The COVID-19 pandemic has further intensified plastic pollution due to the escalated use of single-use gloves and masks, consequently leading to the widespread presence of microplastics (MPs) and nanoplastics (NPs) in major rivers and lakes worldwide. Macrobrachium rosenbergii has become an important experimental subject due to its ecological role and environmental sensitivity. In this study, we sought to comprehend the ramifications of NPs on the widely-distributed freshwater prawn, M rosenbergii, by conducting a detailed analysis of its responses to NPs after both 96 h and 30 days of exposure. The transcriptome analysis revealed 918 differentially expressed unigenes (DEGs) after 30 days of NPs exposure (356 upregulated, 562 downregulated) and 2376 DEGs after 96 h of NPs exposure (1541 upregulated, 835 downregulated). The results of DEGs expression indicated that acute NPs exposure enhanced carbohydrate transport and metabolism, fostering chitin and extracellular matrix processes. In contrast, chronic NPs exposure induced nucleolar stress in M. rosenbergii, impeding ribosome development and mRNA maturation while showing no significant changes in glucose metabolism. Our findings underscore the M. rosenbergii distinct coping mechanisms during acute and chronic NPs exposure, elucidating its vital adaptive strategies. These results contribute to our understanding of the ecological implications of NPs pollution and its impact on aquatic animals.
With the widespread use of plastic products, microplastics and nanoplastics have emerged as prevalent pollutants in coastal aquatic ecosystems. Parasesarma pictum, a common estuarine crab species, was selected as a model organism. P. pictum was exposed to polystyrene (PS) particles of sizes 80 nm (80PS), 500 nm (500PS), and 1000 nm (1000PS), as well as to clean seawater (CK) for 21 days. Histological and fluorescent staining results showed that PS particles of all three sizes induced hepatopancreatic nuclear pyknosis, cell junction damage, and necrosis. The degree of damage was observed as 1000PS > 80PS > 500PS. Transcriptomic analysis revealed that major differentially expressed genes (DEGs) were associated with cellular processes, membrane components, and catalytic activity. The respiratory chain disruptions and immune exhaustion induced by 1000PS were notably stronger than those by 80PS and 500PS. Additionally, necrosis caused hepatopancreas injury in P. pictum rather than apoptosis or autophagy after long-term PS particle exposure. Furthermore, PS particles of all three sizes inhibited innate immunity, while the complement pathway was not significantly affected in the 80PS group. This study elucidated potential distinctions in how plastic particles of varying sizes (nanoplastics, microplastics, and micro/nanoplastics) impact P. pictum, providing a reference for toxicological mechanism research on microplastics and nanoplastics in aquatic organisms. Future research should focus on exploring long-term effects and potential mitigation strategies for microplastics and nanoplastics of more types and a wider range of particle size pollution in aquatic environments.
Plastics are widely produced for industrial and domestic applications due to their unique properties, and studies on the toxic effects of nanoplastics (NPs) on aquatic animals are essential. In this study, we investigated the transcriptomic patterns of Litopenaeus vannamei after NPs exposure. We found that the lysosome pathway was activated when after NPs exposure, with up-regulated DEGs, including glucocerebrosidase (GBA), hexosaminidase A (HEXA), sphingomyelin phosphodiesterase-1 (SMPD1), and solute carrier family 17 member 5 (SLC17A5). In addition, the PI3K-Akt signaling pathway was strongly affected by NPs, and the upstream genes of PI3K-Akt, including epidermal growth factor receptor (EGFR), integrin subunit beta 1 (ITGB1) and heat shock protein 90 (HSP90) were up-regulation. Other genes involved in lipogenesis, such as sterol regulatory element binding transcription factor 1 (SREBP-1c), fatty acid synthase (FASN) and stearoyl-CoA desaturase (SCD-1), were down-regulated. However, the contents of triglycerides (TG) and total cholesterol (TCH) in L. vanname hepatopancreas were reduced, which indicated that the ingestion of NPs led to the disturbance of hepatic lipid metabolism. What more, NPs treatment of L. vannamei also caused oxidative stress. In addition, NPs can damage part of the tissue structure and affect the physiological function of shrimps. The results of this study provide valuable ecotoxicological data to improve the understanding of the biological fate and effects of nanoplastics in L. vannamei.
Plastic pollution pervades both marine and terrestrial ecosystems, fragmenting over time into microplastics (MPs) and nano-plastics (NPs). These particles infiltrate organisms via ingestion, inhalation, and dermal absorption, predominantly through the trophic interactions. This review elucidated the impacts of MPs/NPs on the reproductive viability of various species. MPs/NPs lead to reduced reproduction rates, abnormal larval development and increased mortality in aquatic invertebrates. Microplastics cause hormone secretion disorders and gonadal tissue damage in fish. In addition, the fertilization rate of eggs is reduced, and the larval deformity rate and mortality rate are increased. Male mammals exposed to MPs/NPs exhibit testicular anomalies, compromised sperm health, endocrine disturbances, oxidative stress, inflammation, and granulocyte apoptosis. In female mammals, including humans, exposure culminates in ovarian and uterine deformities, endocrine imbalances, oxidative stress, inflammation, granulosa cell apoptosis, and tissue fibrogenesis. Rodent offspring exposed to MPs experience increased mortality rates, while survivors display metabolic perturbations, reproductive anomalies, and weakened immunity. These challenges are intrinsically linked to the transgenerational conveyance of MPs. The ubiquity of MPs/NPs threatens biodiversity and, crucially, jeopardizes human reproductive health. The current findings underscore the exigency for comprehensive research and proactive interventions to ameliorate the implications of these pollutants.
The extensive use of plastic products has exacerbated micro/nanoplastic (MPs/NPs) pollution in the atmosphere, increasing the incidence of respiratory diseases and lung cancer. This study investigates the uptake and cytotoxicity mechanisms of polystyrene (PS) NPs in human lung epithelial cells. Transcriptional analysis revealed significant changes in cell adhesion pathways following PS-NPs exposure. Integrin α5β1-mediated endocytosis was identified as a key promoter of PS-NPs entry into lung epithelial cells. Overexpression of integrin α5β1 enhanced PS-NPs internalization, exacerbating mitochondrial Ca2+ dysfunction and depolarization, which induced reactive oxygen species (ROS) production. Mitochondrial dysfunction triggered by PS-NPs led to oxidative damage, inflammation, DNA damage, and necrosis, contributing to lung diseases. This study elucidates the molecular mechanism by which integrin α5β1 facilitates PS-NPs internalization and enhances its cytotoxicity, offering new insights into potential therapeutic targets for microplastic-induced lung diseases.