Micro- and Nanoplastics Exposure and Effects on Embryonic Development and Larval Behavior of Zebrafish.

Nanoplastic exposure alters oxidative stress, immunity, and digestive function in Pinctada fucata martensii.

Objective: To investigate the effects of polystyrene nanoplastics (PS-NPs) exposure during gestation on the growth and neurotoxicity of fetal rats. Methods: Twenty-seven SD pregnant rats were randomly divided into 9 groups with three rats in each group. The experimental group of PS-NPs was given 0.5, 2.5, 10 and 50 mg/kg of PS-NPs suspension with different particle sizes (25 and 50 nm) by gavage, wihe the control group was given ultrapure water by gavage. The time of gavage is from the 1st to the 18th day of pregnancy. The morphological changes of the placenta were observed; compare the number of male and female fetuses, live/dead/absorbed fetuses, body weight, body length, placental weight, and organ coefficients of kidney, liver, brain and intestine of fetal rats; the prefrontal cortex, hippocampus and striatum of the fetal rats were taken to measure related biochemical indicators. Results: Compared with the control group, the placenta of the PS-NPs exposed group was found to have structural damage, which increased in a dose-dependent manner. The area ratio of trophoblast was significantly increased (P＜0.05), and the area ratio of labyrinth was significantly decreased (P＜0.05); In the prefrontal cortex, hippocampus and striatum of fetal rats, the levels of IL-1β, IL -6 and TNF-α were significantly increased in the 10 and 50 mg/kg PS-NPs exposed group (P＜0.05), and more significantly elevated in the 25 nm group than those in the 50 nm group at 10 mg/kg exposure (P＜0.05) the CAT activity was significantly decreased in 2.5, 10 and 50 mg/kg PS-NPs exposure groups (P＜0.05), while the SOD and GSH-Px activities were significantly decreased in 25 nm exposure groups and 2.5, 10 and 50 mg/kg 50 nm PS-NPs exposure groups (P＜0.05), the MDA content was significantly increased in 10, 50 mg/kg 25 nm PS-NPs exposure groups and 50 mg/kg 50 nm PS-NPs exposure groups (P＜0.05). Conclusion: Maternal PS-NPs exposure during gestation may affect the growth and development of fetal rats by damaging the placental barrier and produce neurotoxicity in fetal rats, causing oxidative stress and inflammatory responses in various brain regions, and smaller particle sizes and higher doses of polystyrene nanoplastic exposure have more significant neurotoxic effects on the offspring.

Impact and microbial mechanism of continuous nanoplastics exposure on the urban wastewater treatment process

An important disadvantage of plastics is their fragmentation into smaller particles, classi-fied according to size as microplastics and nanoplastics. These plastic particles persist for extended periods in aerial, terrestrial, and aquatic ecosystems and can be incorporated into animal bodies through various routes, including inhalation, dermal contact, and the food chain. The accumulation of these debris generates toxicity on several organs, including the nervous system. In this review article, I will cover the detrimental consequences of plastic exposure on the nervous system, the impact of microplastics and nanoplastics on the gen-esis of neurons both in the embryonic period as well as in adulthood, and the reliability of 5-bromo-2’-deoxyuridine (BrdU) labeling as a tool to analyze the effect of microplastic and nanoplastic exposure on the proliferative behavior of neuronal precursors. BrdU is a marker of DNA synthesis. It is widely used to identify proliferating neuroblasts and follow their fate during embryonic, perinatal, and adult neurogenesis. However, the use of BrdU labeling for analyzing neurogenesis may be inaccurate due to pitfalls and limitations. This is because BrdU exposure can induce apoptosis, cellular senescence, and alterations in DNA methylation. Interestingly, these cellular events also occur following exposure to plastic particles.

An important disadvantage of plastics is their fragmentation into smaller particles, classified according to size as microplastics and nanoplastics. These plastic particles persist for extended periods in aerial, terrestrial, and aquatic ecosystems and can be incorporated into animal bodies through various routes, including inhalation, dermal contact, and the food chain. The accumulation of these debris generates toxicity on several organs, including the nervous system. In this review article, I will cover the detrimental consequences of plastic exposure on the nervous system, the impact of microplastics and nanoplastics on the genesis of neurons both in the embryonic period as well as in adulthood, and the reliability of 5-bromo-2′-deoxyuridine (BrdU) labeling as a tool to analyze the effect of microplastic and nanoplastic exposure on the proliferative behavior of neuronal precursors. BrdU is a marker of DNA synthesis. It is widely used to identify proliferating neuroblasts and follow their fate during embryonic, perinatal, and adult neurogenesis. However, the use of BrdU labeling for analyzing neurogenesis may be inaccurate due to pitfalls and limitations. This is because BrdU exposure can induce apoptosis, cellular senescence, and alterations in DNA methylation. Interestingly, these cellular events also occur following exposure to plastic particles.

Airborne nanoplastics can enter alveolar cells and trigger intracellular oxidative stress primarily. Herein, taking advantage of the high electrochemical resolution of SiC@Pt nanoelectrodes, we achieved the quantitative discrimination of the major ROS/RNS within A549 cells, disclosed the sources of their precursors, and observed that the NO (RNS precursor) level significantly increased, whereas O2˙- (ROS precursor) remained relatively stable during the nanoplastics exposure. This establishes that iNOS or mitochondrion-targeted treatment may be a preventive or therapeutic strategy for nanoplastic-induced lung injury.

Nanoplastic exposure induces mitochondrial dysfunction-driven inflammation and senescence in renal tubular epithelial cells.

Adverse adult-onset and multigenerational effects in zebrafish (Danio rerio) developmentally exposed to polystyrene nanoplastics.

The widespread accumulationof nanoplastics is a growingconcernfor the environmental and human health. However, studies on the mechanismsof nanoplastic-induced developmental toxicity are still limited. Here,we systematically investigated the potential biological roles of nanoplasticexposure in zebrafish during the early developmental stage. The zebrafishembryos were subjected to exposure to 100 nm polystyrene nanoplasticswith different concentrations (0, 100, 200, and 400 mg/L). The resultsindicated that nanoplastic exposure could decrease the hatching andsurvival rates of zebrafish embryos. In addition, the developmentaltoxicity test indicated that nanoplastic exposure exhibits developmentaltoxicity via the inhibition of the heart rate and body length in zebrafishembryos. Besides, behavioral activity was also significantly suppressedafter 96 h of nanoplastic exposure in zebrafish larvae. Further biochemicalassays revealed that nanoplastic-induced activation of the oxidativestress responses, including reactive oxygen species accumulation andenhanced superoxide dismutase and catalase activities, might affectdevelopmental toxicity in zebrafish embryos. Furthermore, a quantitativepolymerase chain reaction assay demonstrated that the mRNA levelsof the base excision repair (BER) pathway-related genes, including lig1, lig3, polb, parp1, pold, fen1, nthl1, apex, xrcc1, and ogg1, were altered in zebrafish embryos for 24 h after nanoplasticexposure, indicating that the activation of the BER pathway wouldbe stimulated after nanoplastic exposure in zebrafish embryos. Therefore,our findings illustrated that nanoplastics could induce developmentaltoxicity through activation of the oxidative stress response and BERpathways in zebrafish.

Chronic nanoplastic exposure induced oxidative and immune stress in medaka gonad

Polystyrene nanoplastics impact the bioenergetics of developing zebrafish and limit molecular and physiological adaptive responses to acute temperature stress.

Temperature shapes the response of marine nitrogen-fixing cyanobacteria to nanoplastics.

Plastic debris in the global biosphere is an increasing concern, and nanoplastic (NPs) toxicity in humans is far from being understood. Studies have indicated that NPs can affect mitochondria, but the underlying mechanisms remain unclear. The liver and lungs have important metabolic functions and are vulnerable to NP exposure. In this study, we investigated the effects of 80 nm NPs on mitochondrial functions and metabolic pathways in normal human hepatic (L02) cells and lung (BEAS-2B) cells. NP exposure did not induce mass cell death; however, transmission electron microscopy analysis showed that the NPs could enter the cells and cause mitochondrial damage, as evidenced by overproduction of mitochondrial reactive oxygen species, alterations in the mitochondrial membrane potential, and suppression of mitochondrial respiration. These alterations were observed at NP concentrations as low as 0.0125 mg/mL, which might be comparable to the environmental levels. Nontarget metabolomics confirmed that the most significantly impacted processes were mitochondrial-related. The metabolic function of L02 cells was more vulnerable to NP exposure than that of BEAS-2B cells, especially at low NP concentrations. This study identifies NP-induced mitochondrial dysfunction and metabolic toxicity pathways in target human cells, providing insight into the possibility of adverse outcomes in human health.

Mechanistic insight into the intensification of arsenic toxicity to rice (Oryza sativa L.) by nanoplastic: Phytohormone and glutathione metabolism modulation

Nanoplastic (NP) pollution has emerged as a growing concern due to its potential impact on human health, although its adverse effects on different organ systems are not yet fully understood. This systematic scoping review, conducted in accordance with international guidelines, aimed to map the current evidence on the biological effects of NPs. In vitro animal studies assessing cellular damage caused by exposure to any type of NP were searched on PubMed, Web of Science, and Scopus. Data on primary outcomes related to genotoxicity and cytotoxicity (cell viability, oxidative stress, inflammation, DNA and cytoplasmic damage, apoptosis) were extracted from the included studies, and overall reporting quality was assessed. A total of 108 articles published between 2018 and 2024, mostly by China (54%), Spain (14%), and Italy (9%), were included. Polystyrene (PS) was the most frequently studied polymer (85%). NP sizes in solution ranged from 15 to 531 nm, with a higher prevalence in the 40-100 nm range (38%). The overall quality of studies was rated as moderate (60%), with many lacking essential details about cell culture conditions (e.g., pH of the medium, passage number, substances used). A higher frequency of negative effects from NP exposure was observed in respiratory cell lines, while immune, digestive, and hepatic cell lines showed greater resistance. Nervous, urinary, and connective tissue systems were impacted by NPs. Positively charged and smaller PS particles were consistently associated with higher toxicity across all systems. In summary, this review highlights the multifactorial nature of NP toxicity, influenced by size, surface charge, and polymer type. It also reveals a significant knowledge gap, stemming from the predominant use of immortalized monocultures exposed to commercially available PS NPs, the limited use of environmentally relevant particles, and the underutilization of advanced experimental models (e.g., organ-on-chip systems) that better mimic physiological conditions.