• Journal of Korean Society of Environmental Engineers
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• v.30 no.11
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• pp.1067-1074
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• 2008

In this study, the organic carbon normalized-sorption coefficients (Koc) for the binding affinity of phenanthrene (PHE) to 16 different soil humic and fulvic acids of various origins were determined by fluorescence quenching. The humic and fulvic acids used in this study were isolated from 6 different domestic soils including Mt. Hanla soil, IHSS standard soil and peat as well as Aldrich humic acid and characterized by elemental composition, ultraviolet absorption at 254 nm, composition of main structural fragments determined by CPMAS $^{13}$C NMR. The Koc values($\times$10$^4$, L/kg C) for each of HA and FA samples were in the range of 1.48$\sim$8.65 and higher in HA compared to that of FA(3.13$\sim$8.65 vs 1.48$\sim$2.48) in the experimental condition([PHE]/[HS] = 0.02$\sim$0.2(mg/L)/(mg-OC/L), pH 6). The correlation study between the structural descriptors of humic and fulvic acids and log Koc values of phenanthrene, show that the magnitude of Koc values positively correlated with the UV$_{254}$ absorptivity([ABS]$_{254}$) and two $^{13}$C NMR descriptors (C$_{Ar-H,C}$, $\sum$C$_{Ar}$/$\sum$C$_{Alk}$), while negatively correlated with the independent descriptors of the(N+O)/C atomic ratios and $^{13}$C NMR descriptors (I$_{C-O}$/I$_{C-H,C}$). These results confirmed that the binding affinity for the hydrophobic organic compound, phenanthrene are significantly influenced by the polarity and aromaticity of soil humc and fulvic acids.

• Toxicological Research
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• v.24 no.3
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• pp.175-182
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• 2008

DNA-dependent protein kinase(DNA-PK) is involved in joining DNA double-strand breaks induced by ionizing radiation or V(D)J recombination and is activated by DNA ends and composed of a DNA binding subunit, Ku, and a catalytic subunit, DNA-PKcs. It has been suggested that DNA-PK might be $2^{nd}$ upstream kinase for protein kinase B(PKB). In this report, we showed that Ser473 phosphorylation in the hydrophobic-motif of PKB is blocked in DNA-PK knockout mouse embryonic fibroblast cells(MEFs) following insulin stimulation, while there is no effect on Ser473 phosphorylation in DNA-PK wild type MEF cells. The observation is further confirmed in human glioblastoma cells expressing a mutant form of DNA-PK(M059J) and a wild-type of DNA-PK(M059K), indicating that DNA-PK is indeed important for PKB activation. Furthermore, the treatment of cells with doxorubicin, DNA-damage inducing agent, leads to PKB phosphorylation on Ser473 in control MEF cells while there is no response in DNA-PK knockout MEF cells. Together, these results proposed that DNA-PK has a potential role in insulin signaling as well as DNA-repair signaling pathway.