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小鼠亚急性吸入臭氧会导致多种器官损伤。

Subacute Inhalation Exposure of Mice to Ozone Induces Damage to Various Organs.

作者信息

Wang Peiwen, Lu Yuan, Lu Kuikui, Xie Daxiao, Ling Min, Lu Luoding, Chen Weiyong, Wu Yu, Liu Qizhan, Bian Qian, Xiao Tian

机构信息

Laboratory of Modern Environmental Toxicology, Environment and Health Research Division, Public Health School and Health Research Centre, Department of Public Health and Preventive Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China.

Center for Global Health, The Key Laboratory of Modern Toxicology, Ministry of Education, School of Public Health, Suzhou Institute of Public Health, Gusu School, Nanjing Medical University, Nanjing 211166, China.

出版信息

Toxics. 2025 May 31;13(6):468. doi: 10.3390/toxics13060468.

DOI:10.3390/toxics13060468
PMID:40559941
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12197127/
Abstract

Ambient ozone (O) pollution, which has become a global problem, is associated with damage to various biological systems, as determined by many studies. However, there is limited experimental evidence regarding the systemic damage induced by O exposure, and there are few associated studies on mice. In the present investigation, we constructed a subacute C57BL/6J female mouse model involving exposure to 0, 0.5, 1, or 2 ppm O for 28 days (3 h/day). Body weights, pulmonary function, hematology, serum biochemistry, inflammatory factors, and injuries to various organs were assessed for O-exposed mice. After O exposure, especially to 2 ppm O, mice showed a loss of body weight, abnormal glucose and lipid metabolism, respiratory and nervous system injuries, an inflammatory response, and pathological changes, which supported the data reported for epidemiology studies. In addition, the IL-6 levels in bronchoalveolar lavage fluid (BALF), the lungs, the livers, the kidneys, and the brains were increased, which indicated that IL-6 was associated with the damage to various organs induced by O exposure. The present report highlights the pathological injury to various organs and provides a basis for further studies of the molecular mechanisms associated with O exposure.

摘要

环境臭氧(O)污染已成为一个全球性问题,许多研究表明,它与各种生物系统的损害有关。然而,关于臭氧暴露引起的全身损害的实验证据有限,且针对小鼠的相关研究较少。在本研究中,我们构建了一个亚急性C57BL/6J雌性小鼠模型,使其暴露于0、0.5、1或2 ppm的臭氧中28天(每天3小时)。对暴露于臭氧的小鼠评估了体重、肺功能、血液学、血清生物化学、炎症因子以及各器官的损伤情况。臭氧暴露后,尤其是暴露于2 ppm臭氧的小鼠出现体重减轻、糖脂代谢异常、呼吸和神经系统损伤、炎症反应及病理变化,这与流行病学研究报告的数据相符。此外,支气管肺泡灌洗液(BALF)、肺、肝、肾和脑中白细胞介素-6(IL-6)水平升高,这表明IL-6与臭氧暴露引起的各器官损伤有关。本报告强调了臭氧对各器官的病理损伤,并为进一步研究与臭氧暴露相关的分子机制提供了依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/65ee/12197127/7c350f11eece/toxics-13-00468-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/65ee/12197127/f7db1567d332/toxics-13-00468-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/65ee/12197127/41762bf502fb/toxics-13-00468-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/65ee/12197127/9da4123d8a85/toxics-13-00468-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/65ee/12197127/2190d4e26e04/toxics-13-00468-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/65ee/12197127/052e72df2aaf/toxics-13-00468-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/65ee/12197127/7c350f11eece/toxics-13-00468-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/65ee/12197127/f7db1567d332/toxics-13-00468-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/65ee/12197127/41762bf502fb/toxics-13-00468-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/65ee/12197127/9da4123d8a85/toxics-13-00468-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/65ee/12197127/2190d4e26e04/toxics-13-00468-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/65ee/12197127/052e72df2aaf/toxics-13-00468-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/65ee/12197127/7c350f11eece/toxics-13-00468-g001.jpg

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Co-exposure to ozone and polystyrene nanoplastic exacerbates cognitive impairment and anxiety-like behavior by regulating neuronal pyroptosis in mice.同时暴露于臭氧和聚苯乙烯纳米塑料会通过调节小鼠神经元焦亡加剧认知障碍和焦虑样行为。
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Effects of co-exposure to heat and ozone on lipid metabolism in the liver and adipose tissue of C57BL/6J male mice.热暴露与臭氧共同作用对C57BL/6J雄性小鼠肝脏和脂肪组织脂质代谢的影响
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