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61,005 resultsShowing papers similar to Synergistic kidney toxicity of polylactic acid nanoplastics and Cr(VI): Ferroptosis aggravated by mitophagy
ClearCo-exposure to environmentally relevant concentrations of cadmium and polystyrene nanoplastics induced oxidative stress, ferroptosis and excessive mitophagy in mice kidney
A mouse study found that combined exposure to cadmium (a toxic metal) and polystyrene nanoplastics caused more kidney damage than either pollutant alone. The combination triggered a harmful chain reaction involving oxidative stress, iron buildup, and excessive breakdown of cellular energy factories called mitochondria. This is significant because people are often exposed to both nanoplastics and heavy metals simultaneously, and their combined effects may be worse than expected.
Iron's silent betrayal: Ferritinophagy-driven mitochondrial damage mediates polylactic acid nanoplastics and Cr(VI)-induced cardiac injury
Researchers found that co-exposure of mice to biodegradable polylactic acid nanoplastics and hexavalent chromium causes synergistic cardiac injury by inducing ferritinophagy — a process where cells break down iron-storage proteins — triggering iron overload and excess mitochondrial reactive oxygen species that damage heart tissue.
Combined exposure to polystyrene nanoplastics and bisphenol A results in mitochondrial damage and ferroptosis via the PI3K-AKT signaling pathway in mice kidneys
Researchers exposed mice to polystyrene nanoplastics combined with bisphenol A for six weeks and found that co-exposure caused significant kidney damage through mitochondrial dysfunction and a form of cell death called ferroptosis. The combined exposure was more harmful than either contaminant alone, operating through the PI3K-AKT signaling pathway. The findings suggest that nanoplastics acting as carriers for co-pollutants like BPA may amplify toxic effects on kidney tissue.
Ferroptosis and hepatic fibrosis induced by cooperative exposure to polylactic acid nanoplastics and copper: Emphasis on gut microbiota dysbiosis
Researchers investigated the combined hepatotoxicity of polylactic acid nanoplastics and copper in mice, focusing on the gut-liver axis. The study found that co-exposure caused synergistic liver damage through ferroptosis, characterized by disrupted glutathione and iron homeostasis, along with gut microbiota dysbiosis and hepatic fibrosis more severe than either pollutant alone.
Polystyrene microplastics modulation of hexavalent chromium toxicity in quails: transcriptomic and toxicological insights
Researchers exposed quails to both polystyrene microplastics and hexavalent chromium — a cancer-causing heavy metal — for 12 weeks, finding that microplastics worsened the kidney damage caused by chromium by disrupting fat metabolism and energy production. The combination triggered severe kidney scarring (fibrosis) that neither pollutant caused as strongly on its own, illustrating how microplastics can amplify the toxicity of other environmental contaminants.
Co-exposure of arsenic and polystyrene-nanoplastics induced kidney injury by disrupting mitochondrial homeostasis and mtROS-mediated ferritinophagy and ferroptosis
Researchers found that arsenic and polystyrene nanoplastics together — but not separately — cause kidney fibrosis in mice by disrupting mitochondrial function and triggering a form of iron-dependent cell death called ferroptosis, with mitochondria-targeted antioxidants significantly reducing the combined damage.
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.
Novel insights into male reproductive toxicity: autophagy-dependent ferroptosis triggered by polylactic acid nanoplastics and copper sulfate
Researchers exposed mice to polylactic acid nanoplastics combined with copper sulfate and found that the combination caused significant testicular damage through a process linking autophagy to ferroptosis, a form of iron-dependent cell death. The combined exposure was more damaging than either substance alone, disrupting sperm production and testicular tissue structure. The study suggests that nanoplastics from biodegradable plastics may amplify the reproductive toxicity of environmental heavy metals.
Microplastics and nanoplastics co-exposure modulates chromium bioaccumulation and physiological responses in rats
Rats exposed to a mix of microplastics and nanoplastics along with hexavalent chromium, a toxic heavy metal, accumulated significantly more chromium in their liver, heart, brain, and skin than rats exposed to chromium alone. This shows that plastic particles can act as carriers that increase the amount of toxic metals absorbed by the body, potentially amplifying the health risks of metal pollution.
Single and joint exposure to nanoplastics and bisphenols: a comparative assessment of in vitro hazards
This study compared the individual and combined toxicity of nanoplastics and bisphenol compounds in biological test systems, finding synergistic effects at certain exposure combinations. The results indicate that co-exposure to these two common plastic-associated contaminants may be more harmful than either alone.
Amplified toxic effects of nanoplastic composite norfloxacin on liver cells in mice: Mechanistic insights and multiscale evaluation
Researchers examined the combined toxic effects of nanoplastics and the antibiotic norfloxacin on mouse liver cells and found that co-exposure was significantly more harmful than either contaminant alone. The nanoplastics acted as carriers that increased antibiotic accumulation inside cells, amplifying oxidative damage and disrupting key protective enzymes. The study highlights that nanoplastics in the environment can worsen the toxicity of co-occurring pollutants like antibiotics.
Combined effect of arsenic and polystyrene-nanoplastics at environmentally relevant concentrations in mice liver: Activation of apoptosis, pyroptosis and excessive autophagy
Researchers investigated the combined toxic effects of arsenic and polystyrene nanoplastics on mouse liver at environmentally relevant concentrations. The study found that co-exposure activated multiple cell death pathways including apoptosis, pyroptosis, and excessive autophagy in liver tissue, suggesting that the interaction between nanoplastics and heavy metals may amplify liver damage.
Implication of ferroptosis in hepatic toxicity upon single or combined exposure to polystyrene microplastics and cadmium
This study found that polystyrene microplastics combined with cadmium caused more severe liver damage in mice than either pollutant alone. The microplastics absorbed cadmium on their surface, increasing the amount of the toxic metal delivered to liver cells, and triggered a type of cell death called ferroptosis. This is concerning because microplastics in the environment commonly carry heavy metals, meaning the combined exposure people face may be more harmful than we thought.
Combined effects of nanoplastics and 3-BHA at environmentally relevant concentrations significantly aggravated kidney injury via TGF-β/SMAD signaling pathway in mice
Researchers investigated combined exposure to nanoplastics and the synthetic antioxidant 3-BHA at environmentally relevant concentrations, finding that the combination caused greater disruption to renal function than either contaminant alone, suggesting synergistic kidney toxicity.
Potential Toxicity in Crucian Carp Following Exposure to Metallic Nanoparticles of Copper, Chromium, and Their Mixtures: A Comparative Study
Copper and chromium nanoparticles were tested for toxicity in crucian carp, finding that mixtures of the two metals caused more harm than either alone. While focused on metal nanoparticles rather than nanoplastics, the findings are relevant because metals commonly attach to the surface of microplastics in water.
Understanding the mechanistic roles of microplastics combined with heavy metals in regulating ferroptosis: Adding new paradigms regarding the links with diseases
This review explores the emerging connection between microplastics combined with heavy metals and a type of cell death called ferroptosis, which involves iron-dependent damage to cell membranes. Researchers found that both microplastics and heavy metals can independently trigger ferroptosis, and their combined presence may amplify this effect in organs like the liver, kidneys, and brain. The study suggests that understanding this cell death pathway could provide new insights into how environmental pollutant mixtures contribute to disease.
Polystyrene nanoplastics exacerbate gentamicin-induced nephrotoxicity in adult rat by activating oxidative stress, inflammation and apoptosis pathways
Researchers co-exposed rats to polystyrene nanoplastics and the antibiotic gentamicin and found that the combination caused significantly greater kidney damage than either substance alone, amplifying oxidative stress, inflammation, and mitochondrial apoptosis in a synergistic manner.
Maternal Exposure to Combined Cadmium and Polystyrene Nanoplastics Induces Offspring Testicular Dysplasia via Mitochondrial Reactive Oxygen Species Overactivating the Peroxisome Proliferator-Activated Receptor α-Mediated Autophagy Signaling Pathway
Researchers investigated the combined effects of maternal exposure to polystyrene nanoplastics and cadmium on offspring in a mouse model. The study found that co-exposure caused testicular developmental abnormalities in offspring through mitochondrial oxidative stress and disrupted autophagy signaling, suggesting that nanoplastics may amplify the reproductive toxicity of co-occurring environmental contaminants.
Synergistic effect of PS-MPs and Cd on male reproductive toxicity: Ferroptosis via Keap1-Nrf2 pathway
A mouse study found that microplastics and the heavy metal cadmium work together to cause more severe damage to male reproductive organs than either pollutant alone. The combination triggered a form of cell death called ferroptosis by disrupting a key protective pathway in the body. This is the first study to show this synergistic reproductive harm, suggesting that microplastics can make other environmental toxins more dangerous.
Synergistic effects of PS-NPs and Cd on ovarian toxicity in adolescent rats: Ferroptosis by induction of mitochondrial redox imbalance via the SIRT3-SOD2/Gpx4 pathway
Researchers studied the combined effects of polystyrene nanoplastics and cadmium on the ovaries of adolescent rats over 28 days. They found that co-exposure was significantly more harmful than either pollutant alone, causing damage to ovarian structure and hormone disruption through a process called ferroptosis triggered by mitochondrial oxidative stress. The study suggests that nanoplastics may act as a carrier that amplifies heavy metal toxicity to the reproductive system during critical developmental periods.
Toxicological interactions of microplastics/nanoplastics and environmental contaminants: Current knowledge and future perspectives
This review examines how the combined presence of micro- and nanoplastics with other environmental contaminants like heavy metals, pesticides, and pharmaceuticals affects toxicity. Researchers found that plastic particles can alter the bioavailability and toxic effects of co-occurring pollutants, sometimes increasing harm to organisms, which complicates environmental risk assessment.
Synergistic Toxicity of Combined Exposure to Acrylamide and Polystyrene Nanoplastics on the Gut–Liver Axis in Mice
Researchers exposed mice to a combination of acrylamide, a common food processing byproduct, and polystyrene nanoplastics through drinking water and found that the combined exposure caused more severe gut and liver damage than either substance alone. The co-exposure disrupted gut barrier integrity, altered gut bacteria composition, and caused widespread metabolic changes. The study suggests that the interaction between nanoplastics and other food contaminants may amplify health risks beyond what each poses individually.
Single and combined toxicity of amino-functionalized polystyrene nanoparticles with potassium dichromate and copper sulfate on brine shrimp Artemia franciscana larvae
Researchers tested the acute toxicity of amino-functionalized polystyrene nanoplastics on brine shrimp (Artemia franciscana) larvae alone and in combination with heavy metal toxicants, finding that nanoplastics generally enhanced the toxicity of chromium and copper co-exposures, demonstrating that realistic multi-contaminant scenarios pose greater risk to zooplankton than single-chemical assessments suggest.
Synergistic toxicity of PFAS and microplastic mixtures across five human cell lines
Researchers tested the combined toxicity of PFAS chemicals and microplastics on five types of human cells representing the kidney, liver, prostate, skin, and lung. They found that mixtures of these common environmental contaminants produced synergistic harmful effects, particularly in kidney and liver cells, including increased oxidative stress and DNA damage. The study suggests that the combined exposure to PFAS and microplastics, which frequently co-occur in the environment, may pose greater health risks than either pollutant alone.