• Biomolecules & Therapeutics
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• 제2권3호
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• pp.298-302
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• 1994

Wistar albino rats were injected subcutaneously with mercuric chloride (5 mg/kg) to define the early biochemical determinants that participate in the pathogenesis of mercuric chloride-induced hepatotoxicity, especially focusing on oxygen free radicals, we studied malondialdehyde(MDA) level and the activities of catalase and superoxide dismutase in the liver of rats at 24, 48 and 72 hr after the injection of mercuric chloride. MDA levels at 24, 48 and 72 hr after the injection of mercuric chloride increased as compared with that of control group. The activities of catalase and superoxide dismutase at 24, 48 and 72hr after the injection of mercuric chloride decreased as compared with that of control group. These results suggest that the depression of the activities of catalase and superoxide dismutase resulting from excessive oxygen free radicals is an important determinant in pathogenesis of mercuric chloride-induced hepatotoxicity.

• Biomolecules & Therapeutics
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• 제7권2호
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• pp.121-126
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• 1999

In an attempt to define the effects of hyperbaric oxygen treatment on the lipid peroxidation and oxygen free radical reactions in rats exposed to carbon monoxide, we studied malondialdehyde (MDA) level and activities of catalase and superoxide dismutase in the kidney of the rats exposed to carbon monoxide. Male Sprague-Dawley albino rats weighing 240 to 260 gm were used. Experimental groups consist of Control group (=breathing with air), HBO group (=exposed to hyperbaric oxygen 〔HBO, 3ATA, 100%〕 after air breath), CO group (=exposed to CO〔3,970 ppm〕after air breath), CO-Air group (=exposed to CO after air breath followed by air breath) and CO-HBO group (=exposed to CO after air breath followed HBO treatment). The CO group showed significantly higher MDA level, catalase activity and SOD activity as compared to that of control group. The CO-HBO group showed significantly lower MDA level as compared to that of CO group, and did not show significantly lower catalase activity and SOD activity as compared to that of CO group. These results suggest that the excessive oxygen free radicals is an important determinant in pathogenesis of CO-induced nephrotoxicity and HBO inhibits the lipid peroxidation caused by excessive oxygen free radicals in the kidney of the rats exposed to carbon monoxide.

• 한국환경과학회지
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• 제17권6호
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• pp.671-677
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• 2008

We studied to determine quantitatively the radical species generated from humic acid (HA) solutions by irradiation(>400 mn). The formation of radical species from HA solutions was investigated with ESR spectroscopy. We gave ESR spectrum with g-value 2.0048 and line width 0.559mT, coincided with those of the semiquinone radical. 0.1 mg/L HA solution generated the radicals of $1.2{\times}10^{-6}M$, increased with increasing HA concentration. Also, pH and ionic strength effect of the amount of the semiquinone radical generate from HA solution. In this study, we have found that the singlet oxygen affects the semiquinone radicals generation in HA solution.

• 대한약리학회지
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• 제32권2호
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• pp.201-209
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• 1996

Restoration of the blood flow after a period of ischemia is accompanied by generation of toxic oxygen radicals. This phenomenon may account for the occurrence of reperfusion-mediated tissue injury in ischemic hearts. In in vitro studies, although oxygen radicals can be generated from a variety of sources, including xanthine oxidase system, activated leucocytes, mitochondria and others, the most important source and mechanism of oxygen radical production in the post-ischemic reperfused hearts is unclear. In the present study, we tested the hypothesis that the respiratory chain of mitochondria might be an important source of oxygen radicals which are responsible for the development of the reperfusion injury of ischemic hearts. Langendorff-perfused, isolated rat hearts were subjected to 30 min of global ischemia at $37^{\circ}C$, followed by reperfusion. Amytal, a reversible inhibitor of mitochondrial respiration, was employed to assess the mitochondrial contributions to the development of the reperfusion injury. Intact mitochonria were isolated from the control and the post-ischemic reperfused hearts. Mitochondrial oxygen radical generation was measured by chemiluminescence method and the oxidative tissue damage was estimated by measuring a lipid peroxidation product, malondialdehyde(MDA). To evaluate the extent of the reperfusion injury, post-ischemic functional recovery and lactate dehydrogenase(LDH) release were assessed and compared in Amytal-treated and -untreated hearts. Upon reperfusion of the ischemic hearts, MDA release into the coronary effluent was markedly increased. MDA content of mitochondria isolated from the post-ischemic reperfused hearts was increased to 152% of preischemic value, whereas minimal change was observed in extramitochondrial fraction. The generation of superoxide anion was increased about twice in mitochondria from the reperfused hearts than in those from the control hearts. Amytal inhibited the mitochondrial superoxide generation significantly and also suppressed MDA production in the reperfused hearts. Additionally, Amytal prevented the contractile dysfunction and the increased release of LDH observed in the reperfused hearts. In conclusion, these results indicate that the respiratory chain of mitochondria may be an important source of oxygen radical formation in post-ischemic reperfused hearts, and that oxygen radicals originating from the mitochondria may contribute to the development of myocardial reperfusion injury.

• Journal of Preventive Medicine and Public Health
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• 제20권2호
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• pp.221-227
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• 1987

In vivo ethane production in rats was used as an index of oxygen toxicity. The rats were allocated to four exposure conditions; hyperbaric oxygenation (HBO=5 ATA, 100% $O_2$), normobaric oxygenation (NBO=1 ATA,100% $O_2$), hyperbaric aeration (HBA=5 ATA, 21% $O_2$) and normobaric aeration (NBA=1 ATA, 21% $O_2$). After 120 minutes of exposure, the rats exposed to high concentration and/or high pressure oxygen exhaled significantly larger amounts of ethane than those exposed to NBA, and the differences in ethane production between any two groups were statistically significant (p<.01). This finding supports the hypothesis that hyperoxia increases oxygen free-radicals and the radicals produce ethane as a result of lipid peroxidation. It is notable that the ethane exhalation level of the HBA group was significantly higher than that of the NBO group. This difference could not be accounted for by the alveolar oxygen partial presure difference between the two groups.

• 대한한의학방제학회지
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• 제10권2호
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• pp.243-249
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• 2002

This study was performed to investigate the effects of fermented extract of Pinus densiflora (FPD) on oxygen radicals and $H_2O_2$-induced damage. The results are as follows: 1. The 1.1-diphenyl-2-picrylhydrazyl (DPPH) free radicals were considerably reduced by FPD and $IC_{50}$ value was showed the concentration of 20 ㎍／㎖. 2. The cytotoxicity did not observe by FPD treatment in A548 cells. 3. The $H_2O_2$-induced cell damage was recovered by FPD pretreatment in A549 cells. These results suggest that FPD, as a natural antioxidant, has scavenging effect of free radicals and protection effect from $H_2O_2$-induced cytotoxicity.

• 약학회지
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• 제43권5호
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• pp.652-658
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• 1999

To reveal the inhibitory mechanism of NO-dependent vasorelaxation by quinone derivatives (OQ1 and OQ21), we have compared the generation of free radicals by oxidative stress and the formation of cellular adducts by arylation. First, we measured oxygen consumption by quinone derivatives as a marker of oxidative stress in order to investigate whether these quinone compounds could generate reactive oxygen species. Both OQ1 and OQ21 generated free radicals and OQ21 was more potent. These results suggested that free radicals be involved in the inhibition of vasorelaxation by quinones. Next, we measured the binding capacity of quinone derivatives with intracellular GSH and protein thiols (-SH) in order to investigate whether these quinones have arylation capacity. Compared to positive control groups (menadione), both OQ1 and OQ21 depleted intracellular GSH and protein thiols very slightly. These compounds have low toxicities in mammalian tissues. From these results, we concluded that the inhibition of vasorelaxation by quinone derivatives (OQ1, OQ21) may be cuased by generation of free radicals.

• Applied Biological Chemistry
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• 제47권3호
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• pp.293-299
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• 2004

거대배아미 에탄올 추출물의 항산화활성을 지질과산화 억제활성 및 활성산소종의 소거활성을 중심으로 일반미와 대조하여 검토하였다. 연구 결과, 발아처리는 전반적으로 환원력 및 지질과산화 억제활성, superoxide radical 및 hydroxyl radical 소거활성을 상승시켰으며, 발아처리에 의한 항산화 활성의 증가현상이 화청거대배아미에서 가장 뚜렷하였다. Superoxide radical 소거작용에 있어서는 남풍거대배아미가 전체적인 소거활성은 높았으나, 발아처리에 의한 활성의 상승률은 역시 화청거대배아미가 가장 높았고, 그 작용기작은 시료에 의한 직접적인 radical 소거에 있는 것으로 나타났다. 생체 독성이 가장 큰 hydroxyl radical 소거활성을 조사한 결과, 화청거대배아미가 전체적인 소거활성 뿐 아니라, 발아처리에 의한 소거활성의 증가율도 가장 높았으며, 그 작용기작도 $Fe^{2+}$의 포족이 아닌 직접적인 라디칼 소거임이 밝혀졌다. 이와 같은 in vitro에서 관찰된 시료의 ROS 소거활성은 TPA하여 유도된 HL-60 세포의 ROS 생산을 억제하는데 유효하게 작용하였다.

• 한국잠사곤충학회지
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• 제42권2호
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• pp.93-98
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• 2000

This study was designed to investigate the effect of silkworm powder on oxygen radicals and their scavenger enzymes in brain membrances of SD rats. Hydroxyl radical (OH) levels resulted in a considerable decreases in brain mitochondria fraction. Superoxide radical (O$_2$) levels were a slightly decreased in brain cytosol fraction. Lipid peroxide (LPO) and Oxidized protein (OP) levels were significantly decreased in brain mitochondria and microsomes fraction. Mn-superoxide dismutase (SOD) activity was remarkably increased in the mitochondria fraction. Cu and Zn-SOD activities were effectively increased in brain cytosol fraction. GSHPx activity was considerably increased in brain cytosol fraction. These results suggest that anti-aging effect of silkworm plays an effective role in attenuating an oxidative stress and increasing a scravenger enzyme activity in brain membranes.

• 동의생리병리학회지
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• 제20권4호
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• pp.980-984
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• 2006

In order to examine the effect of oxygen free radicals on the vascular endothelial cells, cell viability was measured by XTT assay after bovine pulmonary vascular endothelial cell line(BPVEC) was treated only with hydrogen peroxide. In addition, the antioxidant effect of allopurinol on cells treated with hydrogen peroxide was examined by colormetric assay. in this study, the BPVEC treated with hydrogen peroxide showed the significantly decreased cell viability compared with control. Whereas, the viability of cells treated with hydrogen peroxide and allopurinol has significantly increased when compared with that of cells treated only with hydrogen peroxide. These results suggested that hydrogen peroxide, one of the oxygen free radicals showed cytotoxic effect and allopurinol has protective effect on oxygen free radical-induced cytotoxicity.