• 한국약용작물학회지
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• 제12권2호
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• pp.108-112
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• 2004

Four medicinal plants selected from preliminary screening study were evaluated in the aspects of their antioxidant activities in alcohol-intoxicated rats. Rats fed 1% ${\alpha}-tocopherol-supplemented$ diet as positive control and ones done ${\alpha}-tocopherol-deficient$ diet as negative control were compared with ones done the plant extract-supplemented diet (n=8). After the administration of the experimental diets for 4 weeks, typical increments in activities of manganese-superoxide dismutase (Mn-SOD) and glutathione peroxidase (GSH-px) indicated in alcohol-intoxicated rats, were not observed in ones fed Lagerstroemia and Ulmus extract-supplemented diet. The content of thiobarbituric acid reactive substance (TBARS), the product of lipid peroxidation, did not increased in rats fed plant extracts-supplemented diet except for Terminalia. From the results, it is concluded that Lagerstroemia and Ulmus have physiologically efficient antioxidant activities.

• Molecules and Cells
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• 제45권4호
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• pp.193-201
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• 2022

Excessive production of reactive oxygen species (ROS) is a key phenomenon in tumor necrosis factor (TNF)-α-induced cell death. However, the role of ROS in necroptosis remains mostly elusive. In this study, we show that TNF-α induces the mitochondrial accumulation of superoxide anions, not H₂O₂, in cancer cells undergoing necroptosis. TNF-α-induced mitochondrial superoxide anions production is strictly RIP3 expression-dependent. Unexpectedly, TNF-α stimulates NADPH oxidase (NOX), not mitochondrial energy metabolism, to activate superoxide production in the RIP3-positive cancer cells. In parallel, mitochondrial superoxide-metabolizing enzymes, such as manganese-superoxide dismutase (SOD2) and peroxiredoxin III, are not involved in the superoxide accumulation. Mitochondrial-targeted superoxide scavengers and a NOX inhibitor eliminate the accumulated superoxide without affecting TNF-α-induced necroptosis. Therefore, our study provides the first evidence that mitochondrial superoxide accumulation is a consequence of necroptosis.

• Journal of Microbiology
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• 제35권4호
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• pp.309-314
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• 1997

The manganese-containing superoxide dismutase (MnSOD) is a major component of the cellular defence mechanisms against the toxic effects of the superoxide radical. Within the framework of studies on oxidative stress=responsible enzymes in the Candida sp., the gene encoding the MnSOD was isolated and examined in this study. A specific primer was designed based on conserved regions of MnSOD sequences from other organisms, and was used to isolate the gene by PCR on reverse-transcribed Candida poly($A^{+}$) RNA. The PCR product was used to screen a Candida genomic lambda library and the nucleotide wequence of positive clone was determined. The deduced primary sequence encodes a 25kDa protein which has the conserved residues for enzyme activity and metal binding. The 28 N-terminal amino acids encoded by the Candida cDNA comprise a putatice mitochondrial transit peptide. Potential regulatory elements were identified in the 5' flanking sequences. Northern blot analysis showed that the transcription of the MnSOD gene is induced 5-to 10-fold in response to mercury, cadmium ions and hydrogen peroxide.

• Animal Bioscience
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• 제36권7호
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• pp.1022-1033
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• 2023

Objective: p66Shc, a 66 kDa protein isoform encoded by the proto-oncogene SHC, is an essential intracellular redox homeostasis regulatory enzyme that is involved in the regulation of cellular oxidative stress, apoptosis induction and the occurrence of multiple age-related diseases. This study investigated the expression profile and functional characteristics of p66Shc during preimplantation embryo development in sheep. Methods: The expression pattern of p66Shc during preimplantation embryo development in sheep at the mRNA and protein levels were studied by quantitative real-time polymerase chain reaction (RT-qPCR) and immunofluorescence staining. The effect of p66Shc knockdown on the developmental potential were evaluated by cleavage rate, morula rate and blastocyst rate. The effect of p66Shc deficiency on reactive oxygen species (ROS) production, DNA oxidative damage and the expression of antioxidant enzymes (e.g., catalase and manganese superoxide dismutase [MnSOD]) were also investigated by immunofluorescence staining. Results: Our results showed that p66Shc mRNA and protein were expressed in all stages of sheep early embryos and that p66Shc mRNA was significantly downregulated in the 4-to 8-cell stage (p<0.05) and significantly upregulated in the morula and blastocyst stages after embryonic genome activation (EGA) (p<0.05). Immunofluorescence staining showed that the p66Shc protein was mainly located in the peripheral region of the blastomere cytoplasm at different stages of preimplantation embryonic development. Notably, serine (Ser36)-phosphorylated p66Shc localized only in the cytoplasm during the 2- to 8-cell stage prior to EGA, while phosphorylated (Ser36) p66Shc localized not only in the cytoplasm but also predominantly in the nucleus after EGA. RNAi-mediated silencing of p66Shc via microinjection of p66Shc siRNA into sheep zygotes resulted in significant decreases in p66Shc mRNA and protein levels (p<0.05). Knockdown of p66Shc resulted in significant declines in the levels of intracellular ROS (p<0.05) and the DNA damage marker 8-hydroxy2'-deoxyguanosine (p<0.05), markedly increased MnSOD levels (p<0.05) and resulted in a tendency to develop to the morula stage. Conclusion: These results indicate that p66Shc is involved in the metabolic regulation of ROS production and DNA oxidative damage during sheep early embryonic development.

• 한국환경성돌연변이발암원학회:학술대회논문집
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• 한국환경성돌연변이발암원학회 2004년도 KSOT/KEMS Fall Annual Meeting
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• pp.155-155
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• 2004

• 한국동물학회:학술대회논문집
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• 한국동물학회 2000년도 한국생물과학협회 학술발표대회
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• pp.231.2-231
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• 2000

No Abstract, See Full Text

• 한국동물학회:학술대회논문집
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• 한국동물학회 1999년도 한국생물과학협회 학술발표대회
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• pp.233.2-233
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• 1999

No Abstract, See Full Text

• Journal of Preventive Medicine and Public Health
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• 제37권4호
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• pp.306-311
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• 2004

Background : The roles of antioxidants in the placenta and genetic susceptibility to oxidant chemicals in relation to neonatal birth weight have not been elucidated. We determined whether the level of placental manganese superoxide dismutase (MnSOD) and its genetic polymorphism plays any role in oxidative stress and neonatal birth weight. Methods : We measured placental MnSOD and determined MnSOD genetic polymorphism among 108 pregnant women who were hospitalized for delivery and their singleton live births in Korea. Main outcome measurements are maternal urinary malondialdehyde (MDA) and birth weight. Results : Maternal urinary concentrations of MDA were significantly associated with neonatal birth weight (P=0.04). The enzyme level of placental MnSOD was also significantly associated with MDA concentration (P=0.04) and neonatal birth weight (p<0.01). We observed dose-response relationships between placental MnSOD and maternal urinary MDA, and neonatal birth weight after adjusting for maternal weight, height, age, and neonatal sex. After controlling for covariates, MnSOD variant genotype increased maternal urinary MDA concentrations (p<0.01) and reduced birth weight by 149 gm (P=0.08). Conclusions : This study demonstrates that the placental level of MnSOD during pregnancy significantly affects fetal growth by reducing oxidative stress, and that genetic polymorphism of MnSOD probably modulate the effects of oxidants on fetal growth.

• Journal of Microbiology
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• 제37권2호
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• pp.117-122
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• 1999

Protective roles of antioxidant enzymes, copper-zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD), and catalase of Candida albicans against exogenous reactive oxygens and oxidative killing by macrophages were investigated. The initial growth of C. albicans was inhibited by reactive, oxygen-producing chemicals such as hydrogen peroxide, pyrogallol, and paraquat, but it was restored as the production of antioxidant enzymes were increased. The growth inhibition of C. albicans by reactive, oxygen-producing chemicals was reduced by treating the purified candidal SOD and catalase. Also, in the presence of SOD and catalase, the oxidative killing of C. albicans by macrophages was significantly inhibited. These results suggest that antioxidant enzymes, CuZnSOD, MnSOD, and catalase of C. albicans may play important roles in the protection of C. albicans not only from exogenous oxidative stress but also from oxidative killing by macrophages.

• Nutritional Sciences
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• 제4권2호
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• pp.79-84
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• 2001

The influence of Rhodiola extract on tissue antioxidant status, plasma lipid levels, cholesterol contents of liver and fores were investigated in rats find oxidized linoleic acid. Groups of five-week old male Sprague-Dawley rats fed ad libitum with a diet containing 20% oxidized linoleic acid with or without 300 mg/kg body weight freeze-dried Rhodiola water extract. The antioxidant effect of dietary Rhodiola extract supplementation on the peroxidation potential of rats was investigated. The microsomal thiobarbiruric acid reactive substance (TBARS) contents were changed significantly by Rhodiola extract supplementation. Hepatic Catalase activities were increased in Rhodiola supplemented rats, whereas hepatic Manganese Superoxide Dismutase (MnSOD) or Copper Zinc Superoxide Dismutase (CuZnSOD) were not elevated. In addition, plasma cholesterol lowering effect was observed along with the stimulated excretion of cholesterol through the feces were observed with Rhodiola feeding. Supplementation with Rhodiola extract did not alter high density lipoprotein (HDL) cholesterol. These results support that Rhodiola extract may be effective in protection against oxidative stress, and prevention and treatment of blood dyslipidemia. It demonstntes that Rhodiola extract has a potential to exert anti-atherogenic properties antioxidative capacities .