• Animal cells and systems
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• v.7 no.2
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• pp.159-164
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• 2003

The RAD3 gene of Saccharomyces cerevisiae is required for excision repair and is essential for cell viability. The RAD3 encoded protein possesses a single stranded DNA-dependent ATPase and DNA and DNA-RNA helicase activities. To examine the extent of conservation of structure and function of a S. pombe RAD3 during eukaryotic evolution, the RAD3 homolog gene was isolated by screening of genomic DNA library. The isolated gene was designated as HRD3 (homolog of RAD3 gene). Southern blot analysis confirmed that S. pombe chromosome contains the same DNA as HRD3 gene and this gene exists as a single copy in S. pombe. The transcript of 2.8 kb was detected by Northern blot analysis, The level of transcripts increased by ultraviolet (UV) irradiation, indicating that HRD3 is one of the UV-inducible genes in S. pombe. Furthermore, the predicted partial sequence of HRD3 protein has 60％ identity to S. cerevisiae RAD3 gene. This homology was particularly striking in the regions identified as being conserved in a group of DNA helicases. Gene deletion experiments indicate that the HRD3 gene is essential for viability and DNA repair function. These observations suggest evolutionary conservation of other protein components with which HRD3 might interact in mediating its DNA repair and viability functions.

• Toxicological Research
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• v.22 no.1
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• pp.23-30
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• 2006

Among poly aromatic hydrocarbons, dioxin and PCBs are the most controversial environmental pollutants in our modern life. These pollutants are known as human carcinogens, and liver is the most sensitive target in animal cancer models. Specific aims of the study were focused on the mechanism of carcinogenesis in hepatocytes and the structure-activity relation among these diverse environmental chemicals. Because key mechanisms of dioxin-induced carcinogenesis in human epithelial cell model are the alteration of signal transduction pathway and PKC isoforms, the alteration of the signal transduction pathways and other factors associated with carcinogenesis were studied. Rat hepatocytes cultured under the sandwich protocols were exposed with the various concentration of dioxins and PCBs, and signal transduction pathway, protein kinase C isoforms, oxidant stress, and apoptotic nuclei were evaluated. Since it is important to understand the structure-activity relation among these chemicals to properly assess the carcinogenic potentials, the study analyzed the parameters associated with carcinogenic processes, based on their structural characteristics. In addition, signal transduction pathways and PKC isoforms involved in inhibition of UV-induced apoptosis were also analyzed to elaborate the tumor promotion mechanism of these chemicals. Induction of apoptosis by UV irradiation was optimal at $60\;J/m^2$ in primary hepatocyte in culture. Compared to non coplanar PCBs such as PCB 114 and PCB 153, coplanar PCBs such as PCB 77 and PCB126 showed a stronger inhibition of apoptosis induced by UV irradiation. Production of reactive oxygen species (ROS) was more stimulated by non-coplanar PCBs than coplanar PCBs with the most potent induction of ROS by chlorinated non-coplanar PCB. As compared to the level of induction by PCB126, non-coplanar PCB153 showed a higher increase of intracellular concentrations. Besides the alteration of intracellular calcium concentration, translocation of PKC from cytosolic fraction to membrane fraction was clearly observed upon the exposure of non-coplanar PCB. Taken together, the present study demonstrated that there is a potent structure-activity relationship among PCB congeners and the mechanism of PAH-induced carcinogenesis is structure-specific. The study suggested that more diverse pathways of PAH-induced carcinogenesis should be taken into account beyond the boundary of Ah receptor dogma to assess the health impact of PAH with more accuracy.

• Journal of Photoscience
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• v.9 no.2
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• pp.500-502
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• 2002

In vitro and in vivo studies have reported the induction of matrix metaloproteinase (MMP)-1 in the fibroblasts by ultraviolet (UV) A irradiation. We constructed the skin equivalent model using HaCaT cells as keratinocytes and human neonatal dennal fibroblasts as fibroblasts in the present study. The induction of MMP-l in the fibroblasts was confirmed immunohistochemically 6 hours after UVA irradiation using this model. This model was simply composed of human keratinocytes and fibroblasts. To our knowledge, there have been a few papers concerning the skin equivalent model in the field of photobiology. The effect of UVA exposure to fibroblasts through keratinocytes was examined using this model. The cross-talk can be examined between keratinocytes and fibroblasts. This model can be a useful tool in the field of photobiology.

• Proceedings of the Korean Environmental Health Society Conference
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• 2005.11a
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• pp.166-168
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• 2005

The induction of heme oxygenase-1(HO-1) by ultraviolet(UV) radiation provides a protective defense against oxidative stress, and has been well demonstrated in UVA-irradiated skin, but not UVB. In this study in mice, we show that the UVB(290-320nm) radiation can be attributed to the induction of cutaneous heme oxygenase-1. The expression of HO-1 mRNA was assessed in vivo by the reverse transcription-polymerase chain reaction (RT-PCR) analysis, and HO-1 enzyme activity was measured in microsomal preparation from irradiated mice. The mRNA level of HO-1 increases in liver and skin from 24h to 72h after UVB($3KJ/m^3$) radiation. The results of gene expression were same pattern of HO enzyme activity in skin, but not in liver. HO-1 mRNA in liver resulted in a progressive increase to 96h after UVB radiation, but HO activity in liver increased to 48h. This finding indicates that UVB radiation is an important inducer of HO-1 and increases in HO activity may protect tissues directly or indirectly from oxidative stress.

• Journal of Environmental Health Sciences
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• v.34 no.1
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• pp.49-54
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• 2008

The induction of heme oxygenase-1(HO-1) by UV radiation provides a protective defence against oxidative stress, and has been well demonstrated in skin irradiated with UVA, but not UVB. In this study, we show that the induction of cutaneous HO-l can be attributed to UVB radiation. The expression of HO-1 mRNA was assessed in vivo by reverse transcription-polymerase chain reaction (RT-PCR) analysis, and HO-1 enzyme activity was measured in microsomal preparation from irradiated mice. The mRNA level of HO-1 increases in liver and skin from 1d to 3d after UVB $(3KJ/m^2)$ exposure. The results of gene expression were same pattern of HO-1 enzyme activity in skin, but not in liver. HO-1 mRNA in liver resulted in a progressive increase to 4d after UVB exposure, but HO-1 activity in liver increased to 2d. This finding indicates that UVB radiation is an important inducer of HO-1 and increases in HO activity may protect tissue directly or indirectly from oxidative stress.

• Proceedings of the Korean Fiber Society Conference
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• 2002.04a
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• pp.329-332
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• 2002

고밀도 폴리에틸렌(HDPE, High Density Polyethylene) 지오멤브레인은 독성 폐기물 처리시설에서 차수재로 광범위하게 이용되고 있으며, 열이나, 자외선, 그리고 산소와 화학약품에 노출되었을 때의 내구성이 장기성능에 커다란 영향을 미친다 어떤 원인에 의해서 지오멤브레인이 산화될 경우에는 지오멤브레인의 파괴가 가속화되어 구조 시스템의 안정성을 저하시키는 심각한 현상이 발생하게 된다. (중략)

• Proceedings of the Korean Institute of Surface Engineering Conference
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• 2011.05a
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• pp.95-95
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• 2011

도막의 건조는 용액의 조건, 설비특성, 제품의 요구특성에 맞게 다양하게 적용되고 있다. 일반적으로 열풍에 의한 건조방식이 적용되고 있으나 Induction Heater, UV, EB 및 NIR방식 등 다양한 건조방식이 적용되고 있다. 여기서는 건조방법중 NIR에 의한 건조방식을 이용하여 품질특성에 미치는 인자를 검토하였다.

• Journal of Photoscience
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• v.9 no.2
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• pp.479-481
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• 2002

UV-induced DNA damage causes cell killing and mutations leading to carcinogenesis. In normal human cells, UV damage such as cyclobutane pyrimidine dimers (CPDs) and primidine-prymidone (6-4) photoproducts are mainly repaired by nucleotide excision repair mechanism. The molecular processes have been well characterized recently. To know the influence of mitochondrial genome on the nucleotide excision repair mechanism against CPDs, we comparatively examined the production of CPDs by UVC irradiation and their repair kinetics in human cells completely lacking mitochondrial DNA (mtDNA) and the parental HeLa S cells. Whole DNA extracted from the cells exposed to UVC was treated with T4-endonuclease V to break the phosphodiester bond adjacent to CPDs. The DNA was electrophoresed in a denaturing agarose gel, which was visualized by ethidium bromide staining. The relative amount of CPDs was determined by image analysis using NIH Image software. MtDNA- less (rho-O) cells were apparently more sensitive to UVC than HeLa S cells, while the level of induction of CPDs in rho-O and HeLa cells was comparable. The repair of CPDs was less efficient in rho-O cells compared with HeLa cells. The residual amount of CPDs after 24-h repair was larger in rho-O cells than in HeLa cells where more than 90 % of CPDs were repaired by then. The non-repaired CPDs would lead to apoptosis in rho-O cells. These results suggest that mitochondrial genome may contribute to some ATP-dependent steps in nucletide excision repair by supplying sufficient ATP which is generated through a respiratory chain in mitochondria.

• Food Science of Animal Resources
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• v.35 no.1
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• pp.58-70
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• 2015

This study was conducted to examine the effect of egg shell membrane hydrolysates (ESMH) on wrinkle, UV, and moisture protection for cosmetic use. ESMH were fragmented as whole ESMH (before fractioning), Fraction I (> 10 kDa), Fraction II (3-10 kDa), and Fraction III (< 3 kDa). In order to test whether fractionated ESMH can be used for functional cosmetic materials, we examined not only the level of hyaluronic acid and collagen production, but also the MMP-1 activity using a HaCaT and CCD-986Sk cell line. Our study treated each sample of fractionated ESMH with different concentrations (0.01, 0.1, 1 mg/mL). In our in vivo research, we used hairless mice that had been exposed to UV-B to induce wrinkles for 7 wk, then applied Fraction I to the treatment group for 5 wk and then tested skin thickness, minimum erythema dose and moisture content. In addition, Fraction I was high in collagen and HA biosynthesis and it was better than TGF-${\beta}$ in improving of the skin. When TNF-${\alpha}$ caused MMP-1 activity in the CCD-986Sk cells, the whole ESMH and Fraction I proved to be effective in hindering the induction of collagenase depending on the concentration, and also showed outstanding effects in the suppression of skin aging. We found that the treatment group mice's UV-B radiation-induced skin damage was largely mitigated compared to that of the non-treatment group mice. Thus, we have concluded that EMSH helps to mitigate UV-B radiation-induced wrinkles, collagen, HA, MMP-1 activity and can be used for functional cosmetic materials.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.30 no.2
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• pp.247-251
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• 2004

UV radiation exerts various influences in the skin, including photoaging and inflammation (1). The MMPs (Matrix metalloproteinases), which are induced by UV irradiation, can degrade matrix proteins, and these results in a collagen deficiency in photodamaged skin that leads to skin wrinkling. It has been known that the production of PGE$_2$ stimulates MMPs expression, and inhibits procollagen (2). Thus, it is possible that the induction of MMPs and the inhibition of matrix protein synthesis by UV -induced PGE$_2$ may play some role in UV-induced collagen deficiency in photoaged skin. Fructose-1,6-diphosphate (FDP), a glycolytic metabolite, is reported to have cytoprotective effects against ischemia and postischemic reperfusion injury of brain and heart, presumably by augmenting anaerobic carbohydrate metabolism (3). And also, FDP significantly prevent skin aging by decreasing facial winkle compared with vehicle alone after 6 months of use. We studied the mechanism of anti-aging effect of FDP on UVB-irradiated HaCaT keratinocyte model. FDP has protective role in UVB injured keratinocyte by attenuating prostaglandin E$_2$ (PGE$_2$) production and COX-2 expression. And FDP also suppressed UVB-induced MMP-2 expression. Further, to delineate the inhibition of UVB-induced COX-2 and MMPs expression with cell signaling pathways, treatment of FDP to HaCaT keratinocytes resulted in marked inhibition of UVB-induced phosphorylation of ERK1/2, JNK. It also prevents UV induced NFB translocation, which are activated by cellular inflammatory signal. Our results indicate that FDP has protecting effects in UV-injured skin aging by decreasing UVB-induced COX-2 and MMPs expression, which are possibly through blocking UVB-induced signal cascades.