• Korean Journal of Microbiology
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• v.53 no.2
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• pp.118-122
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• 2017

Bacterial growth inhibition by lead, zinc and cadmium was measured by using modified Tris minimal medium. The toxicity against Escherichia coli strain was in the order of zinc> cadmium> lead, and the Escherichia coli strain overexpressing iron-containing superoxide dismutase 2 of Streptomyces coelicolor A3(2) was found to have resistance to heavy metals.

• BMB Reports
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• v.28 no.3
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• pp.249-253
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• 1995

The nonenzymatic glycation of copper, zinc-superoxide dismutase (Cu,Zn-SOD) led to inactivation and fragmentation of the enzyme. The glycated Cu,zn-SOD was isolated by boronate affinity chromatography. The formation of 8-hydroxy-2'-deoxyguanosine (8-OH-dG) in calf thymus DNA and the generation of strand breaks in pBhiescript plasmid DNA by a metal-catalyzed oxidation (MCO) system composed of $Fe^{3+}$, $O_2$, and glutathione (GSH) as an electron donor was enhanced more effectively by the glycated CU,Zn-SOD than by the nonglycated enzyme. The capacity of glycated Cu,Zn-SOD to enhance damage to DNA was inhibited by diethylenetriaminepentaacetic acid (DETAPAC), azide, mannitol, and catalase. These results indicated that incubation of glycated CU,Zn-SOD with GSH-MCO may result in a release of $Cu^{2+}$ from the enzyme. The released $Cu^{2+}$ then likely participated in a Fenton-type reaction to produce hydroxyl radicals, which may cause the enhancement of DNA damage.

• Environmental Mutagens and Carcinogens
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• v.21 no.2
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• pp.67-71
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• 2001

Effects of exposure to a neurotoxicant, fenitrothion on antioxidant enzyme activities in Chironomus riparius Mg. (Diptera, Chironomidae) larvae were evaluated under laboratory conditions. Exposure to this chemical led to an increase of cupper, zinc type superoxide dismutase and manganese type superoxide dismutase activities and to a decrease of glutathion peroxidase activity. An activation of catalase was observed in the larvae exposed to high fenitrothion concentration. The response of superoxide dismutase was rapid and sensitive to low chemical concentrations, but changes in catalase, total peroxidase and glutathion peroxidase were less sensitive. In this study, antioxidant enzyme activities in Chironomus riparius larvae were identified as pertinent biomarkers for environmental monitoring.

• BMB Reports
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• v.32 no.5
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• pp.440-444
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• 1999

Membrane lipid peroxidation processes yield reactive aldehydes that may react with copper,zinc superoxide dismutase (Cu,Zn SOD), one of the key antioxidant enzymes against oxidative stress. We investigated this possibility and found that exposing Cu,Zn SOD to malondialdehyde (MDA) or 4-hydroxynonenal (HNE) caused the loss of dismutase activity, cross-linking of peptides, and an increase in protein oxidation, reflected by the increased level of carbonyl groups. When Cu,Zn SOD that had been exposed to MDA or HNE was subsequently analyzed by amino acid analysis, histidine content was found to be significantly lost. Both MDA-and HNE-treated Cu,Zn SOD were resistant to proteolysis, which may imply that damaged proteins exist in vivo for a longer period of time than the native enzyme. The lipid peroxidation-mediated damage to Cu,Zn SOD may result in the perturbation of cellular antioxidant defense mechanisms, and subsequently lead to a pro-oxidant condition.

• Journal of Photoscience
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• v.9 no.2
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• pp.430-432
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• 2002

The changes in expression of copper-zinc superoxide dismutase (CuZn-SOD), manganese superoxide dismutase (Mn-SOD) and glutathione peroxidase (GPX) in light-damaged rat retinas were examined. Sprague-Dawley rats (male, 6-weeks-old) were maintained on a cyclic photoperiod (12 hours light and 12 hours darkness) for 2 weeks. The illumination intensity during the light period was 80 lux. To induce light damage to the retina, a high-intensity illumination (3000-lux) was applied to the animals for 24 hours. After light exposure, the animals were returned to cyclic lighting. Eyes were enucleated 12 and 24 hours after light exposure started or 1,3, and 7 days after light exposure ended. Eyes were fixed and embedded in paraffin wax. Tissues were cut into 4${\mu}{\textrm}{m}$-thick sections. Sections were immunostained using antibody against CuZn-SOD, Mn-SOD, GPX and 8-hydroxy-deoxyguanocine (8-OHdG) as oxidative stress marker. 8-OHdG was observed in the outer nuclear layer (ONL) and retinal pigment epithelium (RPE) during light exposure. In light-damaged retinas CuZn-SOD labeling was up regulated in the ONL and RPE. Mn-SOD labeling was up regulated in rod inner segments (RIS) during light exposure and that in the RPE was up regulated after exposure. GPX labeling was observed in rod outer segments (ROS) during light exposure. GPX labeling was also observed in the RPE during and after light exposure. All three enzymes were observed in the outer retina, which suffered light damage, but occurred in defferent layers except within the RPE, in which case all three were expressed. These enzymes may play complementary roles as protective factors in light-damaged retinas.

• Journal of the Korean Chemical Society
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• v.38 no.1
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• pp.74-79
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• 1994

The participation of superoxide in initiating tissue damage derived from xenobiotics is best illustrated by paraquat intoxication. In the present study, the roles of superoxide dismutase and catalase on paraquat-induced cell injury were investigated using primary cultured rat skin fibroblast. The degree of cell injury was assassed by the conversion of reduced MTT to a blue formazan. Paraquat produced concentration-and time-related cell injury in cultured rat skin fibroblast. Paraquat induced-cell injury was aggravated by pretreatment of aminotriazol (AT: 10 mM), an catalase inhibitor, and attenuated by addition of catalase (100∼500 unit/ml). However, the effects of diethyldithiocarbamate (DDC : 10 mM), copper- and zinc-containing superoxide dismutase (Cu, Zn-SOD) inhibitor, and Cu, Zn-SOD on paraquat-induced injury were not significant. These results suggest that hydrogen peroxide might be more responsible factor than superoxide in the pathogenesis of paraquat-induced cell injury.

• Toxicological Research
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• v.16 no.3
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• pp.179-185
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• 2000

Zinc is known to generate reactive oxygen species (ROS) including superoxide anion and hydrogen peroxide ($H_2O_2$), which eventually contribute to cytotoxicity in a variety of cell types. Here in, we demonstrated that zinc decreased the viability of C6 glial cells in a time and dose-dependent manner, which was revealed as apoptosis characterized by ladder-pattern fragmentation of genomic DNA. chromatin condensation and DNA fragmentation in Hoechst dye staining. Zinc-induced apoptosis of C6 glial cells was prevented by the addition of catalase and antioxidants including reduced glutathione (GSH), N-acetyl-L-cysteine (NAC) and pyrrolidinedithiocarbamate (PDTC). Wefurther confirmed that zinc decreased intrac-ellular levels of GSH and generated $H_2O_2$in C6 glial cells. Moreover, antioxidants also decreased the generation of zinc-induced $H_2O_2$ in C6 glial cells. These data indicated that zinc-induced the apoptotic death of C6 glial cells via generation of reactive oxygen species such as $H_2O_2$.

• The Journal of Korean Medicine
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• v.22 no.3
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• pp.63-73
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• 2001

Objectives : The objective of the current study is to determine the protective effect of Ukyium(Yougui-yin) on the apoptosis induced by zinc. Methods : Zinc is known to generate reactive oxygen species (ROS), including superoxide anion ($O_2$) and hydrogen peroxide ($H_2O_2$), which eventually contribute to cytotoxicity in a variety of cell types. We investigated the viablity of cells, $H_2O_2$ generation, chromatin condensation and nuclear fragmentation in Hoechst dye staining and $IkB-{\alpha}$ degradation in C6 glial cells of $ZnCl_2$ between pretreatment- and not pretreatment-group with Ukyium. The former methods were researched by Time- and Dose-dependent manners. Results : We demonstrated that pretreatment with Ukyium prevented zinc-induced cell death of C6 glial cells and apoptotic characteristics including chromatin condensation and nuclear fragmentation. Ukyium also prevented $H_2O_2-induced$ cell death. We further confirmed that Ukyium decreased zinc-induced generation of $H_2O_2$ and inhibited degradation of $IkB-{\alpha}$ by zinc in C6 glial ceHs. Conclusions : These data indicated that Ukyium (Yougui-yin) prevents zinc-induced apoptotic death of C6 glial cells via inhibition of ROS generation, such as $H_2O_2$ as well as inhibition of $IkB-{\alpha}$ degradation.

• Journal of Nutrition and Health
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• v.32 no.3
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• pp.277-286
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• 1999

This study was conducted to assess dietary intake and nutritional status of zinc and copper in Korean college women. Dietary survey was conducted by 24-hour recall method and fasting serum samples were collected from 111 apparently healthy subjects. Intake levels of zinc and copper were calculated using newly developed database for Zn & Cu of Korea food. Serum levels of Zn, Cu and activities of ALP, EC-SOD were measured from fasting serum sample. Mean daily zinc and copper intakes were 6.72mg/day(56.0% RDA) and 1.11mg/day respectively. Mean values of serum ALP activity, zinc and copper concentration were 43.9U/L, 14.8umol/1, 15.5umol/1and these values were mostly within normal range. EC-SOD activitis of the subjects were low and had no correlation with intake or serum levels of Zn, Cu. In conclusion, these results show that zinc and copper intake of Koran college women are lower than those from other counties but higher than those of adults in rural area of Korea. Their serum levels of Zn, Cu, ALP are relatively normal. These results indicate that marginal deficiency of Zn and Cu may be quite prevalent in these subjects but serum indicators measured may not be sensitive enough to detect such marginal deficiency. Further study in needed to develop a biochemical index sensitive enough to evaluate Zn and Cu status.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.8
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• pp.4627-4634
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• 2013

Chemoprotection refers to the use of specific natural or synthetic chemical agents to suppress or prevent the progression to cancer. The purpose of this study is to assess the protective effect of aspirin, vitamin C or zinc in a dimethyl hydrazine (DMH) colon carcinoma model in rats and to investigate the effect of these supplements on changes associated with colonic zinc status. Rats were randomly divided into three groups, group 1 (aspirin), group 2 (vitamin C) and group 3 (zinc), each being subdivided into two groups and given subcutaneous injection of DMH (30 mg/kg body wt) twice a week for 3 months and sacrificed at 4 months (A-precancer model) and 6 months (B-cancer model). Groups 1, 2, 3 were simultaneously given aspirin, vitamin C, or zinc supplement respectively from the beginning till the end of the study. It was observed that 87.5% of rats co-treated with aspirin or vitamin C showed normal colonic histology, along with a significant decrease in colonic tissue zinc at both time points. Rats co-treated with zinc showed 100% reduction in tumor incidence with no significant change in colonic tissue zinc. Plasma zinc, colonic CuZnSOD (copper-zinc superoxide dismutase) and alkaline phosphatase activity showed no significant changes in all 3 cotreated groups. These results suggest that aspirin, vitamin C or zinc given separately, exert a chemoprotective effect against chemically induced DMH colonic preneoplastic progression and colonic carcinogenesis in rats. The inhibitory effects are associated with maintaining the colonic tissue zinc levels and zinc enzymes at near normal without significant changes.