• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.2
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• pp.262-266
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• 2002

In order to elucidate the mechanism of cytotoxic effect of oxygen radicals on cultured mouse spinal motor neurons, the neurotoxicity induced by hydrogen peroxide(H₂O₂) was evaluated by MTT assay. The neuroprotective effect of Rhizoma Gastrodiae(RG) against H₂O₂-mediated neurotoxicity was also examined in these cultures by SRB assay. The results were as follows : The value of lethal concentration 50(LC50) of H₂O₂ was estimated at a concentration of 30 uM in these cultures. Cell viability of cultured mouse spinal motor neurons was remarkably decreased by H₂O₂-induced neurotoxicity in a dose- and time-dependent manner. RG was remarkably effective in blocking the neurotoxicity induced by H₂O₂ at a concentration of 120 μM as determined by SRB assay. From above the results, it is suggested that H₂O₂ induce neurotoxicity, and the selective herbal extracted RG was very effective in blocking H₂O₂-mediated neurotoxicity on cultured mouse spinal motor neurons.

• Herbal Formula Science
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• v.7 no.1
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• pp.143-151
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• 1999

To evaluate the neurotoxic effect of oxygen radicals in cultured mouse spinal dorsal root ganglion(DRG) neurons, cytotoxicity was determined by MTT assay after cultured DRG neurons were grown in the media containing various concentrations of glucose oxidase(GO). In addition, neuroprotective effect of herb extract, Epimedium Koreanum Nakai was examined by MTT assay in cultured DRG neurons. Cell viability of cultured DRG neurons was remarkably decreased by GO in dose- and time-dependent manner, and Epimedium Koreanum Nakai protected remarkably GO-induced neurotoxicity in these cultures. From the above results, it is suggested that oxygen radicals is toxic in cultured mouse DRG neurons, and herb extracts such as Epimedium Koreanum Nakai are effective in prevention of the neurotoxicity induced by oxygen radicals in cultured mouse DRG neurons.

• Archives of Pharmacal Research
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• v.18 no.3
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• pp.189-194
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• 1995

The focus of this study was to investigate the influences of enzymatic scavengers of active oxygen metabolites and phospholipase $A_2$ inhibitor on hepatic secretory and microsomal function during hepatic ischemia/reperfusion. Rats were pretreated with free radical scavengers such as superoxide dismutase (SOD), catalase, deferoxamine and phospholipase $A_2$ inhibitor such as quinacrine and then subjected to 60 min. no-flow hepatic ischemia in vivo. After 1, 5 hr of reperfusion, bile was collected, blood was obtained from the abdominal aorta, and liver microsomes were isolated. Serum aminotransferase (ALT) level was increased at 1 hr and peaked at 5 hr. The increase in ALT was significantly attenuated by SOD plus catalase, deferoxamine and quinacrine especially at 5 hr of reperfusion. The wet weight-to-dry weight ratio of the liver was significantly increased by ischemia/reperfusion. SOD and catalase treatment minimized the increase in this ratio. Hepatic lipid peroxidiltion was elevated by ischemia/reperfusion, and this elevation was inhibited by free radical scavengers and quina crine. Bile flow and cholate output, but not bilirubin output, were markedly decreased by ischemia/reperfusion and quinacrine restored the secretion. Cytochrome $P_{450}$ content was decreased by ischemia/reperfusion and restored by free radical scavengers and quinacrine to the level of that of the sham operated group. Aminopyrine N-demethylase activity was decreased and aniline p-hydroxylase was increased by ischemia/reperfusion. The changes in the activities of the two enzymes were prevented by free radical scavengers and quinacrine. Our findings suggest that ischemia/reperfusion diminishes hepatic secretory functions as well as microsomal drug metabolizing systems by increasing lipid peroxidation, and in addition to free radicals, other factors such as phospholipase $A_2$ are involved in pathogenes of hepatic dysfunction after ischemia/reperfusion.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.381.3-382
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• 2002

Free radical-mediated cell damage and free radical attack on polyunsaturated fatty acids result in the formation of lipid radicals. These lipid radicals react readily with molecular oxygen to produce peroxy radicals responsible for initiating lipid peroxidation. The peroxidation of cellular membrane lipid can lead to cell necrosis and considered to be implicated in a number of pathophysiological conditions as well as in the toxicity of many xenobiotics. DPPH is known to abstract labile hydrogen and the ability to scavenge the DPPH radical is related to the inhibition of lipid peroxidation. (omitted)

• Toxicological Research
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• v.17 no.4
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• pp.249-253
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• 2001

Fumonisin B1, a mycotoxin, is thought to induce esophageal cancer in humans and apoptosis in animal cells by inhibiting ceramide synthase. Dumonisin Bl may also generate reactive oxygen species directly or indirectly, leading to DNA damage and lipid peroxidation. In this study, a DNA fragmentation assay, dichlorofluorescein (DCF) analysis, and single cell gel electrophoresis (SCGE) were used to investigate the involvement of cellular free radicals, specifically hydrogen peroxide, in the DNA damaging activity of fumonisin B1. From an in vitro DNA fragmentation assay, E. coli DNA, damage by fumonisin Bl was increased by the addition of superxide dismutase (SOD) and decreased by catalase. SCGE and DCF analysis in vivo showed that the nuclear DNA damage and intracellular free radicals in cultured rat hepatocytes treated with fumonisin B1 were increased with the concentration of fumonisin Bl . DNA damage and free radical generation were inhibited by the addition of catalase. Fumonisin Bl , in the presence of SOD, produces hydrogen peroxide causing oxidative DNA damage and protein malfunction, leading to genotoxicity and cytotoxicity of the toxin.

• Journal of Life Science
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• v.7 no.3
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• pp.180-185
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• 1997

Methylelaiophylin generated superoxide radicals in Bacillus subtilis and showed antibacterial activity against a broad range of gram positive bacteria. The inhibition of DNA synthesis was more sensitive than one of RNA synthesis. A recombination-deficient mutant strain of B. subtilis was 2-fold more sensitive than a wild strain, and this sensitivity was reduced in the presence of an antioxidant, dithiothreitol. Methylelaiophylin generated superoxide radicals in B. subtilis lysates, and this suggests that the antibacterial activity of methylelaiophylin is related to the generation of active oxygen species in the cells.

• Bulletin of the Korean Chemical Society
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• v.14 no.2
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• pp.183-187
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• 1993

Aryl carbenic anion radicals have been generated from the corresponding alkoxy-aryl diazo compounds by unimolecular decomposition reaction in various electrolyte/solvent systems. The electrochemical reductions of alkoxy-aryl diazo compounds in the electrolyte/solvent system are shown to initially be a one-electron process which affords the corresponding anion radicals. The unimolecular loss of nitrogen is favored at the propagation step and accelerated by the oxygen and carbon atoms of alkoxy group adjacent to the diazo function. The structure of the carbene anion radical in the termination is considered to be a resonance hybrid.

• Tuberculosis and Respiratory Diseases
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• v.44 no.1
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• pp.104-113
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• 1997

Background : Toxic oxygen free radicals have been implicated as important pathologic mediators in many clinical disorders. Enhancing the intracellular content of antioxidant enzymes(superoxide dismutase, glutathione peroxidase, and catalase) can provide means of limiting biological damage caused by oxygen free radicals. The oxygen free radicals and changes of antioxidant enzymes are though to play a role in the pathogenesis of chronic obstructive pulmonary disease. Method : To investigate the pulmonary oxygen radical injury and the protective role of antioxidant enzymes in Chronic obstructive pulmonary disease(COPD), author measured the amount of thiobarbituric acid reactants, the activities of antioxidant enzymes and the sulfhydry1 groups of glutathione in serum and red blood cells from the patients with COPD(COPD patients) and the normal controls. Results : The thiobarbituric acid reactant in serum and red blood cells of COPD patients was increased than those of the normal controls, and the superoxide dismutase activity in red blood cells was no statistical difference in both groups. But the glutathione peroxidase and catalase activities in red blood cel1s of COPD patients were significantly lowered than those of the normal controls. The sulfhydry1 groups in serum and red blood cells were no statistically difference in both groups. Conclusion : These results suggest that the increased thiobarbituric acid reactants in serum and RBCs of chronic obstructive pulmonary disease mean oxygen radical toxicity, and the decreased glutathione peroxidase and catalase activities in RBC could take pan in pathogenesis of chronic obstructive pulmonary disease.

• Applied Chemistry for Engineering
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• v.3 no.2
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• pp.256-265
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• 1992

The kinetics for the oxidative coupling of methane over NaCl(30wt%)/ZnO(60wt%)/${\alpha}-Al_2O_3$ catalyst was investigated, and then the active oxygen species were discussed. The conversion rate of methane was measured at the atmospheric pressure with various combinations of partial pressure of methane and oxygen at temperature range of $650^{\circ}C{\sim}750^{\circ}C$, at conversions less than with 10%. These rate data were then used to verify the proposed Langmuir-Hinshelwood kinetic equation. The rate limiting step appeared to be the formation of the methyl radicals by the reactin of the adsorbed methane and the adsorbed oxygen, which were adsorbed on the different active sites of the catalyst. The activation energy of the methyl radical formation was estimated to be ca. 39 kcal/mol. From the kinetic studies, the oxygen species respolsible for the formation of methyl radicals was proposed to be diatomic oxygen such as $O{_2}{^{2-}}$ or $O_2{^-}$ on the surface.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.214.2-215
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• 2003

Reactive oxygen species play an important role in aging. carcinogenesis, and certain neurological disorders of human beings in addition to the host-defensive mechanism of inflammatory response. Murine macrophages Raw264.7 released superoxide anions via NADPH oxidase complex and nitric oxide (NO) via iNOS synthase when the cells were stimulated with unopsonized zymosan binding to complement receptor. (omitted)