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61,005 resultsShowing papers similar to Toxicological effects of microplastics in renal ischemia–reperfusion injury
ClearPolyethylene microplastics disrupt renal function, mitochondrial bioenergetics, redox homeostasis, and histoarchitecture in Wistar rats
Researchers gave rats polyethylene microplastics orally for 28 days and found dose-dependent kidney damage, including impaired filtration, electrolyte imbalances, and tissue inflammation. The microplastics depleted antioxidant defenses, increased oxidative stress markers, and disrupted mitochondrial energy production in kidney cells, identifying the kidneys as a critical target of microplastic toxicity.
Effects of nano- and microplastics on kidney: Physicochemical properties, bioaccumulation, oxidative stress and immunoreaction
Researchers exposed mice to polystyrene nano- and microplastics of varying sizes and tracked their accumulation and effects in the kidneys. They found that the particles changed their physical properties during digestion, accumulated in kidney tissue, and caused oxidative stress and immune responses. The study suggests that plastic particle size plays an important role in determining the extent of kidney-related harm.
Microplastics Exacerbate Cadmium-Induced Kidney Injury by Enhancing Oxidative Stress, Autophagy, Apoptosis, and Fibrosis
Researchers exposed mice to microplastics and cadmium for three months and found that microplastics significantly worsened cadmium-induced kidney injury. The combined exposure enhanced oxidative stress, autophagy, cell death, and tissue scarring in the kidneys beyond what cadmium alone caused. The study suggests that microplastics may act as amplifiers of heavy metal toxicity in organ systems.
The nephrotoxic potential of polystyrene microplastics at realistic environmental concentrations
Researchers tested polystyrene microplastics on human kidney cells at concentrations reflecting real-world environmental levels. They found that the particles attached to and were engulfed by the cells, triggering oxidative stress and inflammatory responses that reduced cell survival. The findings suggest that even realistic low-level microplastic exposure may pose risks to kidney health.
The microplastics exposure induce the kidney injury in mice revealed by RNA-seq
In a mouse study, microplastics of different sizes caused kidney injury including inflammation, oxidative stress, and scarring (fibrosis) after long-term exposure. The smallest particles (80 nanometers) altered immune-related genes, while larger particles disrupted genes tied to the body's internal clock. This research provides evidence that microplastics accumulating in the body over time could contribute to kidney disease in mammals, including humans.
Effects of Microplastic (MP) Exposure at Environmentally Relevant Doses on the Structure, Function, and Transcriptome of the Kidney in Mice
Researchers exposed mice to polystyrene microplastics at doses matching levels found in the environment and examined the effects on kidney structure and function. While the microplastics did not cause obvious physical damage to the kidneys, they altered blood markers of kidney function and changed gene expression patterns related to immune response and metabolism. The study suggests that even low-level microplastic exposure may subtly affect kidney biology at the molecular level.
Microplastic exposure and its consequences for renal and urinary health: systematic review of in vivo studies
This systematic review examines animal studies on how microplastic exposure affects the kidneys and urinary system. The evidence suggests that microplastics can accumulate in kidney tissue and may cause inflammation and oxidative stress, raising concerns about potential long-term effects on human kidney health as our exposure to these particles continues to grow.
Polystyrene microplastics exacerbate experimental chronic kidney disease via inflammatory and oxidative pathways involving NF-κB, ERK/p38 MAPK, and sirtuin-1
Researchers examined the effects of polystyrene microplastics on mice with chronic kidney disease and found that microplastic exposure worsened kidney dysfunction, inflammation, and tissue scarring. Even in healthy mice, microplastics reduced kidney filtration and increased markers of kidney damage. The study suggests that microplastic exposure may aggravate existing kidney conditions through inflammatory and oxidative stress pathways.
Effects of Orally Ingested Microplastics on the Structure and Function of the Kidneys
This study reviewed the structural and functional effects of orally ingested microplastics on kidney tissue, synthesizing experimental evidence from animal and in vitro studies. Microplastic exposure was consistently associated with kidney histopathology including inflammation and fibrosis, with particle size, shape, and polymer type influencing the severity of renal damage.
Microplastics in motion: Genotoxic and redox imbalance impacts of systemic exposure in a murine model
Researchers injected polyethylene microplastics into mice and found the particles accumulated in the blood, liver, and kidneys, with DNA damage detected in peripheral blood. The study revealed complex organ-specific oxidative and nitrosative stress responses, suggesting that systemic microplastic exposure can trigger genotoxicity and disrupt redox balance in multiple tissues.
Polystyrene microplastics facilitate renal fibrosis through accelerating tubular epithelial cell senescence
Mice exposed to polystyrene microplastics at doses relevant to human exposure developed kidney inflammation and scarring (fibrosis) within 28 days. The microplastics caused kidney tube cells to age prematurely, triggering a chain reaction that activated scar-forming cells through a specific signaling pathway. This study provides evidence that microplastic exposure could contribute to chronic kidney damage in people.
The threat of microplastics to human kidney health: Mechanisms of nephrotoxicity and future research directions
This review examines the growing evidence that microplastics can reach and damage human kidneys, where they were first detected in 2023. Short-term exposure triggers oxidative stress and inflammation, while long-term exposure may lead to kidney scarring through a process called ferroptosis, a type of cell death linked to iron buildup. The authors propose that microplastics may also activate the immune system in kidneys through a gut-kidney connection, highlighting that kidney health is an important but overlooked concern in microplastic research.
Kidney and Liver Disorders Due to Microplastic Exposure: Chronic in Vivo Study in Male White Rats
Male white rats were chronically exposed to microplastics (particles 5 mm or smaller) to assess kidney and liver toxicity, with exposure resulting from environmental weathering and ultraviolet irradiation of plastic materials. The study found measurable histopathological and biochemical damage in both organs, confirming that long-term microplastic exposure causes organ-level injury in mammals.
Microplastics and Kidneys: An Update on the Evidence for Deposition of Plastic Microparticles in Human Organs, Tissues and Fluids and Renal Toxicity Concern
This review summarizes the growing evidence that microplastics are found throughout the human body, including in the placenta, lungs, liver, heart, blood, and breast milk. While direct evidence for kidney damage in humans is still lacking, animal studies show that microplastics can cause kidney inflammation, cell death, and oxidative stress. The findings highlight that microplastics are accumulating in virtually every human organ, though the long-term health consequences remain unclear.
Effect of Polystyrene Microplastics Exposure on Blood Parameters in Mice
Researchers exposed mice to polystyrene microplastics in drinking water over four weeks and found increased white blood cell counts, elevated liver enzymes indicating hepatic injury, and altered kidney function markers. The study suggests that subchronic oral microplastic exposure induces inflammatory responses and disrupts liver and kidney function, with no significant recovery observed after a two-week withdrawal period.
Sotagliflozin prevents acute kidney injury by suppressing oxidative stress, inflammation, and apoptosis in renal ischemia/reperfusion rat model
This study found that sotagliflozin, a dual SGLT1/2 inhibitor, protects against acute kidney injury in rats by reducing oxidative stress, inflammation, and cell death in a renal ischemia/reperfusion model. While not directly about microplastics, the study is relevant to understanding kidney protection mechanisms, as microplastics have been detected in kidney tissue and may contribute to renal inflammation.
Effects of microplastics on the kidneys: a narrative review
This review summarizes growing evidence that microplastics can accumulate in the kidneys, where they may trigger inflammation, oxidative stress, and cellular damage that could worsen kidney function. People with chronic kidney disease may be especially vulnerable because impaired kidney filtration could allow microplastics to build up more readily in their bodies.
The Kidney-Related Effects of Polystyrene Microplastics on Human Kidney Proximal Tubular Epithelial Cells HK-2 and Male C57BL/6 Mice
This study found that polystyrene microplastics caused damage to human kidney cells in the lab and accumulated in the kidneys of mice. The microplastics triggered mitochondrial dysfunction, inflammation, and a cellular stress response called autophagy in kidney tissue. These results suggest that long-term microplastic exposure could be a risk factor for kidney disease.
Polystyrene microplastics induce kidney injury via gut barrier dysfunction and C5a/C5aR pathway activation
In a mouse study, polystyrene microplastics caused kidney damage by first breaking down the gut barrier, which then triggered an immune response that attacked the kidneys through a specific pathway called C5a/C5aR. When researchers repaired the gut barrier or blocked this immune pathway, the kidney damage was prevented. This study reveals a gut-kidney connection that could explain how swallowing microplastics might lead to kidney problems in humans.
Chronic exposure to polystyrene microplastics induces renal fibrosis via ferroptosis
Mice exposed to polystyrene microplastics in their drinking water for six months developed kidney scarring (fibrosis) driven by a type of cell death called ferroptosis. The microplastics triggered iron-dependent damage in kidney cells, which then released signals causing surrounding tissue to scar over. This long-term study reveals a new mechanism by which chronic microplastic exposure could lead to progressive kidney disease in humans.
Distribution and toxicity of submicron plastic particles in mice
Researchers found that orally administered submicron-sized microplastics distributed to multiple organs and biofluids in mice over four weeks, causing oxidative stress and inflammation in tissues including the liver, kidneys, and gut.
Microplastics exposure disrupts nephrogenesis and induces renal toxicity in human iPSC-derived kidney organoids
Using human stem cell-derived kidney organoids, researchers showed that microplastic exposure disrupted the formation of key kidney structures during early development. The microplastics triggered oxidative stress, inflammation, and cell death in developing kidney tissue, suggesting that microplastic exposure during pregnancy could potentially interfere with fetal kidney development.
Polystyrene microplastics induced nephrotoxicity associated with oxidative stress, inflammation, and endoplasmic reticulum stress in juvenile rats
This study found that polystyrene microplastics caused kidney damage in young rats through a combination of oxidative stress, inflammation, and a cellular stress response called endoplasmic reticulum stress. The microplastics also reduced body weight growth and affected multiple organs including the heart and ovaries. These findings suggest that microplastic exposure during development could be particularly harmful to kidney health in young, growing organisms.
Micro/nano plastics in the urinary system: Pathways, mechanisms, and health risks.
This review synthesizes emerging evidence on how micro- and nano-plastics reach the urinary system, accumulate in kidney and bladder tissue, and cause damage through oxidative stress, inflammation, and disruption of cellular function. The authors conclude that the urinary system is a primary site of microplastic accumulation and call for more research on long-term health impacts.