Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 4 de 4
Filtrar
Mais filtros










Intervalo de ano de publicação
1.
J Hazard Mater ; 460: 132422, 2023 10 15.
Artigo em Inglês | MEDLINE | ID: mdl-37657322

RESUMO

At present, most ecotoxicological studies are still confined to focusing on the harmful effects of biochar itself on soil fauna. However, the potential ecotoxicity of different components separated from biochar to terrestrial invertebrates remains poorly understood. In this study, the dissolved matter (DM) and particulate matter (PM) were separated from biochar (BC) and then introduced into the soil-earthworm system to investigate the response mechanism of earthworms at the molecular level. The results showed that BC and DM exposure caused an increase in the abundance of Proteobacteria in the cast bacterial community, suggesting the dysbiosis of intestinal microbiota. It was also observed that the cast bacterial communities were more sensitive to DM exposure than PM exposure. Transcriptomic analysis showed that BC and DM exposure induced significant enrichment of functional pathways related to infectious and neuropathic diseases. Metabolomic profiling manifested that DM exposure caused metabolic dysfunction, antioxidant and detoxification abilities recession. Furthermore, significant differences in the responses of earthworms at transcriptomic and metabolic levels confirmed that DM exhibited greater ecotoxicity than PM. This study highlighted the significant contributions of dissolved matter to the ecotoxicity of biochar from the perspective of transcriptomic and metabolomic profiles.


Assuntos
Microbiota , Oligoquetos , Animais , Multiômica , Material Particulado/toxicidade , Solo
2.
Front Public Health ; 10: 959921, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36518583

RESUMO

The harmful effects of air pollution can cause various diseases. Most research on the hazards of air pollution focuses on lung and cardiovascular diseases. In contrast, the impact of air pollution on neurological disorders is not widely recognized. Air pollution can cause various neurological conditions and diseases, such as neural inflammation, neurodegeneration, and cerebrovascular barrier disorder; however, the mechanisms underlying the neurological diseases induced by various components of air pollutants remain unclear. The present paper summarizes the effects of different components of air pollutants, including particulate matter, ozone, sulfur oxides, carbon oxides, nitrogen oxides, and heavy metals, on the nervous system and describes the impact of various air pollutants on neurological disorders, providing ideas for follow-up research.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Doenças do Sistema Nervoso , Humanos , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Exposição Ambiental/efeitos adversos , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Material Particulado/efeitos adversos , Material Particulado/análise , Doenças do Sistema Nervoso/etiologia
3.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-846247

RESUMO

Objective: To analyze and identify the significant different components between Cordyceps hawkesii and Cordyceps sinensis by using method of ultra performance liquid chromatography quadrupole time of flight mass spectrometry (UPLC-Q-TOF-MS). Methods: Mass spectrometry combined with formula finder of PeakView software and database (Human Metabolome Database, Pub Chem, Metlin) and secondary fragmentation analysis, significant different components were identified and analyzed. Results: Through OPLS-DA analysis, it was found that 12 significant different components were identified. Eleven of them were amino acids and their metabolites, and one was phosphatidylcholine. Conclusion: Surprisingly, characteristic components such as cordycepin and adenosine were not identified by significant difference analysis. In this study, it was proved that C. hawkesii can be used as a supplementary resource instead of C. sinensis, which provided scientific support for the further development and utilization of C. hawkesii.

4.
Artigo em Inglês | MEDLINE | ID: mdl-31010106

RESUMO

Background: Studies have found that exposure to fine particulate matter with sizes below 2.5 µm (PM2.5) might cause inflammation response via the NF-κB pathway. To date, only a few studies have focused on the toxicity of different components of PM2.5. We aimed to explore the effects of PM2.5 with different components on the expression levels of NF-κB family gene mRNA and inflammatory molecules in human macrophages. Methods: Human monocytic cell line THP-1-derived macrophages were exposed to water-soluble (W-PM2.5), fat-soluble (F-PM2.5), and insoluble (I-PM2.5) PM2.5. The cell survival rate was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The levels of inflammatory molecules were determined by enzyme-linked immunosorbent assay (ELISA), and the relative mRNA levels of the NF-κB family gene were determined by real time PCR. Results: PM2.5 could decrease the cell viability. After exposure to W-PM2.5, the levels of interleukins (IL)-1ß and IL-12 p70 significantly increased. After exposure to F-PM2.5, the levels of IL-12 p70 significantly increased. The levels of IL-12 p70 and TNF-α after exposure to I-PM2.5 were significantly higher than that in W- and F-PM2.5 treatment groups. The levels of IL-8, C reactive protein (CRP), and cyclooxygenase (COX)-2 increased only after exposure to I-PM2.5. F-PM2.5 increased the mRNA levels of NF-κB genes, especially NF-κB1 and RelA. Conclusions: PM2.5 can decrease the cell survival rate and up-regulate the expression of NF-κB family gene mRNA and inflammatory molecules. The main toxic components of PM2.5 related to inflammatory response in macrophages were the I-PM2.5.


Assuntos
Mediadores da Inflamação/metabolismo , Interleucina-1beta/metabolismo , Macrófagos/efeitos dos fármacos , NF-kappa B/genética , Material Particulado/toxicidade , RNA Mensageiro/metabolismo , Fator de Necrose Tumoral alfa/metabolismo , Sobrevivência Celular/efeitos dos fármacos , Ciclo-Oxigenase 2/genética , Humanos , Macrófagos/metabolismo
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...