• Molecules and Cells
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• v.40 no.8
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• pp.542-549
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• 2017

Cardiomyocyte apoptosis is initiated by various cellular insults and accumulated cardiomyocyte apoptosis leads to the pathogenesis of heart failure. Excessive reactive oxygen species (ROS) provoke apoptotic cascades. Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme that converts cellular ROS into harmless products. In this study, we demonstrate that MnSOD is down-regulated upon hydrogen peroxide treatment or ischemia/reperfusion (I/R) injury. Enhanced expression of MnSOD attenuates cardiomyocyte apoptosis and myocardial infarction induced by I/R injury. Further, we show that miR-23a directly regulates the expression of MnSOD. miR-23a regulates cardiomyocyte apoptosis by suppressing the expression of MnSOD. Our study reveals a novel model regulating cardiomyocyte apoptosis which is composed of miR-23a and MnSOD. Our study provides a new method to tackling apoptosis related cardiac diseases.

• Korean Journal of Plant Tissue Culture
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• v.27 no.2
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• pp.133-136
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• 2000

To evaluate the biological effects of dykellic acid, a novel apoptosis inhibitor, isolated from microorganism on the plant cells, the cell growth, protein contents, and superoxide dismutase (SOD) activity were investigated in suspension cultures of tobacco photomixotrophic cultured (PM) cells on 12 days after different concentration of chemical treatment. The cells were cultured in MS medium containing 0.7 mg/L 2,4-D, 0.3 mg/L kinetin, 30 g/L sucrose and 200 mM NaCl at $25^{\circ}C$ in the light (100 rpm). Dykellic acid strongly inhibited the cell growth by evaluating the cell fresh wt and the ion conductivity in the medium ($IC_{50}$/, about 20 $\mu$M). The results as inhibition of cell growth and cell wall damage were same. The compound significantly increased the protein contents and the SOD specific activity in proportion with the dosage. The results suggested that dykellic acid may have biological activity in plant cells and tobacco PM cells may be suitable biomaterials for in vitro evaluation of the biological activity of natural products.

• Toxicological Research
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• v.13 no.4
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• pp.359-365
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• 1997

Many factors are known to be responsible for cerebral ischemic injury, such as excitatory neurotransmitters, increased intraneuronal calcium, or disturbance of cellular energy metabolism. Recently, oxygen free radicals, formed during ischemia/reperfusion, have been proposed as one of the main causes of ischemia/reperfusion injury. Therefore, to investigate the role of oxygen free radical during ischemia/reperfusion, in the present study the effect of endogenous oxygen free radical scavenger, superoxide dismutase / catalase(SOD / catalase) on the release of [$^3$H]-5-hydroxytryptamine([$^3$H]-5-HT) during hypoxia/reoxygenation in rat hippocampal slices was measured. The hippocampus was obtained from the rat brain and sliced 400 gm thickness with manual chopper. After 30 min's preincubation in the normal buffer, the slices were incubated for 20 min in a buffer containing [$^3$H]-5-HT(0.1 $\mu$M, 74 $\mu$Ci) for uptake, and washed. To measure the release of [$^3$H]-5-HT into the buffer, the incubation medium was drained off and refilled every ten minutes through a sequence of 14 tubes. Induction of hypoxia for 20 min (gassing it with 95% N$_2$/5% CO$_2$) was done in the 6th and 7th tube, and oxygen free radical scavenger, SOD / catalase was added 10 minutes prior to induction of hypoxia. The radioactivity in each buffer and the tissue were counted using liquid scintillation counter and the results were expressed as a percentage of the total activity. When slices were exposed to hypoxia for 20 min, [$^3$H]-5-HT release was markedly decreased and a rebound release of [$^3$H]-5-HT was observed on the post-hypoxic reoxygenation period. SOD / catalase did not changed the release of [$^3$H]-5-HT in control group, but inhibited the decrease of [$^3$H]-5-HT release in hypoxic period and rebound increase of [$^3$H]-5-HT in reoxygenation period. This result suggest that superoxide anion may play a role in the hypoxic-, and reoxygenation-induced change of [$^3$H]-5-HT release in rat hippocampal slices.

• Parasites, Hosts and Diseases
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• v.29 no.3
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• pp.259-266
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• 1991

In cytosolic (raction of adult Paragonimus westermani, superoxide dismutase activity was identified (4.3 units/mg of specific activity) using a xanthine-xanthine oxidase system. The enzyme was purified 150 fold in its activity using the ammonium sulfate precipitation, DEAE-Trisacryl M anion-exchange chromatography and Sephadex G-100 molecular sieve chromatography. The enzyme exhibited the enhanced activity at pH 10.0. The enzyme activity totally disappeared in 1.0mM cyanide while it remained 77.8% even in 10 mM azide. These findings indicated that the ensyme was Cu, Zn-SOD type. Molecular mass of the enzyme was estimated to be 34 kDa by gel filtration and 17 kDa on reducing SDS-polyacrylamide gel electrophoresis which indicated a dimer protein.

• Korean Journal of Microbiology
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• v.43 no.2
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• pp.83-90
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• 2007

Sphingomonas sp. KS 301, which was isolated from oil contaminated soil, was shown to have five different SODs (SODI, II, III, IV, V) which can be separated by DEAE-Sepharose chromatography, and SOD III was finally purified in this study by ammonium sulfate precipitation, DEAE-Sepharose chromatography, Superose 12 gel filtration and Uno-Q1 ion exchange chromatography. The molecular weight of SOD III was 23 kDa as determined by SDS-PAGE and the apparent molecular weight of the native enzyme was estimated to be approximately 71 kDa by Superose-12 gel filtration chromatography. These data suggest that the purified SOD consists of at least two subunits. The specific activity of the SOD III was higher than Mn type or Fe type SOD of Escherichia coli by 5 fold. To determine the type of SOD III, inhibitory effects of $NaN_{3},\;H_{2}O_{2},\;KCN$ were examined. 10 mM $NaN_{3}$ was able to inhibit 56% of the SOD III activity, which indicates that this SOD is Mn type. The optimum pH of the SOD III was 7.0 and the optimum temperature was $20^{\circ}C$. N-terminal amino acid sequence of purified SOD III was most similar to those of Psudomonase ovalis and Vibrio cholerae among bacteria.

• Proceedings of the Microbiological Society of Korea Conference
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• 2004.05a
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• pp.47-50
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• 2004

The defenses against free radical damage include specialized repair enzymes that correct oxidative damages in DNA, and detoxification systems such as superoxide dismutases. These defenses may be coordinated genetically as global responses. We hypothesized that the expression of the SOD and the DNA repair genes would inhibit DNA damage under oxidative stress. Therefore, the protection of E. coli mutants deficient in SOD and DNA repair genes $(sod^-\;xth^-\;and\;nfo^-)$ was demonstrated by transforming the mutant strain with a plasmid pYK9 which encoded Photobacterium leiognathi CuZnSOD and human AP endonuclease. The results show that survival rates were increased in $sod^+\;xth^-\;nfo^+$ cells compared to $sod^-\;xth^-\;ap^+,\;sod^-\;xth^-\;ap^-,\;and\;sod^+\;xth^-\;ap^-$ cells under oxidative stress generated from 0.1 mM Paraquat or 3 mM $H_2O_2$. The data suggested that, at least, SOD and DNA repair enzymes may have collaborate protection and repair of the damaged DNA. Additionally, both enzymes are required for protection against free radicals.

• Asian-Australasian Journal of Animal Sciences
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• v.13 no.10
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• pp.1373-1376
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• 2000

The peroxidation status of tissues was estimated in broilers under acute or chronic heat stress ($32^{\circ}C$, 24 h, $5{\times}24h$) in the present study. The results showed that the lipid peroxide (LPO) concentrations in plasma and liver were elevated (p<0.05) by acute heat stress, and were not influenced in kidney (p>0.05). At the same time, no significant change of superoxide dismutase (SOD) activity in the liver, kidney or plasma was observed. Under chronic heat exposure, the SOD activity in liver was increased (p<0.05) and the LPO concentrations in the liver and plasma were restored to the normal levels. The LPO level in kidney was not affected by chronic heat stress (p>0.05), but SOD activity was significantly decreased (p<0.01). The results suggested that the peroxidation was induced by acute heat stress and disappeared along with the time of heat exposure, and the peroxidation reactions were different among tissues.

• YAKHAK HOEJI
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• v.53 no.4
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• pp.189-193
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• 2009

To investigate the antioxidant effect of lutein on N-nitrosodimethylamine (NDEA)-induced oxidative stress in mice, we measured lipid peroxidation, superoxide dismutase (SOD) and catalase of various tissues. Body weight was almost similar in lutein and control groups during 3 weeks. NDEA increased significantly the activities of typical marker enzymes of liver function (AST, ALT and ALP) in both groups. However, the increase of plasma aminotransferase activity significantly decreased in lutein group. Lipid peroxidation and SOD in various tissues, such as heart, lung, liver, kidney, spleen and plasma were significantly increased by NDEA, which were significantly reduced by lutein at a dose of 50 mg/kg. Catalase activity decreased significantly in control and lutein groups treated with NDEA, the effect being less in lutein group. Lesser effect on SOD and catalase in NDEA-treated lutein group indicates the improvement of protective mechanisms by lutein. Thus, it can be concluded from the present study that lutein can offer a useful protection against NDEA-induced oxidative stress.

• Biomolecules & Therapeutics
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• v.3 no.4
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• pp.260-265
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• 1995

In an attempt to define the early biochemical determinants that participate in the pathogenesis of glycerol-induced nephrotoxicity, especially focusing on oxygen free radicals, we studied malondialdehyde (MDA) level and the activities of catalase and superoxide dismutase in the renal cortex of rats, and the concentrations of blood urea nitrogen(BUH) and serum creatinine of rats at 24hr after the injection of a 50% solution of glycerol. Sprague-Dawley albino rats weighing 240 to 260 mg were injected intramuscularly with a 50% solution of glycerol(2 mι/kg, 4 mι/kg and 8 mι/kg). The group treated with glycerol showed significantlv higher MDA level and catalase activity, lower SOD activity and higher BUN and serum creatinine concentrations at 24 hr after the injection as compared to those of control group. These results suggest that the excessive oxygen free radicals resulting from the depression of SOD activity is an important determinant in the pathogenesis of glycerol-induced nephrotoxicity.

• BMB Reports
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• v.46 no.8
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• pp.404-409
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• 2013

Extracellular superoxide dismutase (EC-SOD) is a metallo-protein and functions as an antioxidant enzyme. In this study, we used lentiviral vectors to generate transgenic chickens that express the human EC-SOD gene. The recombinant lentiviruses were injected into the subgerminal cavity of freshly laid eggs. Subsequently, the embryos were incubated to hatch using phases II and III of the surrogate shell ex vivo culture system. Of 158 injected embryos, 16 chicks (G0) hatched and were screened for the hEC-SOD by PCR. Only 1 chick was identified as a transgenic bird containing the transgene in its germline. This founder (G0) bird was mated with wild-type hens to produce transgenic progeny, and 2 transgenic chicks (G1) were produced. In the generated transgenic hens (G2), the hEC-SOD protein was expressed in the egg white and showed antioxidant activity. These results highlight the potential of the chicken for production of biologically active proteins in egg white.