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Trichloroethylene hypersensitivity syndrome (THS), mainly caused by occupational exposure to trichloroethylene (TCE), can give rise to serious and fatal hepatic damage. To date, the precise mechanisms of hepatic damage in THS remain unclear. Recent studies showed that reactive oxygen species (ROS) play a core role in cell death and inflammatory response. Therefore, the present study sought to explore whether ROS-mediated inflammatory responses contribute to the hepatic damage in TCE sensitization. To this end, a mouse model of TCE sensitization was established; in some cases, hosts were pretreated with tempol, an ROS scavenger. The results showed that TCE sensitization caused hepatic pathological/functional changes, ROS generation, and oxidative stress, alterations of the anti-oxidant defense Nrf2/HO-1/NLRP3 pathway, and pro-inflammatory cytokine formation in the liver. ROS scavenging via pretreatment with tempol was found not only to inhibit the hepatic oxidative stress, but also to regulate Nrf2/HO-1/NLRP3 pathway activity. In all cases, tempol was able to mitigate the pathologic changes induced by TCE sensitization. In summary, the results here demonstrated a novel molecular mechanism wherein ROS-mediated inflammatory responses play a central role in TCE-induced liver damage. Therapies targeting ROS scavenging could help to protect against hepatic damage by regulating Nrf2/HO-1/NLRP3 pathway activities in TCE-sensitized hosts.

ROS-mediated inflammatory response in liver damage via regulating the Nrf2/HO-1/NLRP3 pathway in mice with trichloroethylene hypersensitivity syndrome