Toxicity mechanisms of biomass burning aerosols in in vitro hepatic steatosis models

Michal Pardo*, Chunlin Li, Amani Jabali, Lauren M. Petrick, Ziv Ben-Ari, Yinon Rudich

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease that contributes to the global rise in liver-related morbidity and mortality. Wood tar (WT) aerosols are a significant fraction of carbonaceous aerosol originating from biomass smoldering, contributing to air pollution particles smaller than 2.5 mm (PM2.5). Mechanistic biological associations exist between exposure to PM2.5 and increased NAFLD phenotypes in both cell and animal models. Therefore, this study examines whether an existing NAFLD-like condition can enhance the biological susceptibility of liver cells exposed to air pollution in the form of WT material. Liver cells were incubated with lauric or oleic acid (LA, OA, respectively) for 24 h to accumulate lipids and served as an in vitro hepatic steatosis model. When exposed to 0.02 or 0.2 g/L water-soluble WT aerosols, both steatosis model cells showed increased cell death compared to the control cells (blank-treated cells with or without pre-incubation with LA or OA) or compared to WT-treated cells without pre-incubation with LA or OA. Furthermore, alterations in oxidative status included variations in reactive oxygen species (ROS) levels, elevated levels of lipid peroxidation adducts, and decreased expression of antioxidant genes associated with the NRF2 transcription factor. In addition, steatosis model cells exposed to WT had a higher degree of DNA damage than the control cells (blank-treated cells with or without pre-incubation with LA or OA). These results support a possible systemic effect through the direct inflammatory and oxidative stress response following exposure to water-soluble WT on liver cells, especially those predisposed to fatty liver. Furthermore, the liver steatosis model can be influenced by the type of fatty acid used; increased adverse effects of WT on metabolic dysregulation were observed in the LA model to a higher extent compared to the OA model.

Original languageEnglish
Article number166988
JournalScience of the Total Environment
Volume905
DOIs
StatePublished - 20 Dec 2023

Funding

FundersFunder number
Donald Gordon Foundation
EASVOLEE101095457
Fran Morris Rosman and Richard Rosman
Pudgin Memorial Trust
Merle S. Cahn Foundation
HORIZON EUROPE Framework Programme
Israel Science Foundation928/21

    Keywords

    • Air pollution
    • Aryl hydrocarbon receptor
    • Inflammation
    • Lipid accumulation
    • Oxidative stress

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