Abstract

Hexafluoropropylene oxide dimer acid (HFPO-DA), also known as a GenX, is one type of Poly- and perfluoroalkyl substances (PFASs). PFASs are nonvolatile synthetic substances that could be readily disembogued into the environment during processing and use, making them easy to implement into the soil, drinking water, and the air. Unlike other PFASs, GenX has a comparatively short carbon chain length and has recently been used as a new substitute due to its lower tendency for accumulation in humans. However, the mechanisms and human intoxication, especially as a result of GenX, remain unknown. In this research, GenX apoptotic capacity in human liver cells was investigated. When representative human-derived liver cells, HepG2 cells, were treated to GenX for 12 h, cell viability was reduced, and apoptosis was greatly increased. In addition, GenX increased the generation of intracellular reactive oxidative species (ROS), indicating oxidative stress in a dose-dependent manner. GenX treatment increased major apoptosis-related genes relative to the untreated control group. This research indicates that GenX causes apoptosis through ROS mediation in HepG2 cells and may expand our knowledge of GenX's molecular and toxicological mechanisms.

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