• Journal of Photoscience
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• 제9권2호
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• pp.332-334
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• 2002

We examined the effects of supplementary ultraviolet-B (UV-B) radiation on the changes in synthesis and degradation of ribulose-I, 5-biphosphate carboxylase /oxygenase (Rubisco) and light-harvesting chlorophyll a/b binding protein of PSII (LHCII), as well as mRNA levels for small and large subunits of Rubisco (rbcS and rbcL, respectively) and LHCII (cab) with leaf age in UV-sensitive rice (Norin I) and UV-resistant rice (Sasanishiki). Both Rubisco and LHCII were actively synthesized until the leaf had fully expanded, and then decreased with leaf age. Synthesis of Rubisco, but not LHCII, was significantly suppressed by UV-B in Norin 1. The degradation of Rubisco was enhanced by UV-B around the time of the leaf maturation in the two cultivars. The levels of rbcS and rbcL were reduced by UV-B at the early leaf stages after emergence in both cultivars. The level of cab was first present at the highest level in the two cultivars, but drastically decreased due to UV-B treatment immediately after leaf emergence in Norin 1. It was proved that synthesis and degradation of Rubisco and LHCII greatly changed with leaf age: Rubisco synthesis was significantly suppressed by supplementary UV-B radiation at the transcription step during the early leaf stages. It was also suggested that the difference between the two rice cultivars in sensitivity to UV-B in the synthesis of Rubisco might be due to the specific suppression not only after transcription but also at transcription.

• 한국식물생명공학회:학술대회논문집
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• 한국식물생명공학회 2004년도 생명공학 실용화를 위한 비젼
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• pp.29-34
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• 2004

Reduction in stratospheric ozone layer increases the amount of ultraviolet-B radiation (UVB: 280-320 nm) that reaches the earth ’ s surface. UVB radiationcan damage plants, resulting in decrease in growth and productivity. UVB-augmentation studies have indicated that the sensitivity to UVB radiation in plants varies among the species and cultivars. However. there are no definitive answers for the mechanisms of UVB-resistance in higher plants and for bioengineering design and development of UVB-tolerant plants. We have been studying physiological and biochemical aspects of the effects of UVB radiation on growth and yield of rice COryza sativa LJ. aiming to clarify the mechanism of resistance to UVB radiationin rice. At this meeting. weintroduce our research as followed: (1) supplementary UVB radiation has inhibitory effects on the growth. yield and grain development of rice; (2) UVB sensitivity of rice varies widely among cultivars; (3) among Japanese rice cultivars. Sasanishiki. a leading variety in northeast Japan. is more resistant to UVB. while Norin 1. a progenitor of Sasanishiki. is less resistant; (4)UV-sensitive Norin 1 cultivar is deficient in photorepair of UVB-induced cyclobutane pyrimidine dimer (CPD). and this deficiency results from one amino acid residue alteration of CPD photolyase. These results suggest that spontaneously occurring mutation in CPD photolyase gene could lead to difference in UVB sensitivity in rice. and that CPD photolyase might be a useful target for improving UVB-sensitivity in rice by selective breeding or bioengineering of UVB-tolerant rice.

• IMMUNE NETWORK
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• 제2권2호
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• pp.65-71
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• 2002

The immunological mechanism of the responses to ultraviolet (UV) B radiation in mouse models were investigated by the suppression of contact hypersensitivity (CHS) and delayed type hypersensitivity (DTH), and susceptibility to infection. However, there are some differences in immune suppression according to the different models as well as the irradiation protocols. Therefore, this review focused on the differences in the suppressive effects on CHS and DTH, and susceptibility to infection in relation to the different in vivo models. Recent advances in cytokine knockout mice experiments have the reexamination of the role of the critical cytokines in UVB-induced immune suppression, which was investigated previously by blocking antibodies. The characteristics of the suppressor cells responsible for UVB-induced tolerance were determined. The subcellular mechanism of UVB-induced immune suppression was also explained by the induction of apoptotic cells through the Fas and Fas-ligand interaction. The phagocytosis of the apoptotic cells is believed to induce the production of the immune suppressive cytokine like interleukin-10 by macrophages. Therefore, the therapeutic UVB response to a skin disease, such as psoriasis, by the depletion of infiltrating T cells could be considered in the extension line of apoptosis and immune suppression.

• Ocean and Polar Research
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• 제40권4호
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• pp.281-288
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• 2018

The transmission of solar light according to the distribution of chromophoric dissolved organic matter (CDOM) was measured in the Pacific Arctic Ocean. The Research Vessel Araon visited the ice-covered East Siberian and Chukchi Seas in August 2016. In the Arctic, solar [ultraviolet-A (UV-A), ultraviolet-B (UV-B), and photosynthetically active radiation (PAR)] radiation reaching the surface of the ocean is primarily protected by the distribution of sea ice. The transmission of solar light in the ocean is controlled by sea ice and dissolved organic matter, such as CDOM. The concentration of CDOM is the major factor controlling the penetration depth of UV radiation into the ocean. The relative CDOM concentration of surface sea water was higher in the East Siberian Sea than in the Chukchi Sea. Due to the distribution of CDOM, the penetration depth of solar light in the East Siberian Sea (UV-B, $9{\pm}2m$; UV-A, $13{\pm}2m$; PAR, $36{\pm}4m$) was lower than in the Chukchi Sea (UV-B, $15{\pm}3m$; UV-A, $22{\pm}3m$; PAR, $49{\pm}3m$). Accelerated global warming and the rapid decrease of sea ice in the Arctic have resulted in marine organisms being exposed to increased harmful UV radiation. With changes in sea ice covered areas and concentrations of dissolved organic matter in the Arctic Ocean, marine ecosystems that consist of a variety of species from primary producers to high-trophic-level organisms will be directly or indirectly affected by solar UV radiation.

• Journal of Radiation Protection and Research
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• 제33권3호
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• pp.87-91
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• 2008

C57BL/6 마우스에서 자외선(Ultraviolet, UV) B 조사에 의한 표피 멜라닌세포의 변화에 대한 보중익기탕(Bu-Zhong-Yi-Qi-Tang, BZYQT)의 효과를 관찰하였다. 마우스에 UVB를 매일 $80\;mJ/cm^2$ (0.5 mW/sec)씩 7일간 조사하고, BZYQT를 UV 조사전 또는 조사 후에 복강내주사 또는 피부에 도포하여, 멜라닌세포 형성 억제효과 및 형성된 멜라닌세포에 대한 미백 효과를 dihydroxyphenylalanine (DOPA) 염색으로 관찰하였다. 마우스의 귀등쪽 표피를 분리하여 관찰한바, 정상대조군에서는 $mm^2$ 당 11-16개의 멜라닌세포가 관찰되었으며, UV 조사 일주일 후 발달된 가지를 가진 DOPA양성 멜라닌세포는 급격히 증가하였다. 멜라닌세포 형성 억제 실험에서는 평균치를 기준으로 복강 내 주사군에서 16.3%, 피부도포군에서 26.6%(p<0.01)의 효과가 관찰되었으며, 형성된 멜라닌세포의 감소 효과 실험에서는 평균치를 기준으로 복강 내 주사군의 경우 3주에 24.0%(p<0.01), 6주에 26.0%(p<0.01)의 효과가 관찰되었고, 피부도포군의 경우 3주에 5.2%, 6주에 12.5%(p<0.05)의 효과를 보였다. 이상의 결과는 BZYQT가 UV에 의한 멜라닌세포 형성 억제제 및 미백제로서의 적용 가능성을 제시하였다.

• 대한수의학회지
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• 제45권1호
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• pp.1-6
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• 2005

In this study we assessed the influences of ultraviolet (UV) light B radiation on epidermal cells by apoptotic sunburn cell (SBC) and the effect of green tea treatment on the inhibition of SBC formation in SKH1-hr mouse. The extent of changes following $200mJ/cm^2$ (0.5 mW/sec) was studied at 0, 3, 6, 12, 18, 24, 30 or 36 hours after exposure. SBCs were recognized by 3 hours after irradiation. There was tendency to increase from 3 hours to 24 hours and decrease from then to 36 hours after irradiation. The mice that received 0, 25, 50, 100, 200, 400 or $800mJ/cm^2$ of UVB were examined 24 hours after irradiation. The SBCs were induced as the radiation dose increases from 0 to $200mJ/cm^2$. A further increase of radiation dose has little further effect. The frequency of UVB ($200mJ/cm^2$)-induced SBC formation was reduced by intraperitoneal injection of green tea extract (p<0.01).

• Molecules and Cells
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• 제38권11호
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• pp.982-990
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• 2015

Exposure of the skin to ultraviolet radiation can cause skin damage with various pathological changes including inflammation. In the present study, we identified the skin-protective activity of 1,2,3,4,6-penta-O-galloyl-${\beta}$-D-glucose (pentagalloyl glucose, PGG) in ultraviolet B (UVB) radiation-induced human dermal fibroblasts and mouse skin. PGG exhibited antioxidant activity with regard to intracellular reactive oxygen species (ROS) generation as well as ROS and reactive nitrogen species (RNS) scavenging. Furthermore, PGG exhibited anti-inflammatory activity, inhibiting the activation of nuclear factor-kappaB (NF-${\kappa}B$) and mitogen-activated protein kinase (MAPK) signaling, resulting in inhibition of the expression of pro-inflammatory mediators. Topical application of PGG followed by chronic exposure to UVB radiation in the dorsal skin of hairless mice resulted in a significant decrease in the progression of inflammatory skin damages, leading to inhibited activation of NF-${\kappa}B$ signaling and expression of pro-inflammatory mediators. The present study demonstrated that PGG protected from skin damage induced by UVB radiation, and thus, may be a potential candidate for the prevention of environmental stimuli-induced inflammatory skin damage.

• Journal of Photoscience
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• 제8권1호
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• pp.1-7
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• 2001

The deteriorative effect of ultraviolet-B(UV-B) radiation on photosynthesis was assessed by the simultaneous measurement of O$_2$ evolution and chlorophyll(Chl) fluorescence in green pepper. UV-B was given at the intensity of 1 W$.$m$\^$-2/, a dosage often encountered in urban area of Seoul in Korea, to detached leaves. Both Pmax and quantum yield of O$_2$ evolution was rapidly decreased, in a parallel phase, with increasing time of UV-B treatment. Chl fluorescence parameters were also significantly affected. Fo was increased while both Fm and Fv were decreased. Photochemical efficiency of PSII(Fv/Fm) was also declined, although to a lesser extent than Pmax. Both qP and NPQ were decreased similarly with increasing time of UV-B treatment. However, PS I remained stable. The addition of lincomycin prior to UV-B treatment accelerated the decline in Fv/Fm to some extent, suggesting that D1 protein turnover may play a role in overcoming the harmful effect of UV-B. The amount of photosynthetic pigments was less affected than photosynthetic response in showing decline in Chl a and carotenoids after 24 h-treatment. Presumptive flavonoid contents, measured by changes in absorbance at 270 nm , 300 nm and 330nm, were all increased by roughly 50% after 8 h-treatment. Among antioxidant enzymes, activities of catalase and peroxidase were steadily increased until 12h of UV-B treatment whereas ascorbate perxidase, dehydroascorvate reductase and glutathione reductase did not show any significant change. The results indicate that deteriorative effect of UV-B on photosynthesis precedes the protection exerted by pigment synthesis and antioxidant enzymes.

• Biomolecules & Therapeutics
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• 제23권6호
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• pp.557-563
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• 2015

Skin aging is the most readily observable process involved in human aging. Ultraviolet B (UVB) radiation causes photo-oxidation via generation of reactive oxygen species (ROS), thereby damaging the nucleus and cytoplasm of skin cells and ultimately leading to cell death. Recent studies have shown that high levels of solar UVB irradiation induce the synthesis of matrix metalloproteinases (MMPs) in skin fibroblasts, causing photo-aging and tumor progression. The MMP family is involved in the breakdown of extracellular matrix in normal physiological processes such as embryonic development, reproduction, and tissue remodeling, as well as in disease processes such as arthritis and metastasis. We investigated the effect of diphlorethohydroxycarmalol (DPHC) against damage induced by UVB radiation in human skin keratinocytes. In UVB-irradiated cells, DPHC significantly reduced expression of MMP mRNA and protein, as well as activation of MMPs. Furthermore, DPHC reduced phosphorylation of ERK and JNK, which act upstream of c-Fos and c-Jun, respectively; consequently, DPHC inhibited the expression of c-Fos and c-Jun, which are key components of activator protein-1 (AP-1, up-regulator of MMPs). Additionally, DPHC abolished the DNA-binding activity of AP-1, and thereby prevented AP-1-mediated transcriptional activation. These data demonstrate that by inactivating ERK and JNK, DPHC inhibits induction of MMPs triggered by UVB radiation.

• 한국원자력학회:학술대회논문집
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• 한국원자력학회 2002년도 추계학술발표회요약집
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• pp.389-389
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• 2002