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Fine particulate matter (PM2.5) increases the risks of lung cancer. Epigenetics provides a new toxicology mechanism for the adverse health effects of PM2.5. However, the regulating mechanisms of PM2.5 exposure on candidate gene DNA methylation changes in the development of lung cancer remain unclear. Abnormal expression of the glutathione S transferase (GST) gene is associated with cancer. However, the relationship between PM2.5 and DNA methylation-mediated GST gene expression is not well understood. In this study, we performed GST DNA methylation analysis and GST-related gene expression in human A549 cells exposed to PM2.5 (0, 50, 100 µg/mL, from Taiyuan, China) for 24 h (n = 4). We found that PM2.5 may cause DNA oxidative damage to cells and the elevation of GSTP1 promotes cell resistance to reactive oxygen species (ROS). The Kelch-1ike ECH-associated protein l (Keap1)/nuclear factor NF-E2-related factor 2 (Nrf2) pathway activates the GSTP1. The decrease in the DNA methylation level of the GSTP1 gene enhances GSTP1 expression. GST DNA methylation is associated with reduced levels of 5-methylcytosine (5mC), DNA methyltransferase 1 (DNMT1), and histone deacetylases 3 (HDAC3). The GSTM1 was not sensitive to PM2.5 stimulation. Our findings suggest that PM2.5 activates GSTP1 to defend PM2.5-induced ROS and 8-hydroxy-deoxyguanosine (8-OHdG) formation through the Keap1/Nrf2 signaling pathway and GSTP1 DNA methylation. [ABSTRACT FROM AUTHOR]

Exposure to 2-amino-1-methyl-6-phenylimidazo [4, 5-b] pyridine (PhIP), a typical example of heterocyclic amine compounds, increases colon cancer risk. Seabuckthorn (SBT) seed oil is a biologically active substance extracted from seeds of wildHippophae rhamnoides L. Here, we sought to investigate the toxicological mechanisms underlying oxidative stress and cancer-related gene expression in the rat colons as well as the protective effect of SBT seed oil against colonic oxidative damage. Our results showed that PhIP significantly decreased the anti-oxidative enzyme activities whereas increased the malondialdehyde (MDA) contents, protein carbonyl (PCO) levels and DNA-protein cross-links (DPC) coefficients in the rat colons compared with the solvent-control group. Moreover, PhIP activated expression of c-fos and c-jun and inhibited p16 and Rb expression. Additionally, SBT seed oil plus PhIP significantly improved antioxidant markers and reduced the levels of MDA, PCO and DPC compared to those in rats exposed to PhIP alone. These data indicated that PhIP could induce oxidative stress and abnormal alterations of cancer-related gene expression in the rat colons while SBT seed oil may be beneficial because of its ability to alleviate the PhIP-induced oxidative damage to the rats. [ABSTRACT FROM AUTHOR]

Inhibition of cell apoptosis is an increasingly important factor in modulating airway inflammation in asthma, which is related to environmental pollutants. To investigate the effects of sulfur dioxide (SO2) on the mRNA and protein expressions of apoptosis-related genes in lungs from asthmatic rats, male Wistar rats were challenged by ovalbumin (OVA) or SO2 (2 ppm) inhalation alone or together. Examinations were performed 24 h after the last treatment. The mRNA and protein levels of p53, bax, and bcl-2 were analyzed in lungs using real-time reverse transcription-polymerase chain reaction (RT-PCR) assay and Western blot analysis, respectively. The results indicated that increases of bcl-2 or decreases of p53 and bax mRNA and protein levels were not significant in lungs of rats exposed to SO2 alone, compared with controls, but elevated or reduced levels of these genes appeared in lungs of asthmatic rats exposed to SO2 plus OVA, compared with controls, suggesting that SO2 exposure could result in OVA-induced increases or decreases of transcription and translation levels of these apoptosis-related genes in rat lungs, and may have relations to airway inflammation in asthma. The regulation mechanism of apoptosis in asthma disease exposure to SO2 needs further study. [ABSTRACT FROM AUTHOR]

To study whether sulfur dioxide (SO 2 ) can enter into the different organs of mice exposed to SO 2 , the sulfite contents in brains, hearts, and lungs from male mice were determined by high-performance liquid chromatography with fluorescence detection (HPLC-FD). After reduction and precolumn derivation of tissue homogenates of brains, hearts, and lungs from mice, the mixture was centrifuged, and 5µl of the resulting supernatant was directly injected into HPLC; the mobile phase consisted of methanol–phosphoric acid (12:88, v/v), and for the fluorescence detection ? EX 392 nm and? EM —479 nm were used. The standard curve was linear in the range from 0.126 µg/ml to 126 µg/ml; the minimal detectable concentration was 0.04µg/ml (S/N = 3), the average methodological recoveries were from 97% to 101%, and the within-day and between-day precisions were less than 9%. These results showed that sulfite contents in all organs tested from mice in the SO 2 -exposed groups were significantly increased (p .92) compared with the control groups. These results indicated SO 2 could transform into sulfite in vivo after inhalation, and could distribute into lung and other organs such as brain and heart. These results offered a support for the viewpoint that SO 2 is a systemic toxic agent. [ABSTRACT FROM AUTHOR]

The concentrations of ambient fine particulate matter (PM2.5) and its compositions in urban Taiyuan, China during a typical winter and summer time period in 2017 were measured to investigate the pollution characteristics, source apportionment and health risks assessment of PM2.5 pollution. The results demonstrated that the mean daily mass concentration of PM2.5 in winter (102.6 ± 6.2 μg/m3) was higher than that in summer (65.0 ± 17.2 μg/m3) during sampling. The relatively high concentrations of heavy metals (Zn, Pb, Cu, As, Ni, Cr and Cd), anion (SO42−, NO3−, Cl− and F−) and high-molecular-weight PAHs in PM2.5 were observed. The enrichment factors (EFs) values, special diagnostic ratios like ratios of NO3−/SO42− and individual PAHs concentration ratio showed that coal combustion and vehicle emissions were the major sources of PM2.5 pollution. Health risk assessment illustrated that mean hazard indices for non-cancer and cancer risk of all analyzed metals were within the safe range. However, inhalation exposure to PM2.5-bound PAHs had carcinogenic risk, while not indicating non-carcinogenic risk. Taken together, although PM2.5 pollution was alleviated to some extent, PM2.5 pollution in 2017 was still serious and PM2.5 was mainly originated from coal burning, especially, in which PM2.5-bound PAHs in Taiyuan may pose a potential health risk. [ABSTRACT FROM AUTHOR]

Taiyuan is a center of coal-based electricity production and many chemicals industries, where mixtures of sulfur dioxide (SO2) and particulate matter may be more prominent. The focus of the present study was to determine if there is a link between adverse effects in the brain and the combined-exposure to SO2and fine particulate matter (PM2.5). Rats were exposed alternately to PM2.5with different dosages (1.5, 6.0 and 24.0 mg/kg body weight) and SO2at the level of 5.6 mg/m3. The results showed that the combined exposure to PM2.5and SO2enhanced the mRNA expression and protein level of TNF-α and IL-6 in rat cortex and hippocampus relative to the control, SO2and PM2.5alone. Instead, TGF-β1 mRNA and protein level were down-regulated in the brain. Additionally, PM2.5at medium and/or high dose caused marked increase in Aβ42 level and PM2.5 + SO2induced further increase of Aβ42 level in the cortex and hippocampus. It suggests that SO2and PM2.5can synergistically exert inflammation responses and induce Aβ42 accumulation in the brain. Also, it is notable that the Aβ42 accumulation of rat cortex and hippocampus were closely associated with pro-/anti-inflammatory cytokines ratio. These results clearly demonstrated that the combined exposure to PM2.5and SO2can induce the imbalance of pro-/anti-inflammatory cytokine, resulting in Aβ42 accumulation of rat brain cortex and hippocampus. [ABSTRACT FROM AUTHOR]