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Recommendation: Mitochondria as a target of micro- and nanoplastic toxicity — R1/PR5
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This recommendation document accompanies a peer-reviewed study examining mitochondria as a primary cellular target of micro- and nanoplastic toxicity. The research reviews disruptions to mitochondrial energy production, calcium homeostasis, lipid oxidation, and steroid synthesis caused by plastic particle exposure.
Mitochondria are unique organelles to perform critical functions such as energy production, lipid oxidation, calcium homeostasis, and steroid hormone synthesis in eukaryotic cells. The proper functioning of mitochondria is crucial for cellular survival, homeostasis, and bioenergetics. Mitochondrial structure and function are maintained by the mitochondrial quality control system, which consists of the processes of mitochondrial biogenesis, mitochondrial dynamics (fusion/fission), mitophagy, and mitochondrial unfolded protein response UPRMT. Mitochondrial dysfunction and/or damage is associated with the initiation and progression of several human diseases, including neurodegenerative, cardiovascular, age-related diseases, diabetes, and cancer. Environmental stress and contaminants may exacerbate the sensitivity of mitochondria to damage which causes mitochondrial dysfunction. There is growing evidence about the impact of nanoplastics (NPs) and microplastics (MPs) on mitochondrial health and function. MPs/NPs were reported to trigger oxidative stress and reactive oxygen species production, which eventually change mitochondrial membrane potential. MPs/NPs can cross through the biological barriers in the human body and be internalized by the cells, potentially altering mitochondrial dynamics, bioenergetics, and signaling pathways, thus impacting cellular metabolism and function. This review states the effects of MPs/NPs on mitochondrial homeostasis and function as well as on mitochondrial membrane dynamics, mitophagy, and mitochondrial apoptosis are discussed.
More Papers Like This
Decision: Mitochondria as a target of micro- and nanoplastic toxicity — R1/PR6
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This editorial decision document concerns a peer-reviewed study on mitochondria as a key cellular target of micro- and nanoplastic toxicity. The paper reviews how plastic particles disrupt mitochondrial functions including energy production, calcium homeostasis, and steroid hormone synthesis in eukaryotic cells.
Recommendation: Mitochondria as a target of micro- and nanoplastic toxicity — R2/PR8
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This review examines how micro- and nanoplastics target mitochondria in cells, disrupting energy production, triggering oxidative stress, altering membrane potential and mitochondrial dynamics, and potentially contributing to neurodegenerative, cardiovascular, and metabolic disease development.
Recommendation: Mitochondria as a target of micro- and nanoplastic toxicity — R0/PR2
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This review focuses on mitochondria as a key target of micro- and nanoplastic toxicity, summarizing evidence that MPs and NPs trigger oxidative stress, disrupt mitochondrial membrane potential, alter fusion/fission dynamics, and activate mitophagy. Because mitochondrial dysfunction underlies neurodegenerative disease, diabetes, and cancer, this mechanistic framework helps explain why microplastic exposure may contribute to a wide range of serious human health conditions.
Author comment: Mitochondria as a target of micro- and nanoplastic toxicity — R0/PR1
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This review examines how microplastics and nanoplastics disrupt the function of mitochondria — the cell's energy-producing organelles — by triggering oxidative stress, altering membrane potential, and interfering with cell signaling. Because mitochondrial dysfunction is linked to neurodegenerative disease, cancer, diabetes, and cardiovascular conditions, this work raises concern that microplastic exposure could contribute to or worsen these diseases. The authors call for more targeted research into how plastic particles interact with cellular energy systems.
Author comment: Mitochondria as a target of micro- and nanoplastic toxicity — R1/PR4
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This review details how micro- and nanoplastics disrupt mitochondria — the energy-producing structures inside cells — by generating reactive oxygen species, altering membrane potential, and interfering with the quality-control processes cells use to maintain healthy mitochondria. Because mitochondrial dysfunction is a common driver of neurodegenerative diseases, cancer, diabetes, and cardiovascular disease, these findings suggest a plausible cellular mechanism linking plastic particle exposure to serious chronic illness. The review calls for more research into mitochondria as a key target of plastic toxicity.
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