Abstract

Plastic debris in the global biospheres is an increasing concern and nanoplastic (NPs)
toxicity in humans is far from understood. Studies indicated that NPs could affect mitochondria
but the underlying mechanism remains unclear. The liver and lung have important metabolic
functions and can be easily vulnerable to NP-exposure. In this study, we investigated the effects
of 80-nm-NPs on mitochondrial functions and metabolic pathways in normal human hepatic (L02)
cells and lung (BEAS-2B) cells. NP exposure did not induce mass cell death; however, transmission
electron microscopy analysis showed that the NPs could enter the cells, and cause mitochondrial
damage. These alterations were observed at NP concentrations as low as 0.0125 mg/mL, which
might be comparable to the environmental levels. Nontarget metabolomics confirmed that the
most significantly impacted processes were mitochondrial-related, such as the tricarboxylic acid
cycle, purine metabolism, and glutathione metabolism pathways. The metabolic function of L02
cells was more vulnerable to NP-exposure than BEAS-2B cells, especially at low NP concentrations.
This study identified NP-induced mitochondrial dysfunction and metabolic toxicity pathways in
target human cells, providing insight into the possibility of adverse outcomes in human tissues
and organs.

References:
Lin, et al., (2022). Metabolomics Reveal Nanoplastic-Induced Mitochondrial Damage in Human Liver and Lung Cells. Environmental Science & Technology. (ASAP Article)