BDE-47 induces nephrotoxicity through ROS-dependent pathways of mitochondrial dynamics in PK15 cells
文献类型： 外文期刊
作者： Sun, Shiyao 1 ; Zhao, Zhihui 1 ; Rao, Qinxiong 1 ; Li, XiaoMin 2 ; Ruan, Zheng 3 ; Yang, Junhua 1 ;
作者机构： 1.Shanghai Acad Agr Sci, Inst Agrifood Stand & Testing Technol, Shanghai 201403, Peoples R China
2.Chinese Acad Agr Sci CAAS, Inst Qual Stand & Testing Technol Agroprod, Beijing 100081, Peoples R China
3.Nanchang Univ, Sch Food Sci & Technol, State Key Lab Food Sci & Technol, Nanchang 330047, Jiangxi, Peoples R China
关键词： BDE-47; Nephrotoxicity; Oxidative stress; Mitochondrial fusion and fission
期刊名称：ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY （ 影响因子：6.291； 五年影响因子：6.393 ）
ISSN： 0147-6513
年卷期： 2021 年 222 卷
页码：
收录情况： SCI
摘要： 2,2',4,4'-tetrabromodiphenyl ether (BDE-47)-induced nephrotoxicity is closely associated with oxidative stresses and mitochondrial abnormalities. Mitochondrial fusion and fission dynamics are crucial for maintaining mitochondrial and cellular physiological homeostasis. However, the detailed mechanisms through which BDE-47 disrupts this dynamic and contributes to renal injuries are still not fully understood. The porcine kidney-15 (PK15) cell line, a well-defined in vitro animal renal toxicological model, was exposed to BDE-47 with concentrations of 12.5, 25, 50, and 100 mu M, respectively. Cell viability, the levels of reactive oxygen species (ROS) and adenosine triphosphate (ATP), the mitochondrial membrane potential (MMP), and the expression levels of key mitochondrial fusion and fission proteins were assessed. BDE-47 reduced cell viability and disrupted mitochondrial dynamics by inhibiting mitochondrial fusion and fission simultaneously, leading to MMP decreases, ROS overgeneration, ATP depletion, and cellular disintegration in a dose-dependent manner. Additionally, the mitochondrial division inhibitor (Mdivi-1) with the concentration of 20 mu M observed to restore the downregulation of mitochondrial fusion and fission proteins, alleviate damages in mitochondrial morphology and functionality, correct ROS overproduction, and enable cell survival. The antioxidant N-acety-L-cysteine (NAC) with the concentration of 1 mM also simultaneously reversed the imbalance of mitochondrial dynamics, decreased ROS production, and restored mitochondrial morphology in PK15 cells exposed to BDE-47. Our data provide new insights indicating that BDE-47 disrupts mitochondrial fusion/fission dynamics to induce mitochondrial abnormalities, triggering oxidative stresses and thus contributing to PK15 cell dysfunction. ROSdependent pathways in mitochondrial dynamics may provide a new avenue for developing effective strategies to protect cells against BDE-47-induced nephrotoxicity.
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