病。这组长期症状是1990年至1991年在沙漠风暴行动中服役的美国，澳大利亚和英国等联盟国家的军事人员所特有的。在同一时期，部署在世界其他地区（如波斯尼亚）的士兵报告这些症状的比例要低得多。GWI的确切原因尚不清楚，但联合暴露于N，N-二乙基-间甲苯酰胺（DEET），有机磷如毒死蜱（CPF）和溴化吡啶斯的明（PB）已被假设为一种潜在的机制。已知线粒体功能障碍发生在与GWI具有相同症状的大多数神经退行性疾病中，因此与GWI有关。虽然暴露于这些和其他有毒物质继续被调查为GWI的潜在原因，它们对线粒体生理学的综合影响仍然未知。在这项研究中，在一个常用的和容易获得的永生化细胞系（N2 a），其较高的耗氧率类似于体内的高代谢神经元的组合GWI毒物暴露对线粒体功能的影响进行了测定。我们报告，含有杀虫剂CPF 71 μM、驱虫剂DEET 78 μM和抗毒素PB 19 μM的组合暴露在孵育4小时后导致严重的线粒体功能障碍，导致线粒体呼吸状态降低，而不存在促凋亡信号、质子泄漏或活性氧产生显著增加。
Gulf War Illness (GWI) is defined by the Centers for Disease Control and Prevention (CDC) as a multi-symptom illness having at least one symptom from two of three factors, which include: fatigue, mood-cognition problems, and musculoskeletal disorders. The cluster of long-term symptoms is unique to military personnel from coalition countries including United States, Australia, and the United Kingdom that served in Operation Desert Storm from 1990 to 1991. Reporting of these symptoms is much lower among soldiers deployed in other parts of the world like Bosnia during the same time period. The exact cause of GWI is unknown, but combined exposure to N,N-diethyl-m-toluamide (DEET), organophosphates like chlorpyrifos (CPF), and pyridostigmine bromide (PB), has been hypothesized as a potential mechanism. Mitochondrial dysfunction is known to occur in most neurodegenerative diseases that share symptoms with GWI and has therefore been implicated in GWI. Although exposure to these and other toxicants continues to be investigated as potential causes of GWI, their combined impact on mitochondrial physiology remains unknown. In this study, the effects of combined GWI toxicant exposure on mitochondrial function were determined in a commonly used and readily available immortalized cell line (N2a), whose higher rate of oxygen consumption resembles that of highly metabolic neurons in vivo. We report that combined exposure containing pesticide CPF 71 μM, insect repellants DEET 78 μM, and antitoxins PB 19 μM, causes profound mitochondrial dysfunction after a 4-h incubation resulting in decreased mitochondrial respiratory states in the absence of proapoptotic signaling, proton leak, or significant increase in reactive oxygen species production.
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影响因子：
4.5
作者：
Abdullah, Laila;Evans, James E.;Crawford, Fiona
通讯作者：
Crawford, Fiona
DOI：
10.1093/geronj/44.5.s177
发表时间：
1989-09-01
期刊：
JOURNALS OF GERONTOLOGY
影响因子：
--
作者：
PRUCHNO, RA;RESCH, NL
通讯作者：
RESCH, NL
DOI：
10.1042/cs20140101
发表时间：
2014-09
期刊：
Clinical science (London, England : 1979)
影响因子：
--
作者：
Chacko BK;Kramer PA;Ravi S;Benavides GA;Mitchell T;Dranka BP;Ferrick D;Singal AK;Ballinger SW;Bailey SM;Hardy RW;Zhang J;Zhi D;Darley-Usmar VM
通讯作者：
Darley-Usmar VM
影响因子：
3.4
作者：
Karen, DJ;Li, W;Bloomquist, JR
通讯作者：
Bloomquist, JR
影响因子：
3.5
作者：
Abdullah, Laila;Evans, James E.;Crawford, Fiona C.
通讯作者：
Crawford, Fiona C.