scholarly journals Chemical Characterization of Two Seasonal PM2.5 Samples in Nanjing and Its Toxicological Properties in Three Human Cell Lines

Environments ◽  
2019 ◽  
Vol 6 (4) ◽  
pp. 42 ◽  
Author(s):  
Kai Zhang ◽  
Dongyang Nie ◽  
Mindong Chen ◽  
Yun Wu ◽  
Xinlei Ge ◽  
...  

PM2.5 pollution is of great concern in China due to its adverse health effects. Many diseases have been proven to be associated with PM2.5 components, but the effects of chemical characteristics of PM2.5 on toxicological properties, especially in different human organs, are poorly understood. In this study, two seasonal PM2.5 samples (summer and winter) were collected in Nanjing, and their chemical compositions (heavy metals, water-soluble ions, organic carbon (OC), and elemental carbon (EC)) were analyzed. Human lung epithelial carcinoma cells (A549), human hepatocellular liver carcinoma cells (HepG2), and human neuroblastoma cells (Sh-Sy5y) were employed to evaluate the toxicological properties of the collected PM2.5. The results showed that the average mass concentrations of PM2.5 were lower in summer (51.3 ± 21.4 μg/m3) than those in winter (62.1 ± 21.5 μg/m3). However, the mass fractions of heavy metals, OC, and EC exhibited an opposite seasonal difference. Among all tested fractions, water-soluble ions were the major compositions of particles in both summer and winter, especially the secondary ions (SO42−, NO3− and NH4+). Besides, the ratio of OC/EC in PM2.5 was greater than two, indicating serious secondary pollution in this area. The NO3–/SO42− ratio (< 1) suggested that fixed sources made important contributions. The toxicological results showed that PM2.5 in the summer and winter significantly inhibited cell viability (p < 0.01) and induced intracellular reactive oxygen species (ROS) production (p < 0.01). Moreover, the viability inhibition in A549, Sh-Sy5y, and HepG2 cells was more prominent in summer, especially at high PM2.5 (400 μg/mL) (p < 0.05), and the induction of reactive oxygen species (ROS) in A549 and Sh-Sy5y cells was also more evident in summer. Such seasonal differences might be related to the variations of PM2.5 components.

2022 ◽  
Author(s):  
Jiyan Wu ◽  
Chi Yang ◽  
Chunyan Zhang ◽  
Fang Cao ◽  
Aiping Wu ◽  
...  

Abstract. Excessive reactive oxygen species (ROS) in the human body is an important factor leading to diseases. Therefore, research on the content of reactive oxygen species in atmospheric particles is necessary. In order to more conveniently and accurately detect the content of reactive oxygen in atmospheric particles hour by hour. Here, to modify the instrument, it is added a DTT experimental module that is protected from light and filled with nitrogen at the end, based on the Monitor for AeRosols and Gases in ambient Air (MARGA). The experimental study found that the detection limit of the modified instrument is 0.024 nmol min−1. And the accuracy of the online instrument is determined by comparing the online and offline levels of the samples, which yielded good consistency (slope 0.97, R2 = 0.95). It shows that the performance of the instrument is indeed optimized, the instrument is stable, and the characterization of ROS is accurate. Meanwhile, reactive oxygen and inorganic ions in atmospheric particles are quantified using the online technique in the northern suburbs of Nanjing. It is found that the content of ROS during the day is higher than that at night, especially after it rains, ROS peaks appear in the two time periods of 08:00–10:00 and 16:00–18:00. In addition, examination of the online ROS and water-soluble ions (SO42−, NO3−, NH4+, Na+, Ca2+, K+), BC and polluting gases (SO2, CO, O3, NO, NOx) measurements revealed that photo-oxidation and secondary formation processes could be important sources of aerosol ROS. This method breakthrough enables the quantitative assessment of atmospheric particulate matter ROS at the diurnal scale, providing an effective tool to study sources and environmental impacts of ROS.


2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Amnah M. Alshangiti ◽  
Eszter Tuboly ◽  
Shane V. Hegarty ◽  
Cathal M. McCarthy ◽  
Aideen M. Sullivan ◽  
...  

Neuroblastoma is an embryonal malignancy that arises from cells of sympathoadrenal lineage during the development of the nervous system. It is the most common pediatric extracranial solid tumor and is responsible for 15% of childhood deaths from cancer. Fifty percent of cases are diagnosed as high-risk metastatic disease with a low overall 5-year survival rate. More than half of patients experience disease recurrence that can be refractory to treatment. Amplification of the MYCN gene is an important prognostic indicator that is associated with rapid disease progression and a poor prognosis, highlighting the need for new therapeutic approaches. In recent years, there has been an increasing focus on identifying anticancer properties of naturally occurring chalcones, which are secondary metabolites with variable phenolic structures. Here, we report that 4-hydroxychalcone is a potent cytotoxin for MYCN-amplified IMR-32 and SK-N-BE (2) neuroblastoma cells, when compared to non-MYCN-amplified SH-SY5Y neuroblastoma cells and to the non-neuroblastoma human embryonic kidney cell line, HEK293t. Moreover, 4-hydroxychalcone treatment significantly decreased cellular levels of the antioxidant glutathione and increased cellular reactive oxygen species. In addition, 4-hydroxychalcone treatment led to impairments in mitochondrial respiratory function, compared to controls. In support of this, the cytotoxic effect of 4-hydroxychalcone was prevented by co-treatment with either the antioxidant N-acetyl-L-cysteine, a pharmacological inhibitor of oxidative stress-induced cell death (IM-54) or the mitochondrial reactive oxygen species scavenger, Mito-TEMPO. When combined with the anticancer drugs cisplatin or doxorubicin, 4-hydroxychalcone led to greater reductions in cell viability than was induced by either anti-cancer agent alone. In summary, this study identifies a cytotoxic effect of 4-hydroxychalcone in MYCN-amplified human neuroblastoma cells, which rationalizes its further study in the development of new therapies for pediatric neuroblastoma.


2021 ◽  
Vol 1 (1) ◽  
Author(s):  
Yoo-Hun Noh ◽  
Byung-Ju Jeon ◽  
Seungah Lee ◽  
Jaeho Myeong ◽  
Ga-Young Kim ◽  
...  

1998 ◽  
Vol 275 (6) ◽  
pp. C1640-C1652 ◽  
Author(s):  
Amy R. Simon ◽  
Usha Rai ◽  
Barry L. Fanburg ◽  
Brent H. Cochran

Reactive oxygen species (ROS) play an important role in the pathogenesis of many human diseases, including the acute respiratory distress syndrome, Parkinson’s disease, pulmonary fibrosis, and Alzheimer’s disease. In mammalian cells, several genes known to be induced during the immediate early response to growth factors, including the protooncogenes c- fos and c- myc, have also been shown to be induced by ROS. We show that members of the STAT family of transcription factors, including STAT1 and STAT3, are activated in fibroblasts and A-431 carcinoma cells in response to H2O2. This activation occurs within 5 min, can be inhibited by antioxidants, and does not require protein synthesis. STAT activation in these cell lines is oxidant specific and does not occur in response to superoxide- or nitric oxide-generating stimuli. Buthionine sulfoximine, which depletes intracellular glutathione, also activates the STAT pathway. Moreover, H2O2stimulates the activity of the known STAT kinases JAK2 and TYK2. Activation of STATs by platelet-derived growth factor (PDGF) is significantly inhibited by N-acetyl-l-cysteine and diphenylene iodonium, indicating that ROS production contributes to STAT activation in response to PDGF. These findings indicate that the JAK-STAT pathway responds to intracellular ROS and that PDGF uses ROS as a second messenger to regulate STAT activation.


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