• Journal of Environmental Health Sciences
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• v.28 no.2
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• pp.81-88
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• 2002

Effect of cyclohexanone treatment on the activities oxygen free radical and cyclohexanone metabolizing enzyme in acute liver damaged rats, was investigated. Acute liver damage was induced in rats with pretreatment of 50% $CCl_4$ in olive oil(0.1ml/100g body wt) intraperitoneally 3 times every other day. Cyclohexanone(1.56g/kg body wt, i.p.) was administered to the animals 24 hours after the last Pretreatment of CC1$_4$. Rats were sacrificed at 4 hours after injection of cyclohexanone. On the basis of liver weight/body weight(％), serum levels alanine aminotransferase activity and hepatic protein content, cyclohexanone treatment to acute liver damaged animals led to the more enhanced liver damage. On the other hand, injection of cyclohexanone to the rats led to the increased activities of hepatic cytochrome P-450 dependent aniline hydroxylase and xanthine oxidase. Furthermore, by treatment of cyclohexanone to the acute liver damaged rats hepatic xanthine oxidase activity was more increased than the $CCl_4$ treated rats. In case of oxygen free radical scavenging system, the hepatic glutathione content and the activities of hepatic glutathione S-transferase, catalase, superoxide dismutase were generally increased by injection of cyclohexanone to rats, and the hepatic glutathione content, catalase and alcohol dehydrogenase activities were more decreased in liver damaged rats by the treatment of cyclohexanone. In conclusion, the cyclohexanone treatment to acute liver damaged rats led to enhancement of liver damage that may be due to oxygen free radical together with cyclohexanone.

• Toxicological Research
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• v.4 no.1
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• pp.23-35
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• 1988

The role of calcium in the production of oxygen radical which causes reperfusion damage of ischemic heart has been examined. The reperfusion damage was indrced in isolated Langendorff perfused rat hearts by aortic clamping for 60 min followed by reperfusion with oxygenated Krebs-Henseleit solution with or without 1.25 mM $CaCl_2.$ On reperfusion of the ischemic hearts with the calcium containing solution, the release of cytosolic enzymes (LDH and CPK) increased abruptly. These increased release of enzymes were significantly inhibited by additions of oxygen radical scavengers (SOD, 5,000 U; catalase, 12,500 U) into the reperfusion solution. In the hearts isolated from rats pretreated with allopurinol(20 mg/kg orally, 24 hr and 2 hr prior to the experiments), the levels of enzymes being released during reperfusion were significantly lower than that of the control. However, in the hearts perfused with the calcium-free but oxygenated solution, the increase in the release of cytosolic enzymes during reperfusion was neither inhibited by oxygen radical scavengers nor by allopurinol pretreatment. For providing the evidence of oxygen radical generation during the reperfusion of ischemic hearts in situ, the SOD-inhibitable reduction of exogenously administered ferricytochrome C was measured. In the hearts perfused with the calcium containing solution, the SOD-inhibitable ferricytochrome C reduction increased within the first minute of reperfusion, and was almost completely inhibited by allopurinol pretreatment. When the heart was perfused with the calcium free solution, however, the reduction of ferricytochrome C was not only less than that in the calcium containing condition, but also was not so completely inhibited by allopurinol pretreatment. By ischemia, xanthine oxidase (XOD) in the ventricular tissue was changed qualitatively, but not quantitatively. In the heart made ischemic with the calcium containing condition, the oxygen radical producing O-form of XOD increased, while the D- and D/O-form decreased. However, in the ischemic heart reperfused with the calcium free condition, the D/O-form of XOD was elevated without significant increase in O-form of the enzyme. It is suggested from these results that the calclum may play a contributing role in the genesis of reperfusion damage by promoting the conversion of xanthine oxidase from the D/O-form to the oxygen radical producing O-form in the ischemic myocardium.

• Proceedings of the Korean Vacuum Society Conference
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• 2016.02a
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• pp.208.2-208.2
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• 2016

Many researchers have paid attention to the studies on the interaction between non-thermal plasma and aqueous solutions for biomedical applications. The gas composition in the plasma is very important. Oxygen and nitrogen are the main gases of interest in biological applications. Especially, we focus on the oxygen concentration. In this experiment, we studied the role of oxygen concentration in plasma induced chemical reactions in solution. At first, the amount of ions are measured according to changing the oxygen concentration. And we checked the relationship between these ions and pH value. Secondly, when the oxygen concentration is changed, it identified the type and amount of radical generated by the plasma. In order to confirm the effect of these chemical property change to biological material, hemoglobin and RBCs are chosen. RBCs are one of the common basic biological cells. Thirdly, when plasma treated according to oxygen concentration in nitrogen feeding gas, oxidation of hemoglobin and RBC is checked. Finally, membrane oxidation of RBC is measured to examine the relation between hemoglobin oxidation and membrane damage through relative hemolysis and Young's modulus. Our results suggest that reactive species generated by the plasma differsdepending on the oxygen concentration changes. The pH values are decreased when oxygen concentration increased. OH decrease and NO increase are also observed. These reactive species makes change of chemical properties of solution. We also able to confirm that the difference in these reactive species to affect the oxidation of the Hb and RBCs. The Hb and RBCs are more oxidized with the high oxygen concentration conditions. But membrane is damaged more by plasma treatment with only nitrogen gas. It is shown that red blood cells membrane damage and oxidation of hemoglobin are not directly related.

• Environmental Mutagens and Carcinogens
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• v.20 no.1
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• pp.7-13
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• 2000

The mechanisms of benzene toxicity is not fully elucidated, although the metabolism of benzene is very well understood. In order to study the mechanism of benzene toxicity, we investigated DNA damage induced by benzene metabolite, 1,2,4-benzenetriol (BT) in HL-60 cells by alkaline comet assay. To investigate the mechanism of cellular DNA damage induced by BT, the cells were treated with antioxidant such as vitamin C, SOD, catalase, and chelating agent such as deferoxamine (DFO), bathocuproinedisulfonic acid (BCDS). BT induced DNA damage in dose-dependent manner at concentration between 10$\mu\textrm{m}$ and 100$\mu\textrm{m}$. The antioxidant vitamin C itself induced DNA damage at higher concentration. The DNA damage induced by BT in HL-60 cells was protected at low concentraiton of vitamin C whereas no protective effect was found at high concentration. In hibitory effect of SOD on DNA damage by BT was observed and this suggested that BT produce superoxide anion (O2-) causing DNA damage. Catalase protected BT-induced DNA damage suggesting that BT produce H2O2 during autooxidation of BT. Both Fe(II)-specific cheiating agent, deferoxamine (DFO) and Cu(I)-specific chelating agent, bathocuproinedisulfonic acid (BCDS) inhibited BT0induced DNA damage. This suggested that DNA damage was caused by active species which was produced DAN damage. This suggested that DNA damage was caused by active species which was produced by the autooxidation of BT in the presence of Cu(II) and Fe(III). These findings suggest that reactive oxygen species play an important role in the mechanism of toxicity induced by benzene metabolites.

• Biomedical Science Letters
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• v.9 no.3
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• pp.151-158
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• 2003

In the biological world, there are a number of ecological fights for survival between each organism such as plants, animals and microorganism In such events, an organism can use its natural bioactive products as defence agent against other organisms. Furthermore, natural bioactive products can be utilized for medicine or functional food. Recently, we investigate the effect of Monascus pigment extracted from a fungus, Monascus anke, on the alcohol metabolism and blood lipid profile. In the present study, it is observed that Monascus pigment supplemented dietary may have a hepatoprotective effect on rat's liver damage induced with $CCl_4$ . By treatment with $CCl_4$(3 times, I.P), liver damage was reduced more in the rats fed 2% Monascus pigment extract supplemented diet than those fed standard diet, based on the serum levels of alanine aminotransferase, microsomal glucose-6-phosphatse activity and hepaic malondialdehyde content. On the other hand, oxygen free radical generating enzymes, hepatic P-450 dependent aniline hydroxylase, xanthine oxidase, and oxygen free radical scavenging enzymes, hepatic glutathione S-transferase, catalase, superoxide dismutase activities were generally higher both in $CCl_4$ treated group and control fed 2% Monascus pigment extract supplemented diet than those fed standard diet. In conclusion, the rats fed 2% Monascus pigment extract supplemented diet showed more reduced liver damage than those fed standard diet, which may be due to the acceleration of oxygen free radical metabolism.

• The Korean Journal of Food And Nutrition
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• v.24 no.4
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• pp.803-807
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• 2011

Human umbilical Mesenchymal Stem Cell(uMSC) has been known as one of major component to regenerate connective tissues such as bone, cartilage, fat and others. The effect of low(5%), normotensive(20%) oxygen and freezing-thawing damage on proliferation of uMSC were investigated. low oxygen concentration culture of uMSC resulted in enhanced proliferation significantly($p$ <0.05) than 20% of oxygen culture. After the freezing-thawing injury to uMSC, 5% oxygen culture showed marked proliferation of uMSC than that of 20% oxygen($p$ <0.05) in the 5th passage of uMSC. Expression of antioxidant enzymes such as superoxide anion 1 and glutathione peroxidase 1 appeared marked in 20% oxygen cultured uMSC, which suggest oxidative stress could induce less proliferation of uMSC. Above findings would suggest proliferation of uMSC in 5% of oxygen will give more yields.

• Progress in Medical Physics
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• v.11 no.2
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• pp.157-165
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• 2000

Purpose: For estimation of yields of l)NA damages induced by radiation and enhanced by oxygen, a mathematical model was used and tested. Materials and Methods: Reactions of the products of water radiolysis were modeled as an ordinary time dependant equations. These reactions include formation of radicals, DNA damage, damage repair, restitution, and damage fixation by oxygen and H-radical. Several rate constants were obtained from literature while others were calculated by fitting an experimental data. Sensitivity studies were performed changing the chemical rate constant at a constant oxygen number density and varying the oxygen concentration. The effects of oxygen concentration as well as the damage fixation mechanism by oxygen were investigated. Oxygen enhancement ratio(OER) was calculated to compare the simulated data with experimental data. Results: Sensitivity studies with oxygen showed that DNA survival was a function of both oxygen concentration and the magnitude of chemical rate constants. There were no change in survival fraction as a function of dose while the oxygen concentration change from 0 to 1.0 x 10$^{7}$ . When the oxygen concentration change from 1.0 $\times$ 107 to 1.0 $\times$ 101o, there was significant decrease in cell survival. The OER values obtained from the simulation study were 2.32 at 10% cell survival level and 1.9 at 45% cell survival level. Conclusion: Sensitivity studies with oxygen demonstrated that the experimental data were reproduced with the effects being enhanced for the cases where the oxygen rate constants are largest and the oxygen concentration is increased. OER values obtained from the simulation study showed good agreement for a low level of cell survival. This indicated that the use of the semi-empirical model could predict the effect of oxygen in cell killing.

• BMB Reports
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• v.42 no.8
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• pp.500-505
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• 2009

Anti-oxidative effect of Phellinus linteus (P. linteus) and red ginseng extracts on DNA damage induced by reactive oxygen species (ROS) were investigated in this study. P. linteus (PLE) and red ginseng extracts (RGE) inhibited the breaking of E. coli ColE1 plasmid DNA strands as well as nuclear DNA of rat hepatocytes damaged by oxidative stress. In addition, a reaction mixture of PLE and RGE showed synergistic inhibitory effect against DNA damage. These results suggest that PLE and RGE have a cellular defensive effect against DNA damage induced by ROS.

• Journal of Microbiology and Biotechnology
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• v.9 no.5
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• pp.548-553
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• 1999

A production of $\beta-Carotene$was attempted in a fed-batch culture of Blakeslea trispora by controlling both foam and dissolved oxygen in the presence of surfactant, Span 20. Results obtained from the shake flask cultures indicated that a high concentration of dissolved oxygen was needed for both cell growth and $\beta-Carotene$ synthesis, and the optimal concentration of glucose was found to be in the range of 50-100 g/l. In order to maintain the dissolved oxygen concentration level at higher than 50% of air saturation, pure oxygen was automatically sparged into the medium with air. Foam was controlled by bypassing air from the submerged aeration to the headspace in response to the foam that was caused by Span 20. High agitation speed was found to be detrimental to the cell growth due to shear damage, even though it provided sufficient dissolved oxygen. On the other hand, a low aeration speed caused stagnant regions in the fermentor because of improper mixing. Thus, for the fed-batch operation, agitation speed was increased gradually from 300 to 700 rpm to prevent cell damage at the initial stage of fermentation and to give efficient mixing for a viscous culture broth as the culture proceeded. By controlling dissolved oxygen and foam, a high concentration of $\beta-Carotene$otene (1,190 mg/l) was obtained in 6 days of the fed-batch culture of B. trispora with 2.5% of the dry cell weight, which was approximately 5 times higher than that of the batch cultures.

• Rapid Communication in Photoscience
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• v.4 no.2
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• pp.37-40
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• 2015

To examine the photosensitized biomolecules damaging activity, dimethoxyP(V)tetrakis(2-naphthyl)porphyrin (NP) and dimethoxyP(V)tetraphenylporphyrin (PP) were synthesized. The naphthyl moiety of NP hardly deactivated the photoexcited P(V)porphyrin ring in ethanol. In aqueous solution, the naphthyl moiety showed the quenching effect on the photoexcited porphyrin ring, possibly through electron transfer and self-quenching by a molecular association. Binding interaction between human serum albumin (HSA), a water soluble protein, and these porphyrins could be confirmed by the absorption spectral change. The apparent association constant of NP was larger than that of PP. It is explained by that more hydrophobic NP can easily bind into the hydrophobic pockets of HSA. The photoexcited PP effectively induced damage of the tryptophan residue of HSA, through electron transfer-mediated oxidation and singlet oxygen generation. NP also induced HSA damage during photo-irradiation and the contributions of the electron transfer and singlet oxygen mechanisms were speculated. The electron transfer-mediated mechanism to the photosensitized protein damage should be advantageous for photodynamic therapy in hypoxic condition. The quantum yield of the HSA photodamage by PP was significantly larger than that of NP. The quenching effect of the naphthyl moiety is considered to suppress the photosensitized protein damage. In conclusion, the naphthalene substitution to the P(V)porphyrins can enhance the binding interaction with hydrophobic biomacromolecules such as protein, however, this substitution may reduce the photodynamic effect of P(V)porphyrin ring in aqueous media.