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Decision: Mitochondria as a target of micro- and nanoplastic toxicity — R2/PR9
Summary
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.
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
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