内质网
耳毒性
氧化应激
耳蜗
细胞凋亡
未折叠蛋白反应
外毛细胞
化学
细胞生物学
压力(语言学)
药理学
生物化学
生物
内科学
医学
神经科学
语言学
哲学
化疗
顺铂
作者
Hanyu Liao,Xue Li,Huiming Zhang,Shanshan Yin,Hong Yu,Rong Chen,Fei Gui,Lei Yang,Jing Wang,Jianyun Zhang
标识
DOI:10.1016/j.ecoenv.2024.116936
摘要
Hearing loss is a common chronic sensory deficit that affects millions of people worldwide and has emerged as a significant public health concern. The association between environmental exposure to chemicals and the prevalence of hearing impairment has recently attracted increased attention. Chlorinated paraffins (CPs) are a type of chemical compound that has been widely used and commonly detected in samples of both environmental and human origin. The knowledge of the toxicological effects of CPs, particularly its ototoxicity, remains limited at present. In this study, six commercial CPs were selected and evaluated using cochlea hair HEI-OC1 cells for their cytotoxicity, apoptosis, DNA damage, reactive oxygen species (ROS) accumulation and oxidative response. The cytotoxicity was observed after CPs exposure at high concentrations except for C-40 and was positively related to the chlorine content (Cl-content) in both CCK-8 and trypan blue assays. All 6 CPs induced cells apoptosis through caspase-dependent apoptotic pathway. CPs exposure induced DNA damage and stimulated ROS overproduction. Antioxidant N-acetyl-L-cysteine (NAC) could reverse the cytotoxicity and ROS accumulation caused by CPs exposure. The overexpression of ATF4 and CHOP indicated that endoplasmic reticulum (ER) stress was involved in the CPs induced cytotoxicity. Thus, CPs induced cytotoxicity and apoptosis via ROS accumulation, ER stress and DNA damage and positively related to the Cl-content and our findings indicate that CPs may pose a risk of ototoxicity at environmental relevant exposure levels.
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