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Ambient particulate matter (PM2.5) is a potential risk factor for metabolic damage to the liver. Epidemiological studies suggest that elevated PM2.5 concentrations cause changes in hepatic metabolism, but there is a lack of laboratory evidence. Here, we aimed to evaluate the effects of PM2.5 exposure on liver metabolism in C57BL/6j female mice (10 months old) and to explore the mechanisms underlying metabolic alterations and differential gene expressions by combining metabolomics and transcriptomics analyses. The metabolomics results showed that PM2.5 exposure notably affected the metabolism of amino acids and organic acids and caused hepatic lipid and bile acid accumulation. The transcriptomic analyses revealed that PM2.5 exposure led to a series of metabolic pathway abnormalities, including steroid biosynthesis, steroid hormone biosynthesis, primary bile acid biosynthesis, etc. Among them, the changes in the bile acid pathway might be one of the causes of liver damage in mice. In conclusion, this study clarified the changes in liver metabolism in mice caused by PM2.5 exposure through combined transcriptomic and metabolomic analyses, revealed that abnormal bile acid metabolism is the key regulatory mechanism leading to metabolic-associated fatty liver disease (MAFLD) in mice, and provided laboratory evidence for further clarifying the effects of PM2.5 on body metabolism. [ABSTRACT FROM AUTHOR]

The tremendous potential of graphene quantum dots (gqds) in biomedical applications has raised increasing concerns about their risks to ecosystem and human beings. silicon dioxide nanoparticles (sio2 nps) serve as promising nanofertilizers in enhancing plant tolerance against abiotic stresses, but the knowledge of their role in regulating crop responses to gqd stress is far from sufficient in depth and width. The present work offers insight into the effects of sio2 nps on the root uptake and phytotoxicity of gqds in maize (zea mays L.) seedlings. the addition of sio2 nps significantly decreased the accumulation of gqds in the roots and leaves by 33.3% and 58.8%, respectively. physiologically, the presence of sio2 nps led to substantial enhancement in photosynthesis and antioxidant enzyme activities relative to the plants under the gqds stress. responsive differentially expressed genes were mainly associated with crucial pathways regarding photosynthesis, the mapk signaling pathway in the maize plants, and glutathione metabolism. sio2 nps alleviated the gqds‐induced oxidative stress and helped to re‐establish redox homeostasis by up‐regulating the expression of genes related to antioxidant enzyme activities. these results showed that the root application of sio2 nps alleviated the gqd‐induced inhibition to the photosynthesis and growth of crop plants, which are of great significance for advancing the sustainable utilization of nanofertilizers in agriculture. [ABSTRACT FROM AUTHOR]

Particulate matter of size ≤ 2.5 μm (PM2.5) is a critical environmental threat that considerably contributes to the global disease burden. However, accompanied by the rapid research progress in this field, the existing research on developmental toxicity is still constrained by limited data sources, varying quality, and insufficient in-depth mechanistic analysis. This review includes the currently available epidemiological and laboratory evidence and comprehensively characterizes the adverse effects of PM2.5 on developing individuals in different regions and various pollution sources. In addition, this review explores the effect of PM2.5 exposure to individuals of different ethnicities, genders, and socioeconomic levels on adverse birth outcomes and cardiopulmonary and neurological development. Furthermore, the molecular mechanisms involved in the adverse health effects of PM2.5 primarily encompass transcriptional and translational regulation, oxidative stress, inflammatory response, and epigenetic modulation. The primary findings and novel perspectives regarding the association between public health and PM2.5 were examined, highlighting the need for future studies to explore its sources, composition, and sex-specific effects. Additionally, further research is required to delve deeper into the more intricate underlying mechanisms to effectively prevent or mitigate the harmful effects of air pollution on human health. [ABSTRACT FROM AUTHOR]