Papers

Toxic effects of nanoplastics on biological nitrogen removal in constructed wetlands: Evidence from iron utilization and metabolism

Researchers found that nanoplastics in wastewater disrupt biological nitrogen removal in constructed wetlands by interfering with intracellular iron homeostasis, which cripples the key enzymes and electron transport chains that microbes use for nitrogen metabolism, reducing nitrogen removal efficiency by about 30%.

Polyethylene microplastics induced gut microbiota dysbiosis leading to liver injury via the TLR2/NF-κB/NLRP3 pathway in mice

Mice exposed to polyethylene microplastics developed liver damage that was traced back to disrupted gut bacteria -- the microplastics increased harmful bacteria while decreasing beneficial ones, triggering inflammation through the TLR2/NF-kB/NLRP3 immune pathway. This study provides new evidence that microplastics may harm the liver not just through direct contact, but indirectly by first throwing off the balance of gut bacteria.

Role of biochar toward carbon neutrality

This review examines how biochar, a carbon-rich material made from plant waste, can help fight climate change by reducing greenhouse gas emissions across agriculture, energy, and construction. While not directly about microplastics, biochar is also used as an environmental cleanup tool that can adsorb pollutants from soil and water, including plastic particles.

Migration and remediation of typical contaminants in soil and groundwater: A state of art review

This review covers four major types of soil and groundwater contaminants, including microplastics and PFAS (forever chemicals), examining how they move through the environment and what cleanup methods exist. Understanding how microplastics migrate through soil and water is important because these pathways determine how contamination eventually reaches drinking water sources and affects human health.

Polystyrene-microplastics and DEHP co-exposure induced DNA damage, cell cycle arrest and necroptosis of ovarian granulosa cells in mice by promoting ROS production

Researchers found that co-exposure to polystyrene microplastics and DEHP (a common plastic additive) caused more damage to mouse ovarian cells than either pollutant alone, triggering excessive oxidative stress that led to DNA damage, cell cycle arrest, and cell death. These findings suggest that microplastics combined with their chemical additives may pose a synergistic threat to female reproductive health.

Combined exposure of emamectin benzoate and microplastics induces tight junction disorder, immune disorder and inflammation in carp midgut via lysosome/ROS/ferroptosis pathway

This study found that when carp were exposed to both the pesticide emamectin benzoate and microplastics together, the damage to their gut lining, immune system, and inflammation levels was significantly worse than exposure to either pollutant alone. The findings suggest that microplastics may amplify the harmful effects of pesticides in aquatic food sources, which could have implications for human health through seafood consumption.

Emamectin Benzoate and Microplastics Led to Skeletal Muscle Atrophy in Common Carp via Induced Oxidative Stress, Mitochondrial Dysfunction, and Protein Synthesis and Degradation Imbalance

A study in fish found that combined exposure to the pesticide emamectin benzoate and microplastics caused muscle wasting by triggering oxidative stress, damaging mitochondria (the energy-producing parts of cells), and disrupting the balance between muscle building and breakdown. This suggests that microplastics may worsen the toxic effects of pesticides on muscle health in aquatic organisms.

Microplastics in food: Sources, distribution, health impacts, and regulation

Microplastics induced inflammation and apoptosis via ferroptosis and the NF-κB pathway in carp

Researchers exposed carp to polyethylene microplastics and found they caused serious intestinal damage through two harmful pathways: ferroptosis (a type of iron-dependent cell death) and NF-kB-driven inflammation. The microplastics triggered a buildup of iron and reactive oxygen species in gut tissue, leading to cell death and tissue destruction. Since humans also ingest microplastics that reach the gut, these findings highlight a potential mechanism by which microplastics could damage our digestive system.

Microplastic migration and distribution in the terrestrial and aquatic environments: A threat to biotic safety

This review summarizes how microplastics move through and accumulate in both land and water environments worldwide. Microplastics have been found in nearly every environment on Earth, and they can enter microorganisms, plants, animals, and humans through multiple pathways. The review highlights that despite growing evidence of widespread contamination, researchers still do not fully understand how microplastics of different sizes and shapes migrate and what biological damage they cause.

Microplastics induced endoplasmic reticulum stress to format an inflammation and cell death in hepatocytes of carp (Cyprinus carpio)

Researchers fed carp water containing polystyrene microplastics and found significant liver damage, including inflammation, disrupted cell recycling processes, and cell death. The microplastics triggered a stress response in the cell's protein-folding machinery (endoplasmic reticulum), which set off a chain reaction of inflammation and tissue damage. These findings in freshwater fish suggest that microplastics can cause serious organ damage through specific cellular stress pathways.

Polystyrene microplastics induce endoplasmic reticulum stress, apoptosis and inflammation by disrupting the gut microbiota in carp intestines

Researchers fed carp polystyrene microplastics and found that the particles disrupted their gut bacteria, killing off beneficial species and promoting those linked to diseases. The microplastics triggered a stress response in intestinal cells that led to inflammation, cell death, and tissue damage. Since carp is a widely eaten fish, these gut health effects raise questions about how microplastics in aquatic environments could affect the safety of fish that humans consume.

Exposure to polystyrene microplastics triggers lung injury via targeting toll-like receptor 2 and activation of the NF-κB signal in mice

This mouse study found that inhaling polystyrene microplastics caused serious lung damage, including inflammation, cell death, and scar tissue buildup. Smaller microplastics (1-5 micrometers) caused more harm than larger ones, and the damage worsened with longer exposure. The study identified a specific immune pathway (TLR2/NF-kB) through which inhaled microplastics trigger lung injury, raising concerns about the respiratory effects of airborne microplastics on humans.

Di (2-ethylhexyl) phthalate and polystyrene microplastics co-exposure caused oxidative stress to activate NF-κB/NLRP3 pathway aggravated pyroptosis and inflammation in mouse kidney

When mice were exposed to both polystyrene microplastics and the plasticizer DEHP together, the kidney damage was significantly worse than from either pollutant alone. The combination triggered severe oxidative stress, activated inflammatory pathways, and caused a form of cell death called pyroptosis in kidney tissue. Since microplastics and DEHP frequently occur together in the environment, their combined impact on kidney health deserves serious attention.

Polystyrene microplastics-induced macrophage extracellular traps contributes to liver fibrotic injury by activating ROS/TGF-β/Smad2/3 signaling axis

In a mouse study, polystyrene microplastics caused liver scarring (fibrosis) by triggering immune cells called macrophages to release web-like traps that promoted inflammation. Smaller microplastic particles caused more severe liver damage than larger ones, and the damage involved a specific signaling pathway (ROS/TGF-beta/Smad2/3) that drives tissue scarring. This research reveals a new mechanism by which microplastics may contribute to chronic liver disease.

Polyethylene microplastics induced inflammation via the miR-21/IRAK4/NF-κB axis resulting to endoplasmic reticulum stress and apoptosis in muscle of carp

Researchers found that polyethylene microplastics caused muscle damage in carp through a specific chain reaction: the plastics reduced a protective molecule called miR-21, which activated an inflammatory pathway (NF-kB), leading to stress in the cell's protein-folding machinery and ultimately cell death. This molecular-level finding helps explain how microplastics could damage muscle tissue in fish, with potential implications for the safety of fish consumed by humans.

Intestinal barrier disruption by cadmium and microplastics: Mechanistic insights from integrated metabolomic and proteomic analysis in mice

A mouse study found that combined exposure to cadmium (a toxic metal) and microplastics caused more severe intestinal damage than either pollutant alone. The co-exposure disrupted key metabolic pathways and compromised the gut barrier, potentially promoting cancer cell growth and invasion. Since both cadmium and microplastics are widespread environmental contaminants that humans encounter together, this research highlights the importance of studying how multiple pollutants interact to harm health.

Polystyrene-microplastics and Emamectin Benzoate co-exposure induced lipid remodeling by suppressing PPARα signals to drive ACSL4-dependent ferroptosis and carp splenic injury

Researchers found that carp fish exposed to both polystyrene microplastics and the pesticide Emamectin Benzoate suffered severe spleen damage through a specific cell death process called ferroptosis. The combined exposure was worse than either pollutant alone, disrupting fat metabolism and causing iron-dependent damage to spleen cells. Since microplastics and pesticides often coexist in waterways, this study highlights how their combined effects on fish immune organs could be more dangerous than either pollutant by itself.

Mechanisms of nanoplastic-induced energy metabolism reprogramming in juvenile Sepia esculenta: mRNA profile, miRNA/mRNA network, and ceRNA network

Researchers found that nanoplastics disrupted energy metabolism in juvenile cuttlefish, a popular seafood in China, by suppressing normal energy production pathways and causing oxidative stress. The study used advanced genetic analysis to show how nanoplastics reprogram the way these animals process energy at the molecular level. Since cuttlefish are widely consumed, these effects raise questions about seafood safety in nanoplastic-contaminated waters.

Synthesis of polyvinyl chloride modified magnetic hydrochar for effective removal of Pb(II) and bisphenol A from aqueous phase: performance and mechanism exploration

Scientists created a new material by combining PVC plastic waste with corn straw and iron oxide to make a magnetic filter that can remove lead and bisphenol A from water. The material worked well across a wide range of water conditions and could be reused multiple times. While focused on water cleanup technology, this research shows how recycled plastic waste can be repurposed to help address water contamination, including pollutants often associated with microplastics.

Polystyrene nanoplastics exacerbated lipopolysaccharide‐induced necroptosis and inflammation via the <scp>ROS</scp>/<scp>MAPK</scp> pathway in mice spleen

Researchers found that polystyrene nanoplastics worsened the inflammatory damage caused by bacterial toxins in the spleens of mice. The nanoplastics triggered oxidative stress that activated inflammatory signaling pathways, leading to cell death, and these effects were significantly amplified when nanoplastics were combined with bacterial endotoxin. The study suggests that nanoplastic exposure may compromise the immune system's ability to handle infections and inflammation.

Polystyrene microplastics induce apoptosis and necroptosis in swine testis cells via <scp>ROS</scp>/<scp>MAPK</scp>/<scp>HIF1α</scp> pathway

Researchers exposed swine testis cells to polystyrene microplastics and found that the particles reduced cell viability and triggered both programmed cell death and necroptosis. The damage was driven by excessive production of reactive oxygen species that activated stress signaling pathways. Since pigs are physiologically similar to humans, the findings raise concerns about potential reproductive health effects of microplastic exposure in mammals.

A Practice of Conservation Tillage in the MollisolRegion in Heilongjiang Province of China:A Mini Review

This review summarizes conservation tillage practices in the Mollisol (black soil) region of Heilongjiang Province, China, where intensive farming has caused significant soil degradation. Researchers found that conservation tillage methods like no-till and straw return can help restore soil health, improve microbial diversity, and reduce erosion. The study highlights the importance of sustainable farming practices for protecting one of China's most important agricultural regions.

High-fat diet disrupts the gut microbiome, leading to inflammation, damage to tight junctions, and apoptosis and necrosis in Nyctereutes procyonoides intestines

Researchers found that a high-fat diet disrupted gut bacteria, caused intestinal inflammation, and triggered cell death in the intestines of raccoon dogs. While this study focuses on diet rather than microplastics, the biological pathways it examines, including gut microbiome disruption, inflammation, and damage to the intestinal lining, are the same pathways through which microplastics are known to cause harm. The findings reinforce that a compromised gut may be more vulnerable to additional stressors like microplastic exposure.