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Author comment: Mitochondria as a target of micro- and nanoplastic toxicity — R2/PR7
Summary
This author comment contributes to the peer review discussion of a paper on mitochondria as targets of micro- and nanoplastic toxicity, addressing reviewer feedback on the evidence for mitochondrial dysfunction, mechanisms of plastic particle internalization, and disease implications.
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.
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Author comment: Mitochondria as a target of micro- and nanoplastic toxicity — R0/PR1
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
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.
Recommendation: Mitochondria as a target of micro- and nanoplastic toxicity — R2/PR8
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
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.
Decision: Mitochondria as a target of micro- and nanoplastic toxicity — R2/PR9
This review summarizes evidence on how microplastics and nanoplastics target mitochondria in cells, disrupting energy production, triggering oxidative stress, altering mitochondrial dynamics and membrane potential, and potentially contributing to chronic disease development.