聚苯乙烯纳米塑料-植物蛋白冠的形成与特征

为探究聚苯乙烯纳米塑料-植物蛋白冠的形成过程以及蛋白冠的形成对植物可能造成的影响,本研究选用3种平均粒径为200nm不同表面修饰的聚苯乙烯纳米塑料微球和新几内亚凤仙(Impatiens hawkeri)为对象,将3种聚苯乙烯纳米塑料分别与新几内亚凤仙的叶蛋白提取物进行反应,反应时间分别为2、4、8、16、24、36 h。利用扫描电镜(scanning electron microscopy, SEM)观察其形貌变化,原子力显微镜(atomic force microscopy, AFM)进行表面粗糙度测定,使用纳米粒度和zeta电位分析仪测定水合粒径及zeta电位,液相色谱-串联质谱(liquid chromatography-tandem mass spectrometry, LC-MS/MS)鉴定蛋白冠的蛋白成分。从生物学过程、细胞组分以及分子功能3个方面对蛋白进行分类,研究不同表面修饰的纳米塑料对蛋白的吸附选择,探究聚苯乙烯纳米塑料-植物蛋白冠的形成与特征,预测蛋白冠对植物造成的可能影响。结果表明：随着反应时间增加,纳米塑料的形貌变化越发明显,表现为尺寸和粗糙度的增加和稳定性的增...     

Perspectives and challenges of micro/nanoplastics‐induced toxicity with special reference to phytotoxicity

Plastic pollution has become a global concern for ecosystem health and biodiversity conservation. Concentrations of plastics are manifold higher in the terrestrial system than the aquatic one. Micro/nanoplastics (M/NP) have the ability to alter soil enzymatic system, soil properties and also affect soil borne microorganisms and earthworms. Despite, the knowhow regarding modulatory effects of plastics are acquired from the study on aquatic system and reports on their phytotoxic potentials are limited. The presence of cell wall that could restrict M/NP invasion into plant roots might be the putative cause of this limitation. M/NP inhibit plant growth, seed germination and gene expression; and they also induce cytogenotoxicity by aggravating reactive oxygen species generation. Dynamic behavior of cell wall; the pores formed either by cell wall degrading enzymes or by plant–pathogen interactions or by mechanical injury might facilitate the entry of into roots M/NP. This review also provides a possible mechanism of large sized microplastics‐induced phytotoxicity especially for those that cannot pass through cell wall pores. As M/NP affect soil microbial community and soil parameters, it is hypothesized that they could have the potential to affect N₂ fixation and research should be conducted in this direction. Reports on M/NP‐induced toxicity mainly focused only on one polymer type (polystyrene) in spite of the toxicological relevancies of other polymer types like polyethylene, polypropylene etc. So, the assessment of phytotoxic potential of M/NP should be done using other plastic polymers in real environment as they are known to intract with other environmental stressors as well as can alter the the soil–microbe–plant interaction.     

Molecular toxicity of nanoplastics involving in oxidative stress and desoxyribonucleic acid damage

Microplastic pollution attracted extensive attention because of its global presence and adverse effects on ecosystem. However, it is insufficient to clear the effects of nanoplastics on organisms at the molecular level. Herein, a nanopolystyrene (50 nm) was used to examine molecular responses of superoxide dismutase (SOD) and desoxyribonucleic acid (DNA) using spectroscopy (UV‐vis, circular dichroism spectra, and fluorescence measurements) and single cell gel electrophoresis methods. Results showed that nanopolystyrene induced oxidative stress, involving in the increase of SOD activity and malondialdehide (MDA) content, and DNA damage because of the significant increase of olive tail moment, head optical density, and tail DNA percentage in the groups at exposure concentrations above 5 × 10^?6 mol/L. The second structural and microenvironment of aromatic amino acids of SOD were changed with nanopolystyrene exposure. The fluorescence of SOD was quenched by nanopolystyrene at exposure concentration above 1 × 10^?5 mol/L, and the quenching mode could be ascribed to the static type. The results and the combined methods are favorable to explore the molecular toxicity of other nanoplastics and the interaction mechanism.     

Microplastics as an emerging threat to terrestrial ecosystems

Microplastics (plastics <5 mm, including nanoplastics which are <0.1 μm) originate from the fragmentation of large plastic litter or from direct environmental emission. Their potential impacts in terrestrial ecosystems remain largely unexplored despite numerous reported effects on marine organisms. Most plastics arriving in the oceans were produced, used, and often disposed on land. Hence, it is within terrestrial systems that microplastics might first interact with biota eliciting ecologically relevant impacts. This article introduces the pervasive microplastic contamination as a potential agent of global change in terrestrial systems, highlights the physical and chemical nature of the respective observed effects, and discusses the broad toxicity of nanoplastics derived from plastic breakdown. Making relevant links to the fate of microplastics in aquatic continental systems, we here present new insights into the mechanisms of impacts on terrestrial geochemistry, the biophysical environment, and ecotoxicology. Broad changes in continental environments are possible even in particle‐rich habitats such as soils. Furthermore, there is a growing body of evidence indicating that microplastics interact with terrestrial organisms that mediate essential ecosystem services and functions, such as soil dwelling invertebrates, terrestrial fungi, and plant‐pollinators. Therefore, research is needed to clarify the terrestrial fate and effects of microplastics. We suggest that due to the widespread presence, environmental persistence, and various interactions with continental biota, microplastic pollution might represent an emerging global change threat to terrestrial ecosystems.     

Oral feeding of nanoplastics affects brain function of mice by inducing macrophage IL-1 signal in the intestine

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Polystyrene nanoplastics aggravates lipopolysaccharide-induced apoptosis in mouse kidney cells by regulating IRE1/XBP1 endoplasmic reticulum stress pathway via oxidative stress

Nanoplastics (NPs) pollution poses a huge threat to the ecosystem and has become one of the environmental pollutants that have attracted much attention. There is increasing evidence that both oxidative stress and endoplasmic reticulum stress (ERS) are associated with polystyrene nanoplastics (PS-NPs) exposure. Lipopolysaccharide (LPS) has been shown to induce apoptotic damage in various tissues, but whether PS-NPs can aggravate LPS-induced apoptosis in mouse kidneys through oxidative stress-regulated inositol-requiring enzyme 1 (IRE1)/X-box binding protein 1 (XBP1) ERS pathway remains unclear. In this study, based on the establishment of in vitro and in vivo PS-NPs and LPS exposure models alone and in combination in mice and HEK293 cells, the effects and mechanisms of PS-NPs on LPS-induced renal cell apoptosis were investigated. The results showed that PS-NPs could aggravate LPS-induced apoptosis. PS-NPs/LPS can induce ERS through oxidative stress, activate the IRE1/XBP1 pathway, and promote the expression of apoptosis markers (Caspase-3 and Caspase-12). Kidney oxidative stress, ERS, and apoptosis in PS-NPs + LPS combined exposure group were more severe than those in the single exposure group. Interestingly, 4-phenylbutyric acid-treated HEK293 cells inhibited the expression of the IRE1/XBP1 ERS pathway and apoptotic factors in the PS-NPs + LPS combined exposure group. N-acetyl-L-cysteine effectively blocked the activation of the IRE1/XBP1 ERS pathway, suggesting that PS-NPs-induced oxidative stress is an early event that triggers ERS. Collectively, these results confirmed that PS-NPs aggravated LPS-induced apoptosis through the oxidative stress-induced IRE1/XBP1 ERS pathway. Our study provides new insights into the health threats of PS-NPs exposed to mammals and humans.