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Toxicological effects of micro- and nanoplastic exposure reveal resistance mechanisms to programmed cell death in hepatic cells
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This study exposed human liver cells in a lab to tiny plastic particles called microplastics and nanoplastics, including polyethylene and polyethylene terephthalate. The treated cells showed changes in proteins that control cell death, becoming more resistant to dying, including when exposed to a cancer drug.
Microplastics (MPs) contamination is an emerging environmental issue. Due to their small sizes, MPs can usually enter to human body and impair human health. Although the toxicological effects of MPs have been increasingly investigated, the existing literature has predominantly focused on polystyrene (PS) particles, whereas data on other commonly used polymers, particularly polyethylene (PE) and polyethylene terephthalate (PET), remain comparatively limited in human hepatic cells. In this context, our study sought to analyze the possible impacts of environmental micro- and nanoplastics (EMPs/ENPs), particularly that of PET and PE (10µg /ml). First, we focused on the intrinsic apoptotic pathway in HepG2 cells by analysing pro-survival proteins such as (Bcl-2, MCL-1, Bcl-w, and Bcl- xL) and pro-apoptotic protein levels (Bad, NOXA). Second, we analyzed cytochrome c release and the production of caspase-3. Our data illustrated that MPs treatment provoked the activation of Bcl-2 phosphorylation, as well as a resistance to programmed cell death. Moreover, we demonstrated that MPs/NPs-treated HepG2 cells exhibit increased resistance to doxorubicin, It is noteworthy that this study breaks new ground by examining the repercussions of PE and PET on the intrinsic apoptotic pathway in HepG2 cell line.
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Researchers investigated how nanoplastics are internalized by human liver cancer cells (HuH-7) and assessed the cellular damage that follows, characterizing the dynamics of particle uptake and the resulting cytotoxic effects relevant to hepatic health.
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This scoping review examines hepatotoxic mechanisms of micro- and nanoplastics in animal models, identifying oxidative stress, inflammation, lipid peroxidation, and epigenetic alterations as the primary pathways through which plastic particles damage liver tissue.
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This thesis tested tiny plastic particles, including polystyrene, PLA, and PCL, on human intestinal, liver, and neuronal cells grown in the lab. Smaller particles caused more cell damage, including stress to cell structures and disrupted genes, with effects varying by polymer type and cell type. Biodegradable plastics also caused cell stress, similar to conventional plastics.
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Researchers tested the effects of polymethyl methacrylate micro- and nanoplastics on human liver cells, varying the particle concentration, exposure duration, size, and surface chemistry. They found that smaller particles and those with specific surface modifications caused greater cellular damage, including reduced viability and increased oxidative stress. The study suggests that the physical and chemical properties of microplastics play a critical role in determining their potential toxicity to human tissues.
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