Upregulation of oxidative stress by triphenyl phosphate (TPhP) exposure causes antioxidant insult and apoptotic process in Epithelioma papulosum cyprini (EPC) cells

• Published in: Environmental science and pollution research international Vol. 30; no. 56; pp. 119217 - 119227
• Main Authors: Xiong, Ning-Xia, Fang, Zi-Xuan, Kuang, Xu-Ying, Wang, Fei, Ou, Jie, Luo, Sheng-Wei
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.12.2023; Springer Nature B.V
• Subjects: Animals; Antioxidants; Antioxidants - metabolism; Apoptosis; Aquatic Pollution; Atmospheric Protection/Air Quality Control/Air Pollution; Bioengineering; Biotechnology; Carcinoma; Cell activation; Cell death; Cell viability; Cytotoxicity; Developmental biology; Earth and Environmental Science; Ecotoxicology; Environment; Environmental Chemistry; Environmental Health; Environmental science; Enzymes; Experiments; Exposure; Fibroblasts; Fish; Flame retardants; Flame Retardants - metabolism; Flame Retardants - toxicity; Genes; Lipids; Organophosphates; Organophosphates - toxicity; Oxidative Stress; Physiological effects; Protein folding; Proteins; Reactive oxygen species; Research Article; Up-Regulation; Waste Water Technology; Water Management; Water Pollution Control; Zebrafish; Fish cell lines; Oxidative stress; Triphenyl phosphate; Gene expressions
• ISSN: 1614-7499; 0944-1344; 1614-7499
• DOI: 10.1007/s11356-023-30697-0

Triphenyl phosphate (TPhP) is the predominant compound of organophosphate flame retardants (OPFRs), which can elicit a toxicological effect on physiological response and tissue development of fish. In this study, we investigated the effect of TPhP exposure on cell viability, antioxidant capacities, and apoptosis in EPC cells. Current study revealed that TPhP exposure could decrease cell viability and promote intracellular oxidative stress in EPC cells. In addition, high-dose TPhP exposure could facilitate antioxidant insults and cause mitochondrial collapse in a dose-dependent manner, along with increased gene expressions involved in apoptosis and unfolded protein response (UPR). These results indicated that reactive oxygen species (ROS)-induced cytotoxic stress and cell death were involved in antioxidant insults and apoptotic activation in TPhP-exposed fish cells.