직업과 생활 습관, 그리고 CYP1A1, GSTM1, GSTT1 유전자 다형성이 요중 1-hydroxypyrene과 2-naphthol 농도에 미치는 영향

김헌,강종원,임현술,이호익,김용대,남홍매,이철호 大韓産業醫學會 1999 대한직업환경의학회지 Vol.11 No.4

Objectives : This study was performed to describe the distribution patterns of urinary 1-hydroxypyrene (1-OHP) and 2-naphthol concentration in coke oven workers and workers not occupationally exposed to polycyclic aromatic hydrocarbons (PAH), and to determine the effects of occupation, life style, and genetic polymorphism of cytochrome P450 1A1(CYP1A1), glutathione S-transferase mu 1 (GSTM1) and theta 1 (GSTT1) on urinary 1-OHP and 2-naphthol concentration. Methods : The study subjects were 19 coke oven workers and 156 shipyard workers. A questionnaire was used to obtain data about detailed smoking and food intake history. Urinary 1-OHP and 2-naphthol concentration and genetic polymorphism of CYP1A1, GSTM1, and GSTT1 were analyzed. Results : The urinary 1-OHP and 2-naphthol concentration was higher in the coke oven workers and in smokers. Urinary 1-OHP concentration was significantly correlated with time after last intake of roasted in non-smoking coke oven workers, whereas urinary 2-naphthol concentration was with amount of cigarette smoking at the sampling day in smoking shipyard workers. Urinary 1-OHP, but not 2-naphthol, concentration of the shipyard workers with Ile/Ile type of CYP1A1 was significantly lower than that of the shipyard workers with other CYP1A1 genotype. Conclusions : Urinary 1-OHP would be a better marker for occupational exposure to PAH in coke oven workers, and urinary 2-naphthol might be better for non-occupational inhalation exposure to PAH. CYP1A1 would not play an important role in the metabolism of naphthalene but in the metabolism of pyrene.

Effect of KIOM-79 against mitochondrial damage induced by streptozotocin in pancreatic beta-cells.

Kang, Kyoung Ah,Kim, Jin Sook,Zhang, Rui,Piao, Mei Jing,Ko, Dong Ok,Wang, Zhi Hong,Heo, Young Jun,Park, Doek Bae,Maeng, Young Hee,Hyun, Jin Won Taylor Francis 2009 Journal of toxicology and environmental health. Pa Vol.72 No.20

<P>The present study examined the effects of KIOM-79 on streptozotocin (STZ)-induced mitochondrial oxidative stress in rat pancreatic beta-cells (RINm5F). KIOM-79 is a mixture of plant extracts from parched Puerariae radix, gingered Magnoliae cortex, Glycyrrhizae radix, and Euphorbiae radix. A marked increase in mitochondrial reactive oxygen species (ROS) was observed in STZ induced diabetic cells, which returned to control conditions after KIOM-79 treatment. Mitochondrial manganese superoxide dismutase (Mn SOD) activity and its protein expression were downregulated by STZ treatment but upregulated by KIOM-79 treatment. In addition, KIOM-79 treatment restored the loss of the mitochondrial membrane potential (Deltapsi) produced by STZ treatment. KIOM-79 induced an increase in Bcl-2 and a decrease in phospho Bcl-2 and Bax, which are related to permeability of the mitochondrial membrane. Further, KIOM-79 inhibited the translocation of cytochrome c from the mitochondria to the cytosol and elevated the ATP level, which was reduced by STZ treatment. These results suggest that KIOM-79 exhibits a protective effect through activation of antioxidant defense mechanisms and by attenuation of mitochondrial dysfunction in STZ-induced diabetic cells.</P>

Myricetin Protects Cells against Oxidative Stress-Induced Apoptosis via Regulation of PI3K/Akt and MAPK Signaling Pathways

Kang, Kyoung Ah,Wang, Zhi Hong,Zhang, Rui,Piao, Mei Jing,Kim, Ki Cheon,Kang, Sam Sik,Kim, Young Woo,Lee, Jongsung,Park, Deokhoon,Hyun, Jin Won Molecular Diversity Preservation International (MD 2010 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.11 No.11

<P>Recently, we demonstrated that myricetin exhibits cytoprotective effects against H<SUB>2</SUB>O<SUB>2</SUB>-induced cell damage via its antioxidant properties. In the present study, myricetin was found to inhibit H<SUB>2</SUB>O<SUB>2</SUB>-induced apoptosis in Chinese hamster lung fibroblast (V79-4) cells, as shown by decreased apoptotic bodies, nuclear fragmentation, sub-G<SUB>1</SUB> cell population, and disruption of mitochondrial membrane potential (Δψ<I><SUB>m</SUB></I>), which are increased in H<SUB>2</SUB>O<SUB>2</SUB>-treated cells. Western blot data showed that in H<SUB>2</SUB>O<SUB>2</SUB>-treated cells, myricetin increased the level of Bcl-2, which is an anti-apoptotic factor, and decreased the levels of Bax, active caspase-9 and -3, which are pro-apoptotic factors. And myricetin inhibited release of cytochrome c from mitochondria to cytosol in H<SUB>2</SUB>O<SUB>2</SUB>-treated cells. Myricetin-induced survival correlated with Akt activity, and the rescue of cells by myricetin treatment against H<SUB>2</SUB>O<SUB>2</SUB>-induced apoptosis was inhibited by the specific PI3K (phosphoinositol-3-kinase) inhibitor. Myricetin-mediated survival also inhibited the activation of p38 mitogen activated protein kinase (MAPK) and c-Jun <I>N</I>-terminal kinase (JNK), which are members of MAPK. Our studies suggest that myricetin prevents oxidative stress-induced apoptosis via regulation of PI3K/Akt and MAPK signaling pathways.</P>

Inhibitory Effects of Triphlorethol-A on MMP-1 Induced by Oxidative Stress in Human Keratinocytes via ERK and AP-1 Inhibition

Kang, Kyoung Ah,Zhang, Rui,Piao, Mei Jing,Ko, Dong Ok,Wang, Zhi Hong,Lee, Kyung,Kim, Bum Joon,Shin, Taekyun,Park, Jae Woo,Lee, Nam Ho,Yoo, Byoung Sam,Hyun, Jin Won Taylor Francis 2008 Journal of toxicology and environmental health. Pa Vol.71 No.15

<P> Oxidative stress is known to generate reactive oxygen species (ROS) in cells, which subsequently induce the synthesis of matrix metalloproteinases (MMP) and an aging phenomenon. The protective effects of triphlorethol-A, derived from Ecklonia cava, were investigated against hydrogen peroxide (H2O2)-induced damage using human skin keratinocytes. Data showed that triphlorethol-A inhibited ROS formation, induced catalase expression, inhibited DNA damage, and increased cell viability in keratinocytes. Triphlorethol-A treatment significantly reduced MMP-1 expression and production, compared to H2O2-treated cells. In addition, triphlorethol-A abrogated the activation of extracellular signal regulated protein kinase (ERK), which originates upstream of MMP-1 expression, and was induced by H2O2 treatment. Moreover, triphlorethol-A inhibited DNA binding activity of activator protein-1 (AP-1), a downstream transcription factor of ERK. Data indicate that the antioxidative properties of triphlorethol-A involve the inhibition of MMP-1 via ERK and AP-1 inhibition.</P>

청소년의 자아상 발달에 대한 횡문화적 비교 연구

홍강의,신민섭,표미자,우종인,조수철,정도언,하규섭 大韓神經精神醫學會 1998 신경정신의학 Vol.37 No.6

목 적: 문화적이거나 민족적인 요인이 청소년들의 자아상 발달에 미치는 영향을 알아보기 위해 한국 청소년들과 조선족, 한족 청소년들을 대상으로-횡문화적 비교연구를 수행하였다. 방 법 : 서울과 충주에 위치한 중,고등학생 1576명(남 891, 여 685)과, 중국 연변 룡정시에 위치한 한족 중,고등학생 634명 (남 305.·여 329). 그리고 조선족 중.고등학생 665명(남 317.여 348)이 피험자로 참여하였으며, 세 집단의 연령범위는 중1에서 고3까지 13∼18세였다. 연구도구로는 한국판 Offer 자아상 척도(KOSIQ-R)가 사용되었다 한국 청소년들에게는 본 연구자가 학급별로 KOSIQ-R을 실시하였고. 조선족과 한족 청소년들에게는 연변에 거주하는 조선족 정신과의사가 KOSIQ-R을 중국어로 번안한 후 학급별로 실시하였다. 변량분석방법을 사용하여 KOSIQ-R의 12개 하위척도점수와 전체 자아상점수의 평균치상에서 각 민족 집단간의 차이를 성별과 연령별로 비교. 분석하였다. 결 과: 12개 하위척도 점수와 전체 자아 상 점수에서 민족 집단간의 차이가 유의미하게 나타났다. 성별과 연령 변인에 상관없이 성 척도를 제오한 모든 척도 점수에서 한국 청소년 집단이 가장 높은 점수를 보였으며, 한족과 조선족 집단간에는 신체상과 정신건강 척도를 제외한 10개 하위척도와 잔체 자아상 점수에서 유의미한 차이가 있었다. 조선족 청소년들은 윤리적 가치, 이타성, 가족기능, 사회적 기능, 충동 조절, 자신감 척도와 전체 자아상점수에서 더 높은 점수를 보인 반면, 한족 청소년 들은 정서상태, 성, 직업에 대한 태도, 자기-신뢰척도에서 조선족 청소년집단에 비해 유의미하게 더 높은 점수를 보였다. 결론 : 청소년들의 자아상 발달에 민족적인 요인(한민족-한족)과 문화적인 요인(민주주의-사회주의)이 중요한 영향을 준다고 볼 수 있다. 조선족 청소년들은 여러 하위척도에서 한국과 한족 청소년들의 중간 점수를 보여, 중국과 한국문화사이에서 이중적응을 하고 있음이 시사되었다. 그러나 사회적으로 바람직하게 보이려는 측면에서는 한국청소년들과 유사한 특성을 보였으며, 이는 조선족 청소년들이 비록 다른 문화권에서 성장했다할 지라도 사회적인 관계에서 예절과 체면, 도덕성을 강조하는 한민족 전통의 가치관이 가정내에서 학습되어 내제화되었음을 시사해주었다. Objectives : In order to investigate the effect of cultural and ethnic differences on the development of self-image, we conducted a cross-cultural study on Korean, Korean-Chinese and Chinese adolescents. Methods : A total of 1576 Koreans middle and high school students in Seoul/choongju, 665 Korean-Chinese students and 634 Chinese students living in Yunbyun, China participated in this study. The Korean version of the Offer Self-Image Questionnaire was administered to Korean students, and the Chinese version of the questionnaire was administered to Korean-chinese and Chinese students. The data obtained from all subjects were analyzed according to ethnicity and age variable through AN0VA. Results : A significant difference across ethnicity was found in the 12 subscales and the total self-image score of OSIQ-R Korean adolescents obtained significantly higher scores in all of the 11 subscales except the sexuality subscale than Korean-Chinese and Chinese adolescents. Korean-Chinese adolescents obtained significantly higher scores on the ethical value, idealism, family functioning, social functioning, impulse control, self-confidence and total self-image scores than Chinese adolescents, whereas Chinese adolescents obtained significantly higher stores in the subscales of emotional tone, sexuality, vocational attitudes, and self-reliance than Korean - Chinese adolescents . Conclusion : The results suggest the possibility that the difference in ethnicity(Korean versus Chinese), the tradition associated with earth ethnic group, and the cultural-political factor (democracy versus socialism) significantly affects the development of self-image in adolescents. Although Korean-Chinese adolescents seemed to show cultural pluralism between Korean and Chinese cultures, they were similar to Korean adolescents in their tendency to respond in socially desirable ways, which suggests that although raised under the different cultural systems, traditional Korean ethical values were learned and internalized within the family.

기체크로마토그래피법을 이용한 오가피 중 아칸토산과 그 이성질체의 분석

강지연,정영희,임은희,이은주,주홍매,정수진,배기환,김영호,강종성 충남대학교 약학대학 의약품개발연구소 2005 藥學論文集 Vol.20 No.-

Acanthoic acid, continentalic acid and kaurenoic acid are bioactive diterpenoids which were structural isomers isolated from Acanthopanax species. For the quality evaluation of Acanthopanax species a gas chromatographic method for the separation and quantitation of these isomers was developed. Three compounds were successfully separated from the extracts of leaves, stems and roots of Acanthopanax species. GC-MS provided the identification of components separated from the extracts. Adequate separation of the components from Acanthopanax species was achieved on a fused-silica dimethyl polysiloxane capillary column (15 m x 0.25 ㎜, 0.25 ㎛ film thickness) operated with temperature programming from 160℃ held 0.5 min, increased at 11℃/min to 290℃ held 0.5 min with the carrier gas flow-rate (helium) of 5.1 ㎖/min. Among six Acanthopanax species only two species (A. koreanum and A. trifoliatus) contained the diterpenoids indication that the two species might possess the taxonomical similarity.

Pretreatment of Macrophages with Paclitaxel Inhibits iNOS Expression

Mei Hong Li,Jong Soon Kang,Hwanmook Kim,Young Jin Jeon 한국독성학회 2006 Toxicological Research Vol.22 No.2

We demonstrate that paclitaxel, an antitumor agent derived from yew tree, inhibits LPS-induced expression of iNOS gene in RAW 264.7 cells. Previously, paclitaxel has been known to induce iNOS gene expression in macrophages. However, in this report we described that the pretreatment of macrophages with paclitaxel (0.1 μM) for 8 h inhibited LPS-induced iNOS gene expression. Pretreatment of RAW 264.7 cells with paclitaxel significantly inhibited LPS-stimulated nitric oxide (NO) production. Western immunoblot of iNOS and RT-PCR analysis showed that the decrease of NO was due to the inhibition of iNOS gene expression in RAW 264.7 cells. Immunocytochemical staining of iNOS further confirmed that pretreatment of macrophages with paclitaxel inhibited macrophage activation. Electrophoretic mobility shift assay showed that paclitaxel inhibited NF-κ/Rel DNA binding. Collectively, these series of experiments indicate that paclitaxel inhibits iNOS gene expression by blocking NF-κB/Rel activation.

Ischemic postconditioning protects cardiomyocytes against ischemia/reperfusion injury by inducing MIP2

Hong-Lin Zhu,Kang-Kai Wang,Xing Wei,Shun-Lin Qu,Chi Zhang,Xiao-Xia Zuo,Yan-Sheng Feng,Qi Luo,Guang-Wen Chen,Mei-Dong Liu,Lei Jiang,Xian-Zhong Xiao 생화학분자생물학회 2011 Experimental and molecular medicine Vol.43 No.8

Cardiomyocytes can resist ischemia/reperfusion (I/R)injury through ischemic postconditioning (IPoC)which is repetitive ischemia induced during the onset of reperfusion. Myocardial ischemic preconditioning up-regulated protein 2 (MIP2) is a member of the WD-40family proteins, we previously showed that MIP2 was up-regulated during ischemic preconditioning (IPC). As IPC and IPoC engaged similar molecular mechanisms in cardioprotection, this study aimed to elucidate whether MIP2 was up-regulated during IPoC and contributed to IPoC-mediated protection against I/R injury. The experiment was conducted on two models,an in vivo open chest rat coronary artery occlusion model and an in vitro model with H9c2 myogenic cells. In both models, 3 groups were constituted and randomly designated as the sham, I/R and IPoC/hypoxia postconditioning (HPoC) groups. In the IPoC group, after 45 min of ischemia, hearts were allowed three cycles of reperfusion/ischemia phases (each of 30 s duration)followed by reperfusion. In the HPoC group, after 6 h of hypoxia, H9c2 cells were subjected to three cycles of 10 minute reoxygenation and 10 minute hypoxia followed by reoxygenation. IPoC significantly reduced the infarct size, plasma level of Lactate dehydrogenase and creatine kinase MB in rats. 12 h after the reperfusion,MIP2 mRNA levels in the IPoC group were 10 folds that of the sham group and 1.4 folds that of the I/R group. Increased expression of MIP2 mRNA and attenuation of apoptosis were similarly observed in the HPoC group in the in vitro model. These effects were blunted by transfection with MIP2 siRNA in the H9c2cells. This study demonstrated that IPoC induced protection was associated with increased expression of MIP2. Both MIP2 overexpression and MIP2 suppression can influence the IPoC induced protection.

Toxic effects of lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on development of male reproductive system: Involvement of antioxidants, oxidants, and p53 protein

Jin, Mei Hua,Hong, Chang Hee,Lee, Hye Young,Kang, Hyo Jin,Han, Sang Won Wiley Subscription Services, Inc., A Wiley Company 2010 Environmental toxicology Vol.25 No.1

<P>2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent endocrine disruptor compound and induces multiple organ dysfunctions. The effect of TCDD exposure both in adults and in utero has been well established. However, little is known about the effects of TCDD acquired through mother's milk on the development of the male reproductive system. The aim of this study was to investigate the effects and mechanisms of TCDD from lactational exposure. TCDD (1 μg/kg) was administered to C57BL/6 mouse mothers for 4 days from the day of delivery. On postnatal day 30 (PND 30) and postnatal day 60 (PND 60), body weight, body length, and anogenital distance (AGD) of male offspring were measured. The weights of the testes and epididymides were also measured. Epididymides were used for sperm counts, and testes were used to measure the activity of antioxidant enzymes (SOD, CAT, GPX, GR), the parameters of oxidative stress (hydrogen peroxide, MDA), and testosterone. In addition, expression of p53 and the proapoptotic protein, Bax, were analyzed by Western blot. TCDD exposure decreased body weight, body length, and AGD in both PND 30 and PND 60 groups compared with the control group. The activity of all antioxidant enzymes at PND 60 was decreased after TCDD treatment. TCDD treatment decreased testicular testosterone levels in both the PND 30 and PND 60 groups. The expression of p53 and Bax were also upregulated by TCDD and did not return to normal levels by PND 60. These data suggest that TCDD affects development of male offspring when the mother is exposed to TCDD during lactation. In addition, oxidative stress is a major mediator of TCDD-induced adverse effects, and p53 may play an important role in this mechanism. © 2008 Wiley Periodicals, Inc. Environ Toxicol, 2010.</P>

Pretreatment of Macrophages with Paclitaxel Inhibits iNOS Expression

Li Mei-Hong,Kang Jong-Soon,Kim Hwan-Mook,Jeon Young-Jin Korean Society of ToxicologyKorea Environmental Mu 2006 Toxicological Research Vol.22 No.2

We demonstrate that paclitaxel, an antitumor agent derived from yew tree, inhibits LPS-induced expression of iNOS gene in RAW 264.7 cells. Previously, paclitaxel has been known to induce iNOS gene expression in macrophages. However, in this report we described that the pre-treatment of macrophages with paclitaxel ($0.1{\mu}M$) for 8 h inhibited LPS-induced iNOS gene expression. Pretreatment of RAW 264.7 cells with paclitaxel significantly inhibited LPS-stimulated nitric oxide (NO) production. Western immunoblot of iNOS and RT-PCR analysis showed that the decrease of NO was due to the inhibition of iNOS gene expression in RAW 264.7 cells. Immunocytochemical staining of iNOS further confirmed that pretreatment of macrophages with paclitaxel inhibited macrophage activation. Electrophoretic mobility shift assay showed that paclitaxel inhibited $NF-_{\kappa}/Rel$ DNA binding. Collectively, these series of experiments indicate that paclitaxel inhibits iNOS gene expression by blocking $NF-_{\kappa}B/Rel$ activation.