• Title/Summary/Keyword: oxy radical-scavenging system

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Methods for Evaluation of Antioxidant Activity: Application to Taurine (항산화 활성의 평가를 위한 연구법: 타우린의 적용)

  • Kim, Bong-Hee;Oh, Jung-Min;Yun, Kang-Uk;Kim, Chung-Hyeon;Kim, Sang-Kyum
    • Toxicological Research
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    • v.23 no.3
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    • pp.263-269
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    • 2007
  • Although taurine (2-aminoethanesulfonic acid) can inhibit oxidative stress in both animal and epidemiological studies, it is obscure whether taurine directly scavenges oxy-radicals or indirectly regulates oxidant production and/or antioxidant defense system. The reason for this discrepancy remains unknown but may be due, in part, to the lack of a validated assay system for evaluating oxy-radical scavenging capacity. The antioxidant activities of taurine and hypotaurine (2-aminoethanesulfinic acid), a precursor of taurine, against peroxyl radicals, hydroxyl radicals and peroxynitrites were determined by the total oxy-radical scavenging capacity (TOSC) assay and cell-based assay using H4IIE cells. tert-Butylhydroperoxide or hydrogen peroxide-induced cell toxicity determined by MTT assay was markedly inhibited by 10mM taurine or hypotaurine. The tert-butylhydroperoxide- or hydrogen peroxide-induced changes in oxidative stress markers, such as cellular glutathione and malondialdehyde, were ameliorated by 10mM taurine or hypotaurine. However, specific TOSC values calculated from the slope of the linear regression for taurine against peroxyl radicals, hydroxyl radicals or peroxynitrites were all less than 1 TOSC/mM. On the other hand specific TOSC values for hypotaurine against peroxyl radicals, hydroxyl radicals or peroxynitrites were 48, 2096, or 69 TOSC/mM, respectively. These results suggest that taurine protects cells against oxidative insults, which is not ascribed to directly scavenging activity of taurine against oxy-radicals. These results support the idea that the oxidation state of sulfur in antioxidants may be a determinant of oxy-radical scavenging capacity.

Evaluation of Oxy-radical Scavenging Capacity of Fucoidan (Fucoidan의 Oxy-radical 포획능 평가)

  • Kim, Bong-Hee;Oh, Jung-Min;Kang, Keon-Wook;Kwak, Sang-Hoon;Yun, Sei-Young;Lee, Chul-Ho;Lee, Hyun-Sun;Kim, Sang-Kyum
    • Environmental Analysis Health and Toxicology
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    • v.23 no.1
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    • pp.41-45
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    • 2008
  • Algal fucoidan is a marine polysaccharide containing sulfur with a wide variety of biological activities including anti-inflammatory and anti-thrombotic effects. Although antioxidants can inhibit inflammatory signals through inhibiting activator protein-1 and/or nuclear factor-kappaB activation, it is obscure whether fucoidan directly scavenges oxy-radicals or indirectly regulates oxidant production and/or antioxidant defense system. The antioxidant activities of fucoidan against peroxyl radicals, peroxynitrites and hydroxyl radicals were determined by the total oxy-radical scavenging capacity (TOSC) assay. The specific TOSC values of fucoidan against peroxyl radicals, peroxynitrites or hydroxyl radicals were $282{\pm}60$, $43{\pm}1$ or $40{\pm}1\;TOSC/mg/mL$, respectively. These specific TOSC values against peroxyl radicals, peroxynitrites or hydroxyl radicals are 23, 12, or 13% of the specific TOSC values of glutathione, a positive control, respectively. These results suggest that fucoidan has direct oxy-radical scavenging capacity, which may be related with anti-inflammatory effect of fucoidan.

Antioxidant Action of Malotilate on Prolonged Hepatic Injury Induced by Carbon Tetrachloride Alone or in Combination with Ethanol in Rat (사염화탄소 및 에탄올에 의해 유도된 만성간 손상에 미치는 말로틸레이트의 항산화 작용)

  • Kim, Hyoung-Chun;Hur, In-Hoi
    • YAKHAK HOEJI
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    • v.34 no.4
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    • pp.267-276
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    • 1990
  • To achieve a better understanding of antioxidant action manifested by malotilate, the dithiol malonates, we monitored the oxy radical-scavenging system against the chronic hepatic damage induced by $CCl_4$ alone or in combination with ethanol. Malotilate was given orally at a dose of 100 mg/kg/day and $CCl_4$ 1.5 ml/kg was injected subcutaneously twice a week for 4 weeks. In each group receiving ethanol, drinking water was replaced by 20% aqueous solution or glucose, isocaloric amounts of ethanol, as a control of ethanol was diluted in its drinking water. Each rat was killed as a starved state at 18 hours after the period of the experiment, four weeks. The results were summarized as follows: 1) Malotilate inhibited the rate of generation of superoxide radicals, the accumulation of lipoperoxides, and promoted the synthesis of glutathione in the liver. 2) Malotilate stimulated the enhancement of activity of superoxide dismutase in hepatic mitochondria. 3) Malotilate had no effects on the hepatic $H_2O_2$ contents. 4) Malotilate showed the increase of catalase activity in the liver poisoned with $CCl_4$, and also gave a tendency to increase it in the liver intoxicated with ethanol. Thus, our data suggested that the activation of hepatic antioxidant system in the presence of malotilate would play a role in protecting liver against the toxic effects of oxy radical and/or lipid peroxides under the hepatotoxic conditions induced by $CCl_4$ with or without ethanol. However, the effects of malotilate against the ethanol-induced hepatotoxicity appear to be insignificant.

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Evaluation of Antioxidant Activity of Sugar Alcohols Using TOSC (Total Oxy-radical Scavenging Capacity) Assay (TOSC 법을 이용한 당알코올의 항산화 활성 평가)

  • Kang, Keon-Wook;Kwak, Sang-Hoon;Yun, Sei-Young;Kim, Sang-Kyum
    • Toxicological Research
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    • v.23 no.2
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    • pp.143-150
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    • 2007
  • Although animal and epidemiological studies have suggested oxidative stress as an etiological factor in pathogenesis including cancer, inflammation, sepsis, fibrosis, cardiovascularlneurodegenerative diseases and aging-related disorders, conflicting results have been obtained in clinical trial with antioxidants. The reason for this discrepancy remains unknown but may be due, in part, to the lack of a validated assay system for evaluating antioxidant capacity. The antioxidant activity of a series of sugar alcohols against peroxyl radicals, hydroxyl radicals and peroxynitrites was determined by the total oxy-radical scavenging capacity (TOSC) assay and cell-based assay using H4IIE cells. Specific TOSC values calculated from the slope of the linear regression for erythritol, xylitol, sorbitol or mannitol against peroxyl radicals was $2.1{\pm}0.2,\;3.7{\pm}0.3,\;9.1{\pm}0.3$ or $8.7{\pm}1.1$ TOSC/mM, respectively. Specific TOSC values for erythritol, xylitol, sorbitol or mannitol against peroxynitrite was $1.9{\pm}0.3,\;3.9{\pm}0.4,\;7.8{\pm}0.7$ or $7.7{\pm}0.5$ TOSC/mM, respectively. These results suggest that oxy-radical scavenging capacity is dependent on the number of aliphatic hydroxyl group in sugar alcohols of monosaccharide. Tert-butylhydroperoxide (t-BHP)-induced cell toxicity determined by MTT assay was marginally attenuated by 10 mM erythritol, but completely inhibited by 10 mM xylitol, 2 mM sorbitol or 0.75 mM maltitol, a disaccharide alcohol. Oxidative stress markers, such as glutathione (GSH) and malondial-dehyde (MDA) levels, were measured in t-BHP-treated cells using HPLC equipped with a fluorescence detector and a reverse phase column. Erythritol did not change the levels of GSH and MDA in H411E cells treated with t-BHP. The t-BHP-induced changes in cellular GSH and MDA levels were ameliorated by 10 mM xylitol and completely blocked by 10 mM sorbitol and maltitol. These results indicate that sugar alcohols protect cells against oxidative stress via scavenging oxy-radical and suggest that TOSC assay in conjunction with cell-based assay is a valid method for evaluating antioxidant capacity of natural and synthetic chemicals.

Protective Effect of Copper against Pancreatic Insult in Streptozotocin-induced Diabetogenic Rat

  • Kim, Hyoung-Chun;Jhoo, Wang-Kee;Kim, Kyeong-Ho;Kim, Jin-Tae;Lee, Sang-Joon;Hur, In-Hoi
    • Archives of Pharmacal Research
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    • v.13 no.2
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    • pp.121-125
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    • 1990
  • The present study examined the alterations in endogenous oxy-radical scaverging system of pancreatic tissue associated with the dose of 45 mg/kg steptozotocin (STZ) alone or with various combinations. The activities of pancreatic Min-superoxide dismutase (SOD) and catalase were no apparent changes in the other groups except for the Cu(II) 4 mg/kg pretreated group. The presence of 4 mg/kg of Cu(II) with or without 125 mg /kg of diethylenetriaminepentaacetic acid (DTPA) markedly attenuated the fall in activity of Cu, Zn-Sod by STZ stress. In particular, STZ-induced superoxide generation was dramatically abolished by prior administration of Cu(II) 4 mg/kg. Conculsively, We suggested the possible involvement that copper may enhance the defence mechanism of pancreatic oxidative damage by STZ challenge.

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