Methylated derivatives of polycyclic aromatic hydrocarbons in road dust, green belt soil and parking lot dust: occurrence, spatial distribution and emission sources.

Convenient transportation facilities not only bring the higher standard of living to big cities, but also bring some environmental pollution problems. In order to understand the presence and sources of methylated polycyclic aromatic hydrocarbons (Me-PAHs) in environmental samples and their association with total organic carbon (TOC), 49 Me-PAHs were analyzed in road dust, green belt soil and parking lot dust samples in Harbin. The results showed that the ranges of the total Me-PAHs (ΣMe-PAHs) content in road dust were 221-5826 ng/g in autumn and 697-7302 ng/g in spring, and those in green belt soil were 170-2509 ng/g and 155-9215 ng/g in autumn and spring, respectively. And ΣMe-PAHs content in parking lot dust ranged from 269 to 2515 ng/g in surface parking lots and from 778 to 10,052 ng/g in underground parking lots. In these samples, the composition profile of Me-PAHs was dominated by 4-ring Me-PAHs. The results of diagnostic ratios and principal component analysis (PCA) indicated that petrogenic and pyrogenic sources were the main sources of Me-PAHs in the samples. Spearman correlation analysis showed that there was no correlation for Me-PAHs in road dust and green belt soil on the same road. Furthermore, there was a significant positive relationship (0.12 ≤ R2 ≤ 0.67, P < 0.05) between Me-PAHs concentrations and the TOC content. This study demonstrated the presence of Me-PAHs with high concentrations in the road environment samples of Harbin.

Aniline antioxidants in road dust, parking lot dust, and green-belt soil in Harbin, a megacity in China: Occurrence, profile, and seasonal variation.

Aniline antioxidants (ANs) are widely used as industrial chemicals in products composed of rubber. ANs originate mainly from vehicles, where tire wear particles end up in dust and soil after being deposited on roads. Nowadays, limited information is available on the fate and seasonal variation of ANs in the road environment. In this study, we investigated the occurrence of 32 ANs in dust and soil from different road environments, including road dust, garage dust, parking lot dust, and green-belt soil. The total concentrations of ANs were 369 ng g-1 in road dust, 712 ng g-1 in garage dust, and 687 ng g-1 in parking lot dust. These concentrations are several times higher than that in green-belt soil (128 ng g-1). The highest concentrations of N-(1,3-dimethylbutyl)-N'-phenyl-1,4-phenylenediamine (6PPD) were found in dust and soil. Furthermore, notable seasonal differences were observed, with significantly higher concentrations of ANs in autumn than those in spring. In the main urban area, roads with high traffic volume exhibited higher concentrations of ANs than those with low traffic volume, indicating that ANs were produced by vehicle-related sources.

Occurrence, Sources, and Health Risks of Polycyclic Aromatic Hydrocarbons in Road Environments from Harbin, a Megacity of China.

To obtain a comprehensive understanding about that occurrence, sources, and effects on human health of polycyclic aromatic hydrocarbons (PAHs) in road environmental samples from Harbin, concentrations of 32 PAHs in road dust, green belt soil, and parking lot dust samples were quantified. The total PAH concentrations ranged from 0.95 to 40.7 µg/g and 0.39 to 43.9 µg/g in road dust and green belt soil, respectively, and were dominated by high molecular weight PAHs (HMW-PAHs). Despite the content of PAHs in arterial roads being higher, the composition profile of PAHs was hardly influenced by road types. For parking lot dust, the range of total PAH concentrations was 0.81-190 µg/g, and three-ring to five-ring PAHs produced the maximum contribution. Compared with surface parking lots (mean: 6.12 µg/g), higher total PAH concentrations were detected in underground parking lots (mean: 33.1 µg/g). The diagnostic ratios of PAHs showed that petroleum, petroleum combustion, and biomass/coal combustion were major sources of PAHs in the samples. Furthermore, according to the Incremental Lifetime Cancer Risk model, the cancer risks of three kinds of samples for adults and children were above the threshold (10-6). Overall, this study demonstrated that PAHs in the road environment of Harbin have a certain health impact on local citizens.

Fuzheng Qingjie granules potentiate the anticancer effect of cyclophosphamide by regulating cellular immune function and inducing apoptosis in Hepatoma 22 tumor-bearing mice.

Fuzheng Qingjie (FZQJ) is a polyherbal Chinese medicine that has previously been implemented as an adjuvant therapy for gastrointestinal cancer. The present study investigated whether FZQJ is able to potentiate the anticancer effect of cyclophosphamide (CTX). Hepatoma 22 tumor-bearing mice were randomly divided into a vehicle group, CTX group, FZQJ group and combination (CTX+FZQJ) group. In addition, untreated mice without H22 cells served as blank controls. Seven days post-treatment, the mice were sacrificed and the tumors were weighed. Blood cells were evaluated using an automatic hemocytometer analyzer and flow cytometer. The expression levels of interleukin (IL)-2 and tumor necrosis factor (TNF)-α were evaluated using a radioimmunoassay. Apoptotic cells were observed using a terminal deoxynucleotidyl transferase dUTP nick-end labeling assay. Alanine transaminase, aspartate aminotransferase, blood urea nitrogen and creatinine were examined using an automatic biochemical analyzer. The results demonstrated that the tumor inhibitory rate and apoptosis index were higher in the combination group, compared with those in the CTX group. Notably, FZQJ was able to alleviate CTX-induced decreases in the numbers of white blood cells and platelets, CD3+ and CD4+ T lymphocyte subsets, and the concentration of hemoglobin, body weight and thymus index, and increase serum TNF-α and IL-2 levels without overt hepatorenal toxicity. These results suggest that FZQJ granules may enhance the anticancer effect of CTX, in addition to alleviating the side effects.

Ethyl acetate extract from Jiedu Xiaozheng Yin inhibits the proliferation of human hepatocellular carcinoma cells by suppressing polycomb gene product Bmi1 and Wnt/ß-catenin signaling.

Jiedu Xiaozheng Yin (JXY) is a Chinese herbal decoction used to treat hepatocellular carcinoma (HCC). Previous studies have demonstrated that JXY can inhibit HCC cell proliferation via induction of G0/G1 phase arrest. In this study, we investigated whether the inhibitory effect of JXY on HCC cells is associated with the inhibition of the Wnt/ß­catenin pathway and the polycomb gene product Bmi1. Ethyl acetate extract from JXY (EE-JXY) was prepared. Methyl thiazolyl tetrazolium (MTT) and colony formation assays were used to measure cell proliferation. Immunofluorescence was used to analyze the expression and location of ß-catenin and Bmi1. Immunohistochemistry was used to examine the expression of proliferating cell nuclear antigen (PCNA), c-myc and cyclin D1. ß-catenin, Bmi1, c-myc, cyclin D1 and p16INK4A mRNA levels were detected by RT-PCR. The results demonstrated that EE-JXY inhibited the expression of PCNA, c-myc, cyclin D1 and Bmi1, and upregulated the expression of p16INK4A. We also found that EE-JXY could facilitate ß-catenin translocation from the cytoplasm and nuclei to the cytomembrane. Finally, suppression of cell proliferation and expression of Bmi1 and Wnt/ß-catenin by EE-JXY was confirmed in a mouse xenograft model of HCC. Thus, EE-JXY can inhibit the proliferation of HCC partially via suppression of the Bmi1 and Wnt/ß-catenin signaling pathways.

Fuzheng Qingjie recipe induces apoptosis in HepG2 cells via P38 MAPK activation and the mitochondria-dependent apoptotic pathway.

Fuzheng Qingjie (FZQJ) recipe is a polyherbal Chinese medicine capable of suppressing tumor growth and is used as an adjuvant therapy for various types of cancer. However, its anticancer mechanisms are yet to be fully elucidated. In the present study, we explored whether p38 mitogen-activated protein kinase (MAPK) was involved in FZQJ-mediated mitochondria-dependent apoptosis in human hepatocellular carcinoma cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays were used to measure the viability of HepG2 cells. 4,6-Diamidino-2-phenylindole (DAPI) and Annexin-V fluorescein isothiocyanate (FITC) were used to analyze the apoptosis of HepG2 cells. The mitochondrial membrane potential (∆ψ) and phosphorylated P38 MAPK protein were examined by a flow cytometer following 5,5',6,6'-tetrachloro­1,1',3,3'-tetraethylbenzimidazolcarbocyanine iodide (JC-1) and Alexa Fluor® 647 mouse anti-phosphorylated P38 MAPK antibody staining, respectively. The activation of caspase-9 and caspase-3 were measured using colorimetric assays. Additionally, Bcl-2 and Bax expression were examined using reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis. The results demonstrated that water extract of FZQJ was able to induce apoptosis of HepG2 cells in vitro. FZQJ-induced apoptosis was accompanied by the loss of ∆ψ, downregulation of Bcl-2 and upregulation of Bax expression, and the activation of caspase-3, -9 and P38 MAPK. These results indicated that FZQJ induced apoptosis in HepG2 cells at least via P38 MAPK activation and the mitochondria-dependent apoptotic pathway.