ABSTRACT
Polycyclic aromatic hydrocarbons [PAHs] in the priority controlling list of US EPA were systematically evaluated in surface sediments in Dianchi Lake and its estuaries. Total PAH concentrations [IPAHs] varied from 210 to 11,070 ng/gdry weight [d.w] in Dianchi Lake, and from 230 to 12,271 microg/g d.w. in the estuaries. IPAHs in sediments from Caohai section were higher than those from Waihai section. The occurrences of PAHs in the Lake were closely related to the distributions of rivers, indicating that the river runoff was an important pathway of PAHs into the Lake. Compared with the US Sediment Quality Guidelines [SQGs], IPAHs in most area were below the effect range low [ERL], which implied that the adverse biological effects would occur rarely. The toxic equivalent concentrations of potentially carcinogenic PAHs [TEQ[carc]] varied from 19to967ngTEQ/gd.w., and the higher values were found in northern Caohai area. The proportions of the toxic equivalent quantity [TEQ[carc]] to the total TEQs in sediments were all above 96%, suggesting that the carcinogenicity of PAHs could be occurred. Significantly positive correlations between total organic carbon [TOC] and less molecular weight PAHs [2, 3-ring] [LPAHs] were observed in the Lake. Diagnostic ratios showed that the primary source of PAHs in Dianchi Lake and most estuaries is biomass combustion, but is petroleum combustion or petrogenic origin in several other estuaries
ABSTRACT
Epoxyeicosatrienoic acids [EETs], which are cytochrome P450 epoxygenase metabolites of arachidonic acid, have anti-inflammatory effects, modulate smooth muscle proliferation, and inhibit smooth muscle migration. This study was designed to determine whether exogenous EETs have any effect on the cell proliferation and apoptosis of carcinoma cell as well as the possible signaling pathways of EETs in this regulation. The effects of EETs on the proliferation and anti-apoptosis of human carcinoma cells were measured by MTT assay and flowcytometric analysis, and the regulation of PPARy, epithelial growth factor receptor [EGFR], extracellular signal-regulated kinase [ERK], phosphatidylinositol 3 [PI3]-Kinase/AKT pathways was investigated by reverse transcriptase polymerase chain reaction [RT-PCR] and western blot analysis. Results of this study suggested that 14, 15-EET may activate the expression of PPARy in Tea-8113 cells. 14,15-EET may stimulate cell proliferation, and increase the percentage of cells during S-G2-M phase in Tea-8113 cells significantly. The levels of EGFR, ERK, and PI3 kinase/AKT proteins were significantly induced by treatment of 14, 15-EET and 14,15-EET/ AUDA, but no significant changes were observed by addition of GW9662. These findings suggest that exogenous 14,15-EET has potent inhibitory effect on proliferation, and could induce apoptosis in Tea-8113 cell, and these changes are related to the expression of PPARganna, the activation of EGFR, ERK, and PI3 kinase/AKT proteins