• 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)

• Journal of Navigation and Port Research
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• v.34 no.10
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• pp.757-762
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• 2010

The purposes of this study were to examine the effects of aerobic exercise capacity on free oxygen radicals in blood(FORB) during submaximal exercise in rowing ergometer and as for study purposes, a set of experiments were conducted using one group of 6 rowing players(RP) and the other group of 6 non rowing players(NRP) at the maximum heart rate reserve(HRR) 85~90% exercise intensity. Oxygen free radical was sampled 5 times including a rest period(ARP), immediate after exercise(IAE), 10 minutes after exercise(10MAE), 20 minutes after exercise(20MAE) and 30 minutes after exercise(30MAE). Accordingly, following findings were derived from current study. The effects of interaction between groups and times were significant in oxygen free radical(p<.05) and post hoc tests revealed that significant differences occurred between 10MAE and 20MAE and between 20MAE and 30MAE. In conclusion, the aerobic exercise capacity excellence RP group had more positive recovery pattern than that in the NRP group from FORB of negative influence to the human body

• Biomedical Science Letters
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• v.8 no.3
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• pp.155-159
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• 2002

To evaluate the physiological significance of xanthine oxidase (XO) in rat skin, the activity of XO (type O) in skin was compared with that of small intestine or liver. Concomitantly, XO activities in some partial portions (scalp, leg, dorsal and ventral part) of skin were determined and then compared with each partial portion. XO activity of skin was lower than that of small intestine and rather higher than that of liver. Furthermore, the activity of XO in skin, after clipping of hairs and then in 5 days, was more increased than that of rat which was clipped before having been sacrificed. As for activities of free radical scavenging system (GPx, GST, SOD), skin is lower than liver and small intestine. Although it is hewn that the oxygen free radical generated by XO system lead to injurious effect on the cell, the XO activity of ventral part which is to be less exposed to xenobiotics and biological agents was the lowest among those of ventral, dorsal, leg and scalp parts in skin. In conclusion, it may be hypothesized that XO system in skin act on defence mechanism.

• Korean Journal of Pharmacognosy
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• v.38 no.4
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• pp.372-375
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• 2007

Reactive oxygen species(ROS) or free radicals are produced in the pathogenesis of human diseases including atherosclerosis, diabetes, cancer, and aging. Antioxidants are associated with the prevention of ROS-induced tissue and cellular damage in the various diseases. This study investigated the antioxidative activities of the methanol extract of Alisma plantagoaquatica var. orientale and its main component under conditions of radical generation using allophycocyanin and ferric-thiocyanate assay. Alisol B 23-acetate as a main component was isolated from the methanol extract of Alisma plantago-aquatica var. orientale. In results, the extract of Alisma plantago-aquatica var. orientale showed inhibitory activity on AAPH [2,2'-azobis(2-amidinopropane)dihydrochloride]-induced protein oxidation. Also, the extract of Alisma plantago-aquatica var. orientale and alisol B 23-acetate inhibited lipid peroxidation. These results indicate that Alisma plantago-aquatica var. orientale and alisol B 23-acetate show promise as therapeutic agents for various damages involving free radical reactions.

• Journal of Acupuncture Research
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• v.15 no.2
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• pp.135-145
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• 1998

Bupleury radix has been used for the treatment of fever, liver disease, inflammation in traditional medicine. The present study was carried out to evaluate the antioxidant effects of Bupleury radix aqua-acupuncture solution (BRAS) in vitro. Oxygen derived free radicals produced in the course of normal aerobic life, such as superoxide anion radical($O_2^-$ ), hydroxyl radicaI( OH), hydrogen peroxide($H_2O_2$) and singlet oxygen($^1O_2$) can attack polyunsaturated fatty acid in cell membranes, enzymes, other cell compounds, and give rise to lipid peroxidation, DNA damage, lipofuscin accumulation, structure alteration of cell membrane and cell death. In this study, antioxidant effects of BRAS on lipid peroxidation were determined according to the method of TBA. BRAS inhibited markedly peroxidation of linoleic acid during the autoxidation, and also inhibited lipid peroxidation induced by hydroxyl radical derived from $H_2O_2-Fe^{2+}$ in rat liver homogenate. And BRAS showed 30% scavenging effect on DPPH radical, also exhibited a 30% inhibitory effect on superoxide generation from xanthine-xanthine oxidase system. In addition, BRAS protected the cell death induced by tert-butyl hydroperoxide(t-BHP) and significantly increased cell viability in the normal rat liver cell(Ac2F).

• Toxicological Research
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• v.11 no.1
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• pp.57-62
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• 1995

To investigate the ultrastructural changes of kidney and clarify to a cause of its changes in lead intoxicated rats, the 0.5% lead acetate administed orally to the rats and those were sacrifled at 2 day, 1, 2, 4, 6 and 8 week after the treatment of lead acetate. Each extirpated kidney was histopathologically examined under the electron microscopy and histochemical examination was also carried out. Concomitantly, the activity of free radical metabolizing enzyme was determined. The blood levels of lead concentration showed a gradual increase from the first group reaching the plateau at the one or two week group with the slightly decreasing value throughout the whole course of the experiment. And the urinary ALA concentration showed a gradual increase from the first group to the 8 week group. In the kidney tissue of rat sacrified at 6 week, the proximal tubular cells showed dilatation of endoplasmic reticulum, mitochondrial swelling, increased numbers of secondary lysosomes and myelin figure-like residual bodies on electron microscope and oxygen free radicals are identified by histochemistry on light microscope whereas there were no differences in the activity of catalase and glutathione peroxidase between the lead acetate treated group and control group. But the activity of xanthine oxidase was more increased in lead acetate treated rats than control group. Furthermore, the superoxide dismutase activity was significantly increased in the experimental group than the control group. In conclusion, it is assumed the kidney damage in lead intoxicated rat may be induced by free radicals.

• Tuberculosis and Respiratory Diseases
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• v.38 no.4
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• pp.357-371
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• 1991

To identify the pathogenetic role of reactive oxygen free radical-induced oxidation reaction in endotoxin-induced acute lung injury, we infused endotoxin into 8 domestic pigs; endotoxin only (n=3), pretreatment with dimethylthiourea (DMTU) (n=5). We observed the sequential changes in hemodynamic parameters, the concentration of plasma oxidized glutathione (GSSG) in pulmonary arterial and venous blood, and albumin content in bronchoalveolar lavage fluid (BALF). The results were as follows. 1) While cardiac output decreased, mean pulmonary arterial pressure, pulmonary vascular resistance, and alveolar-arterial oxygen difference increased over phase 1 (0-2 hr) and phase 2 (2-4.5 hr) by endotoxin, DMTU attenuated the above changes only during phase 2. 2) While the concentration of plasma GSSG increased significantly by endotoxin during phase 2, there were no significant differences between pulmonary arterial and venous GSSG contents during both phases. The increase in plasma GSSG content was attenuated by DMTU. 3) The content of BALF albumin was significantly lower in DMTU group than that of endotoxin group. These results suggest that reactive oxygen free radical-induced oxidation reaction may have an important pathogenetic role in endotoxin-induced acute lung injury in pigs, which seems to be greater during phase 2 rather than phase 1.

• Journal of Chest Surgery
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• v.21 no.5
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• pp.803-815
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• 1988

The present experiments were performed to confirm the hypothesis that xanthine oxidase[XOD], as a source and mechanism of oxygen radical production, plays an important role in the genesis of the reperfusion injury of ischemic myocardium. The experimental ischemic-reperfusion injury was induced in isolated, Langendorff preparations of rat hearts by 60 min. Of global ischemia with aortic clamping followed by 20 min. of reperfusion with oxygenated Krebs-Henseleit solution[pH 7.4, 37*C]. The results were as follows: 1. The releases of creatine phosphokinase and a lipid peroxidation product, malondialdehyde[MDA] into the coronary effluent were abruptly increased upon reperfusion of ischemic hearts. The increases of the enzyme and MDA were suppressed significantly in the hearts removed from rats pretreated with allopurinol, a specific XOD inhibitor[20mg/kg, oral, 24 hrs and 2 hrs before study]. This effect of allopurinol was comparable to that of oxygen radical scavengers, superoxide dismutase[5, 000U] and catalase[12, 500 U]. 2. The increased SOD-inhibitable reduction of ferricytochrome C, which was infused to the hearts starting with reperfusion, was significantly suppressed in allopurinol pretreated hearts. 3. Activities of myocardial XOD were compared in the normal control hearts and the ischemic ones. Total enzyme activities were not different in both hearts. However, comparing with the control, the ischemic ones showed higher activity in 0-form and lower activities in D-form and D/O-form. 4. In the ischemic hearts, phenylmethylsulfonyl fluoride, a serine protease inhibitor, prevented significantly the increase of 0-form and the decreases of D and D/O-form, while thiol reagents did not affect the changes of the enzyme. 5. The increase of 0-form and the decreases of D and D/0-form were not significant in both calcium-free perfused and pimozide, a calmodulin inhibitor, treated ischemic hearts. 6. The SOD-inhibitable reduction of ferricytochrome C were suppressed by PMSF and pimozide treatment as well as by calcium-free perfusion. It is suggested from these results that in the ischemic rat myocardium, xanthine oxidase is converted to oxygen radical producing 0-form by calcium, calmodulin-dependent proteolysis and plays a contributing role in the genesis of ischemic-reperfusion injury by producing oxygen free radicals.

• Biomedical Science Letters
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• v.14 no.3
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• pp.193-198
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• 2008

In order to evaluate on the effect of kaempferol on the cytotoxicity of oxygen tree radicals, XTT assay was performed to determine the cell viability after skin fibroblasts derived from human (Detroit 51) that were treated with various concentrations of hydrogen peroxide $(H_2O_2)$. And also, the effect of kaempferol on the cytotoxicity induced by H202 that was examined by cell viability, lactate dehydrogenase (LDH) activity and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity in these cultures. $H_2O_2$ decreased cell viability in dose-dependent manner in these cultures and the $XTT_{90}\;and\;XTT_{50}$ values were determined at concentration of $35{\mu}M\;and\;90{\mu}M$ of $H_2O_2$ after skin fibroblasts derived from human were treated with $15{\sim}90{\mu}M$ of $H_2O_2$ for 6 hours, respectively. $H_2O_2$ was highly toxic on cultured skin fibroblasts derived from human by toxic criteria of Brenfreund and Puerner (1984). In the protective effect of kaempferol on $H_2O_2$-induced cytotoxicity, kaempferol increased DPPH radical scavenging activity and significantly decreased LDH activity. From these results, it is suggested that oxygen tree radical, $H_2O_2$, was highly toxic on cultured skin fibroblasts derived from human, and also kaempferol of flavonoid showed the protection on $H_2O_2$-induced cytotoxicity.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.288.3-289
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• 2002

Increasing evidence regarding free radical generating agents and inflammatory processes suggests that accumulation of reactive oxygen species can cause hepatotoxicity. A short-chain analog of lipid hydroperoxide, t-butyl hydroperoxide (t-BHP), can be metabolized to free radical intermediates by cytochrome P-450 in hepatocytes. which in turn can initiate lipid peroxidation, affect cell integrity and result in cell injury. (omitted)