Plastic debris in the global biosphere is an increasing
concern,
and nanoplastic (NPs) toxicity in humans is far from being understood.
Studies have indicated that NPs can affect mitochondria, but the underlying
mechanisms remain unclear. The liver and lungs have important metabolic
functions and are 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, as evidenced by overproduction of
mitochondrial reactive oxygen species, alterations in the mitochondrial
membrane potential, and suppression of mitochondrial respiration.
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. The metabolic function of L02 cells was
more vulnerable to NP exposure than that of BEAS-2B cells, especially
at low NP concentrations. This study identifies NP-induced mitochondrial
dysfunction and metabolic toxicity pathways in target human cells,
providing insight into the possibility of adverse outcomes in human
health.
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