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61,005 resultsShowing papers similar to The Mitochondrial Battleground: A Review of Microplastic-Induced Oxidative Stress and Inflammatory Pathways in Human Health
ClearMicroplastics/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.
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.
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.
Micro- and nano-plastics activation of oxidative and inflammatory adverse outcome pathways
This review maps the biological harm caused by micro- and nanoplastics to formal toxicity pathways, finding that oxidative stress is a common starting point for damage at every level from cells to whole organisms. Researchers found that in ecological settings, this oxidative damage cascades into growth inhibition and behavioral changes, while in human health contexts it may trigger inflammatory responses. The study highlights that more mammalian research is needed to fully define the health risks of plastic particle exposure.
Microplastics, Endocrine Disruptors, and Oxidative Stress: Mechanisms and Health Implications
This review examines how microplastics and nanoplastics trigger oxidative stress as a central mechanism of toxicity across multiple organ systems, including reproductive, cardiovascular, hepatic, and neurological tissues. The study highlights that these particles often carry endocrine-disrupting chemicals like bisphenol A and phthalates, which together generate reactive oxygen species, impair mitochondrial function, and compromise antioxidant defenses.
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.
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.
Mitochondria-Targeted Biomaterials-Regulating Macrophage Polarization Opens New Perspectives for Disease Treatment
This review explores how new biomaterials can be designed to target mitochondria inside immune cells called macrophages, steering them between pro-inflammatory and anti-inflammatory states to treat diseases. While not directly about microplastics, the review is relevant because microplastic exposure is known to cause mitochondrial damage and trigger inflammatory immune responses through these same pathways. Understanding how to control macrophage behavior through mitochondria could lead to treatments for inflammation caused by environmental pollutants like microplastics.
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.
Microplastics and Oxidative Stress—Current Problems and Prospects
This review examines how microplastics cause oxidative stress, a condition where harmful molecules called free radicals damage cells. Microplastics have been linked to DNA damage, cell membrane disruption, mitochondrial problems, inflammation, and cell death, all driven by oxidative stress. These effects may contribute to serious health conditions including cancer and cardiovascular disease, though the authors note that more research is needed to fully understand the risks.
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.
Cellular and Systemic Impacts of Microplastics and Nanoplastics
This review synthesized evidence on how micro- and nanoplastics cause cellular and systemic harm through inflammation, oxidative stress, mitochondrial dysfunction, and endocrine disruption across multiple organ systems. The authors emphasize that exposure is ubiquitous and that health impacts are no longer speculative.
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.
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.
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.
Molecular and Cellular Effects of Microplastics and Nanoplastics: Focus on Inflammation and Senescence
This review summarizes research showing that micro- and nanoplastics trigger oxidative stress, inflammation, and premature cell aging across many experimental models. These are the same biological processes linked to heart disease, brain disorders, and other age-related conditions. Particularly concerning, studies in animals show that plastic-related damage can be passed from parents to offspring, suggesting potential long-term generational health effects.
Oxidative and Inflammatory Potential of Nano/Microplastics in Living Organisms
This review examines the growing body of evidence that microplastics and nanoplastics trigger oxidative stress and inflammatory responses across a wide range of animals, though the findings are often inconsistent and sometimes contradictory. The authors conclude that plastic particle weathering can alter these effects in complex ways, and call for standardized, systematic research to establish clearer dose-response relationships before firm regulatory conclusions can be drawn.
Do microplastics induce oxidative stress in marine invertebrates?
This review examined whether marine invertebrates exposed to microplastics show evidence of oxidative stress — a common cellular response to toxic injury — finding support for this effect across multiple species and polymer types. Oxidative stress is a key mechanism by which microplastics may harm marine organisms.
Recent consequences of micro-nanaoplastics (MNPLs) in subcellular/molecular environmental pollution toxicity on human and animals
This review examines the subcellular and molecular mechanisms by which micro- and nanoplastics cause toxicity in humans and animals, focusing on oxidative stress, inflammation, cell death pathways, and endocrine disruption at the cellular level.
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.
Effects of Microplastics on Human Physiology: Mechanisms of Toxicity and Health Risks
This systematic review of 48 studies confirmed that microplastics are present in human blood, placenta, and reproductive tissues. The research consistently shows these particles cause oxidative stress, inflammation, mitochondrial damage, and hormonal disruption, pointing to potential links with reproductive problems, cardiovascular issues, and other chronic health conditions.
Molecular mechanisms underlying mitochondrial damage, endoplasmic reticulum stress, and oxidative stress induced by environmental pollutants
This review examines how environmental pollutants including microplastics, heavy metals, and pesticides damage cells by disrupting mitochondria, triggering endoplasmic reticulum stress, and generating harmful reactive oxygen species. Researchers describe the molecular signaling pathways through which these pollutants cause cell dysfunction and death. The study highlights the interconnected nature of these cellular stress responses and their relevance to understanding pollution-related health effects.