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20 resultsShowing papers similar to Mitochondria as a target of micro- and nanoplastic toxicity
ClearMitochondria as a target of micro- and nanoplastic toxicity
This review examines how micro- and nanoplastics damage mitochondria, the energy-producing structures inside cells. Studies show that plastic particles can disrupt energy production, cause harmful oxidative stress, and interfere with the cell's ability to repair or recycle damaged mitochondria. Since mitochondrial damage is linked to many chronic diseases including heart disease, neurodegeneration, and diabetes, this helps explain why microplastic exposure may have widespread health effects.
Impact of Micro- and Nanoplastics on Mitochondria
This review examines how micro- and nanoplastics can damage mitochondria, the energy-producing structures inside cells that are critical for metabolism and cell survival. Researchers found that plastic particle exposure can trigger oxidative stress, disrupt mitochondrial membrane function, and interfere with energy production pathways. Since mitochondrial dysfunction is linked to numerous health conditions, the study suggests this may be a key mechanism through which plastic pollution affects human health.
Environmental nanoplastics induce mitochondrial dysfunction: A review of cellular mechanisms and associated diseases
This review summarizes how nanoplastics, which are small enough to enter individual cells, damage mitochondria (the energy-producing structures inside cells) by disrupting their shape, function, and ability to produce energy. This mitochondrial damage has been linked to a range of diseases including neurodegeneration, diabetes, cardiovascular disease, and reproductive problems. The findings help explain why nanoplastic exposure may contribute to multiple chronic health conditions through a common cellular mechanism.
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.
Microplastics/nanoplastics contribute to aging and age-related diseases: Mitochondrial dysfunction as a crucial role
This review examines how microplastics and nanoplastics may contribute to aging and age-related conditions by damaging mitochondria, the energy-producing structures inside cells. Researchers describe how these tiny plastic particles enter the body through food, water, and air, and accumulate in various organs where they can disrupt normal mitochondrial function. The study suggests that microplastic-driven mitochondrial damage could be an underappreciated factor in the aging process and related health decline.
Assessing micro and nanoplastics toxicity using rodent models: Investigating potential mitochondrial implications
This review examines recent rodent studies investigating how micro- and nanoplastics affect cellular health, with a focus on potential mitochondrial impacts. Researchers found that while no study has directly targeted mitochondrial effects, several reported molecular and biochemical changes consistent with disrupted mitochondrial function, including oxidative stress. The study suggests that mitochondria may be an important but understudied target of micro- and nanoplastic toxicity.
The Impact of Micro-Nanoplastics on Mitochondria in the Context of Diet and Diet-Related Diseases
This review examines how micro- and nanoplastics may worsen diet-related diseases like obesity and type 2 diabetes by damaging mitochondria, the energy-producing structures inside cells. Studies suggest that microplastic exposure combined with unhealthy diets can amplify metabolic problems like insulin resistance and high blood sugar. The findings point to mitochondrial damage as a key link between microplastic exposure and the growing epidemic of metabolic diseases.
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.
Nanoplastics and Human Health: Hazard Identification and Biointerface
This review covers what we know about nanoplastics and their potential effects on human health, including how they enter the body and what happens when they get inside cells. Nanoplastics can penetrate cell membranes and damage internal structures like mitochondria, which are responsible for producing energy in cells. The review also discusses strategies to reduce nanoplastic levels in the environment to protect human health.
Decision: Mitochondria as a target of micro- and nanoplastic toxicity — R0/PR3
Microplastics and nanoplastics can enter human cells and directly damage mitochondria — the organelles that power every cell — by triggering oxidative stress, disrupting energy production, and activating cell death pathways. Because mitochondrial dysfunction underlies diseases ranging from neurodegeneration to cancer and diabetes, this review argues that mitochondrial harm should be treated as a central mechanism linking plastic exposure to chronic disease risk.
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.
Micro- and nanoplastic-induced mitochondrial dysfunction and organelle miscommunication: A toxicological perspective
This review examined how micro- and nanoplastics disrupt mitochondrial function and inter-organelle communication in cells. The evidence indicates that these particles cause oxidative stress, calcium dysregulation, impaired energy production, and activation of stress responses including autophagy and cell death, with cascading effects on lysosomes, the endoplasmic reticulum, and nuclear function.
Influence of Micro- and Nanoplastics on Mitochondrial Function in the Cardiovascular System: A Review of the Current Literature
This review examined the limited but growing research on how micro- and nanoplastics may affect mitochondrial function in the cardiovascular system. Researchers noted that these plastic particles can trigger oxidative stress and disrupt normal mitochondrial processes, which are critical for heart and blood vessel health. The study highlights the need for more comprehensive research given the rising levels of plastic particle contamination and the importance of mitochondrial health in preventing cardiovascular problems.
Metabolomics Reveal Nanoplastic-Induced Mitochondrial Damage in Human Liver and Lung Cells
Researchers exposed normal human liver and lung cells to 80-nanometer plastic particles and found that the nanoplastics damaged mitochondria, the energy-producing structures inside cells, without causing widespread cell death. Using metabolomics analysis, they identified specific disruptions to energy metabolism and lipid processing pathways in both cell types. This study reveals a subtle but important way that nanoplastics could impair organ function in humans by disrupting cellular energy production.
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.
Micro/nanoplastics and human health: A review of the evidence, consequences, and toxicity assessment
This review summarizes evidence that micro and nanoplastics have been found in multiple human organs and body fluids, where they can alter cell shape, damage mitochondria, reduce cell survival, and cause oxidative stress. The health effects depend heavily on the size, shape, and chemical makeup of the particles, with smaller nanoplastics generally posing the greatest risk because they penetrate deeper into tissues. The review provides a framework for assessing how dangerous different types of plastic particles are to human health.
The Mitochondrial Battleground: A Review of Microplastic-Induced Oxidative Stress and Inflammatory Pathways in Human Health
This review synthesizes research on how microplastics damage mitochondria through oxidative stress and inflammation across aquatic, terrestrial, and mammalian systems. Researchers found that microplastics generate reactive oxygen species that disrupt mitochondrial function, with smaller and aged particles causing greater toxicity, while inflammatory signaling creates a feedback loop that worsens cellular damage.
Author comment: Mitochondria as a target of micro- and nanoplastic toxicity — R2/PR7
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.
Polystyrene nanoplastics target electron transport chain complexes in brain mitochondria
Researchers investigated the effects of polystyrene nanoplastics on mitochondrial function in rat brain tissue. They found that nanoplastic exposure significantly impaired the electron transport chain, specifically disrupting electron flow between respiratory complexes I-III and II-III in both synaptic and non-synaptic mitochondria. The findings reveal a potential mechanism by which nanoplastics could contribute to brain energy metabolism deficits and neurotoxicity.