ArticleEnvironmental science and pollution research international2021
Effects of reactive oxygen species generation induced by Wonju City particulate matter on mitochondrial dysfunction in human middle ear cell.
Article in Environmental science and pollution research international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Environmental exposure to air pollution and climate: Intersecting the impact on ear and nose health and chemosensory function (Review).International journal of molecular medicine · 2026Review
- Identification of mitochondrial related gene characteristics and potential molecular mechanism of acute otitis media.Frontiers in molecular biosciences · 2025Article
- Deep Learning Techniques for Ear Diseases Based on Segmentation of the Normal Tympanic Membrane.Clinical and experimental otorhinolaryngology · 2023Article
- Particulate matter 10 induces oxidative stress and apoptosis in rhesus macaques skin fibroblast.PeerJ · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Atmospheric particulate matter (PM) contains different components that can elicit varying adverse health effects in humans and animals. Studies on PM toxicity and its underlying mechanisms in the middle ear are limited, and they generally use a PM standard. However, as PM composition varies temporally and geographically, it is crucial to identify the toxic PM constituents according to season and region and investigate their associated health effects. Thus, we sought to determine whether PM induces cytotoxicity and inflammatory factor and reactive oxygen species (ROS) generation in human middle ear epithelial cells obtained from patients with otitis media. The cells were treated with both standard urban PM and PM directly captured from the atmosphere in Wonju City. The association between mitochondrial dysfunction and PM was investigated. PM exposure significantly increased COX-2 and TNF-α mRNA expression, increased ROS generation, induced inflammatory responses, and caused abnormalities in mitochondrial motility and function. Furthermore, PM induced cell apoptosis, which consequently reduced cell survival, particularly at the concentration of 100 μg/mL. Overall, our study provides new insights into the toxic effects of standard and atmospheric PM on middle ear cell line.
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Registered trials
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