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61,005 resultsShowing papers similar to The Impact of Micro-Nanoplastics on Mitochondria in the Context of Diet and Diet-Related Diseases
ClearImpact 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.
Mitochondria 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.
Mitochondria as a target of micro- and nanoplastic toxicity
This review examines how micro- and nanoplastics damage mitochondria, the energy-producing structures inside our cells. Research shows these tiny plastic particles can cross biological barriers, enter cells, and disrupt mitochondrial function by triggering oxidative stress and altering energy production. Since mitochondrial damage is linked to diseases like cancer, diabetes, and neurodegeneration, this represents a key concern for human health.
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.
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.
Adipose tissue as target of environmental toxicants: focus on mitochondrial dysfunction and oxidative inflammation in metabolic dysfunction-associated steatotic liver disease
This review examines how environmental toxicants, including micro and nanoplastics, target fat tissue and contribute to metabolic diseases like obesity, diabetes, and fatty liver disease. These pollutants disrupt mitochondria (the energy-producing parts of cells) and trigger a cycle of oxidative stress and inflammation that damages both fat tissue and the liver. The findings suggest that microplastic exposure could be one of several environmental factors contributing to the rising rates of metabolic disease worldwide.
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 oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications
This review examines how high blood sugar in diabetes triggers excessive production of reactive oxygen species (ROS) in mitochondria, leading to a destructive cycle of cellular damage that drives complications in the heart, kidneys, and blood vessels. While focused on diabetes, this mechanism is relevant to microplastic research because microplastics are also known to increase ROS production and mitochondrial dysfunction in human cells.
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.
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.
Microplastics induce insulin resistance by causing mitochondrial dysfunction associated with mROS in skeletal muscle in vitro
Researchers exposed human muscle cells to polystyrene micro and nanoplastics and found that the particles caused insulin resistance, meaning the cells could not properly absorb sugar from the blood. The plastics damaged the cells' mitochondria (the energy-producing structures) and triggered harmful oxidative stress, but a mitochondria-protecting antioxidant reversed the damage. This study suggests that microplastic exposure could contribute to metabolic problems like type 2 diabetes by impairing how muscles process sugar.
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.
Exploring the micro- and nanoplastics–diabetes nexus: Shattered barriers, toxic links, and methodological horizons
This review examines growing evidence that micro- and nanoplastics may contribute to diabetes by disrupting blood sugar regulation, insulin signaling, and fat metabolism through oxidative stress and inflammation. Animal studies show that plastic particles can damage the pancreas, liver, and gut in ways that mirror the development of diabetes, though human studies are still limited. The review calls for more research into whether everyday microplastic exposure could be a hidden factor in the global rise 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.
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.
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.
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.
Biological exposure to microplastics and nanoplastics and plastic additives: impairment of glycolipid metabolism and adverse effects on metabolic diseases
This review examines how exposure to micro- and nanoplastics disrupts the body's ability to process sugars and fats, potentially contributing to diabetes, obesity, and atherosclerosis. The plastics cause inflammation and oxidative stress, damage gut bacteria, trigger insulin resistance, and increase fat buildup in the liver. For people who already have metabolic conditions, plastic exposure may make their disease worse.
Role of Mitochondria in Inflammatory Bowel Diseases: A Systematic Review
This systematic review found that mitochondrial dysfunction plays a significant role in inflammatory bowel diseases through multiple mechanisms, including disrupted energy production, impaired mucosal repair, altered gut microbiota signaling, and weakened intestinal barrier integrity. The findings are relevant to microplastic research because plastic particle exposure has been shown to cause mitochondrial damage in gut tissues.
Cellular mechanisms of microplastic and nanoparticle exposure and its relationship with metabolic diseases: Literature review
This literature review examined how microplastic and nanoparticle exposure affects cellular mechanisms related to metabolic disease, finding evidence that these contaminants disrupt insulin signaling, alter lipid metabolism, and may contribute to the development of metabolic syndrome.
Cellular Distribution of Polystyrene Nanoplastics from Food Chain and Their Effects on Mitochondrial Quality in H9C2 Cells
Researchers investigated the cellular distribution of polystyrene nanoplastics entering via the food chain and examined their effects on mitochondrial quality in H9C2 cardiac cells, assessing how nanoplastic accumulation disrupts mitochondrial function.
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.
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.