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Author comment: Mitochondria as a target of micro- and nanoplastic toxicity — R0/PR1
Summary
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.
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.