• Title/Summary/Keyword: Oxidative damage

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Physiological effects of copper on the freshwater alga Closterium ehrenbergii Meneghini (Conjugatophyceae) and its potential use in toxicity assessments

  • Wang, Hui;Sathasivam, Ramaraj;Ki, Jang-Seu
    • ALGAE
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    • v.32 no.2
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    • pp.131-137
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    • 2017
  • Although green algae of the genus Closterium are considered ideal models for testing toxicity in aquatic ecosystems, little data about the effects of toxicity on these algal species is currently available. Here, Closterium ehrenbergii was used to assess the acute toxicity of copper (Cu). The median effective concentration ($EC_{50}$) of copper sulfate based on a dose response curve was $0.202mg\;L^{-1}$, and reductions in photosynthetic efficiency ($F_v/F_m$ ratio) of cells were observed in cultures exposed to Cu for 6 h, with efficiency significantly reduced after 48 h (p < 0.01). In addition, production of reactive oxygen species significantly increased over time (p < 0.01), leading to damage to intracellular organelles. Our results indicate that Cu induces oxidative stress in cellular metabolic processes and causes severe physiological damage within C. ehrenbergii cells, and even cell death; moreover, they clearly suggest that C. ehrenbergii represents a potentially powerful test model for use in aquatic toxicity assessments.

Mitochondria-Targeted Vitamin E Protects Skin from UVB-Irradiation

  • Kim, Won-Serk;Kim, Ikyon;Kim, Wang-Kyun;Choi, Ju-Yeon;Kim, Doo Yeong;Moon, Sung-Guk;Min, Hyung-Keun;Song, Min-Kyu;Sung, Jong-Hyuk
    • Biomolecules & Therapeutics
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    • v.24 no.3
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    • pp.305-311
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    • 2016
  • Mitochondria-targeted vitamin E (MVE) is designed to accumulate within mitochondria and is applied to decrease mitochondrial oxidative damage. However, the protective effects of MVE in skin cells have not been identified. We investigated the protective effect of MVE against UVB in dermal fibroblasts and immortalized human keratinocyte cell line (HaCaT). In addition, we studied the wound-healing effect of MVE in animal models. We found that MVE increased the proliferation and survival of fibroblasts at low concentration (i.e., nM ranges). In addition, MVE increased collagen production and downregulated matrix metalloproteinase1. MVE also increased the proliferation and survival of HaCaT cells. UVB increased reactive oxygen species (ROS) production in fibroblasts and HaCaT cells, while MVE decreased ROS production at low concentration. In an animal experiment, MVE accelerated wound healing from laser-induced skin damage. These results collectively suggest that low dose MVE protects skin from UVB irradiation. Therefore, MVE can be developed as a cosmetic raw material.

Effects of Danchun-hwan on Oxidative Damage of Human Neural Cell (단천환이 사람신경세포의 산화적 손상에 미치는 영향)

  • 한상혁;김명선;이지현;김도환;나영훈;조광호;박래길;문병순
    • The Journal of Korean Medicine
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    • v.21 no.4
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    • pp.183-192
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    • 2000
  • Objectives : The present study was carried out to investigate the effects of Danchun-hwan(DCH) on the peroxynitrite-induced neural cell death in human neuroblastoma cell line, SH-SY5Y. Methods : The cultured cells were pretreated with DCH and exposed to 3-morpholinosydnonimine(SIN-1) that simultaneously generates NO and superoxide, thus possibly forming peroxynitrite. The cell damage was assessed by using MTT assay and crystal violet staining. Results : Exposure of the cells to SIN-1 for 24hr induced 75% apoptotic cell death, as evaluated by the occurrence of morphological nuclear changes characteristic of apoptosis using 4', 6-diamidino-2-phenylinole(DAPI). However, pretreatment of SH-SY5Y with the water extracts of DCH, inhibited the apoptotic cell death in a dose-dependent manner. DCH also inhibited SIN-1-induced apoptotic caspase 3-like protease activity in a dose-dependent manner. DCH recovered the depleted glutathione levels by SIN-1. Conclusions : Taken together, it is suggested that DCH protected human neuroblastoma cell line, SH-SY5Y, from the free radical injury mediated by peroxynitrite by a mechanism of elevating antioxidant, GSH.

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The Chemopreventive Effects of Antioxidant Enzyme (항산화효소의 암 예방 효과 및 발암 억제 기전)

  • Jung Hwa-Jin;Choi Yoon-Joo;Won Chang-Won;Seo Young-Rok
    • Environmental Mutagens and Carcinogens
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    • v.26 no.2
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    • pp.45-47
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    • 2006
  • The reactive oxygen species (ROS) caused the damage of macro molecules, many degenerative disease and cancer, which was produced in process of the aerotropic metabolic pathway as well as in response to the various genotoxic stresses. Recently, redox systems including the number of antioxidant proteins such as catalase, glutathione peroxidase, heam-containing peroxidase, peroxiredoxin and superoxide dismutase (SOD) has been reported to have chemopreventive effects. Antioxidant proteins has been known to have the activity directly removing ROS and affecting the protein-protein interaction and cell signaling to induce the cellular responses. We need to understand the mechanism of antioxidants prevent DNA damage from oxidative stresses for researching the cancer prevention and providing the development of cancer therapeutic drug.

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Heme Oxygenase-1 as a Potential Therapeutic Target for Hepatoprotection

  • Farombi, Ebenezer Olatunde;Surh, Young-Joon
    • BMB Reports
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    • v.39 no.5
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    • pp.479-491
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    • 2006
  • Heme oxygenase (HO), the rate limiting enzyme in the breakdown of heme into carbon monoxide (CO), iron and bilirubin, has recently received overwhelming research attention. To date three mammalian HO isozymes have been identified, and the only inducible form is HO-1 while HO-2 and HO-3 are constitutively expressed. Advances in unveiling signal transduction network indicate that a battery of redox-sensitive transcription factors, such as activator protein-1 (AP-1), nuclear factor-kappa B (NF-${\kappa}B$) and nuclear factor E2-related factor-2 (Nrf2), and their upstream kinases including mitogen-activated protein kinases play an important regulatory role in HO-1 gene induction. The products of the HO-catalyzed reaction, particularly CO and biliverdin/bilirubin have been shown to exert protective effects in several organs against oxidative and other noxious stimuli. In this context, it is interesting to note that induction of HO-1 expression contributes to protection against liver damage induced by several chemical compounds such as acetaminophen, carbon tetrachloride and heavy metals, suggesting HO-1 induction as an important cellular endeavor for hepatoprotection. The focus of this review is on the significance of targeted induction of HO-1 as a potential therapeutic strategy to protect against chemically-induced liver injury as well as hepatocarcinogenesis.

Antioxidant Effects of Plant Extracts on Free Radicals and Lipid Peroxidation

  • Na, Min-Kyun;An, Ren-Bo;Jin, Wen-Yi;Min, Byung-Sun;Yoo, Jae-Kuk;Kim, Young-Ho;Bae, Ki-Hwan
    • Natural Product Sciences
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    • v.9 no.4
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    • pp.226-231
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    • 2003
  • Reactive oxygen species damage biomolecules such as lipids, proteins, sugars and DNA, which can not only lead to various disease but also oxidative damage resulting aging. In order to search for antioxidants from plants, the antioxidant effects of the MeOH extracts from 182 plants were evaluated. The results showed that thirteen plant extracts exhibited antioxidant activity (>80%) in DPPH radical assay, seven plant extracts demonstrated antioxidant activity (>40%) in the hydroxyl radical assay and eighteen plant extracts were active (>80%) in the lipid peroxidation assay. In particular, the extracts of Distylium racemosum (Hamamelidaceae), Astilbe koreana (Saxifragaceae), Astilbe chinensis and Euphorbia supina (Euphorbiaceae) were identified as potent principles of antioxidant activity in all the assay systems.

Liver Protective Effects of Jageum-Jung in Alcohol-induced liver injury mice model (알코올 유발 간 손상 마우스 모델에서 자금정의 간 보호 효과)

  • Kim, Kwang-Youn;Park, Kwang-Il;Cho, Won-Kyung;Ma, Jin-Yeul
    • Herbal Formula Science
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    • v.28 no.2
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    • pp.179-187
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    • 2020
  • Objectives : This study investigated the hepatoprotective effects effects of Jageum-jung extract on alcohol-induced liver disease mice model. Methods : Alcoholic liver disease was induced by Ethanol in C57/BL6 male mice, which were fed Lieber-DeCarli liquid diet containing ethanol. Jageum-jung (100,200 and 300 mg/kg bw/day) were orally administered daily in the alcoholic fatty liver disease mice for 16 days. Results : The results indicate that Jageum-jung promotes hepatoprotective effects by significantly reducing aspartate transaminase (AST) and alanine transaminase (ALT) levels as indicators of liver damage in the serum. Furthermore, Jageum-jung decreased accumulation of triglyceride and total cholesterol, increased levels of superoxide dismutase (SOD) and glutathione (GSH) in the serum of the alcoholic fatty liver disease mice model. Additionally, it improved the serum alcohol dehydrogenase (ADH) activity. Conclusions : This study confirmed the anti-oxidative and hangover elimination effects of Jageum-jung extract, and suggests the possibility of using Jageum-jung to treat alcholic liver disease.

Effects of Total Dietary Restriction on the Contents of Thiobarbituric Acid-Reactive Substance and Antioxidant Enzymes in the Liver and Kidney of Rats (절식이 흰쥐의 간과 신장의 Thiobarbituric Acid-Reactive Substance량 및 항산화효소 활성도에 미치는 영향)

  • 박평심;고춘남;박재윤
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.28 no.2
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    • pp.471-476
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    • 1999
  • The effects of total dietary restriction(100% restriction of energy intake) on thiobarbituric acid reactive substance(TBARS) contents and intracellular antioxidant enzymes activities in the liver and kidney of young male Sprague Dawley rats were studied. The TBARS contents were reduced in both liver and kidney, up to 77% and 79% of the control rats, fed ad libitum, respectively at 7 days after dietary restriction . Superoxide dismutase(SOD) activities in the liver and kidney of rats were increased significantly by total dietary restriction. However, the activity of catalase in kidney was decreased 27% at 6 days after dietary restriction, but this enzyme activity did not change in liver. The changes of glutathione peroxidae(GSHPx) and catalase activities in the liver and kidney of rats with dietary restriction were not significant. These result suggested that dietary restriction reduce the free radical induced by tissue damage, as determined by TBARS content, in both the liver and kidney but the changes of activities of antioxidant enzymes may not be a contributory factor in reducing oxidative damage to tissue.

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Effects of Platycodi Radix on Passive Smoking in Rats (간접흡연에 노출시킨 흰쥐의 폐조직 손상에 대한 길경의 보호효과)

  • Kim, Bum-Hoi
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.26 no.1
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    • pp.40-46
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    • 2012
  • Cigarette smoking is known to be associated with various chronic pulmonary and cardiovascular diseases ranging from inflammation to cancer. Not only first-hand smoke but also second-hand smoke is suggested to be a factor of health risk. This study was to investigate whether Platycodi Radix extract administration would alter oxidative stress in lung leading to protection of cigarette smoke-induced lung damage. Sprague-Dawley rats were randomly divided into 3 groups; Intact, Smoke+PR and Smoke+Vehicle. In Smoke+PR and Smoke+Vehicle group, the exposure to cigarette smoke was performed for 15 min/day for 4 weeks in ventilated smoking chamber. The Platycodi Radix extract and saline were orally administrated to Smoke+PR and Smoke+Vehicle group each. The rats of Intact group were just kept in ventilated chamber without cigarette smoke. After the experiment for 4 weeks, the lung tissues were collected for histological observation and immunohistochemistry. In Results, airspace enlargement and goblet cell hyperplasia were observed after 4 weeks' exposure to cigarette smoke. Whereas, the oral administration of Platycodi Radix extract for 4 weeks reduced airspace enlargement and goblet cell hyperplasia. Moreover, the alterations of BAX/Bcl-2 proteins in lung tissues were observed. These results suggest that Platycodi Radix extract ameliorates lung damage in cigarette smoke-exposed rats and has protective effects on second-hand smoke injury.

Multiple Roles of Peroxiredoxins in Inflammation

  • Knoops, Bernard;Argyropoulou, Vasiliki;Becker, Sarah;Ferte, Laura;Kuznetsova, Oksana
    • Molecules and Cells
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    • v.39 no.1
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    • pp.60-64
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    • 2016
  • Inflammation is a pathophysiological response to infection or tissue damage during which high levels of reactive oxygen and nitrogen species are produced by phagocytes to kill microorganisms. Reactive oxygen and nitrogen species serve also in the complex regulation of inflammatory processes. Recently, it has been proposed that peroxiredoxins may play key roles in innate immunity and inflammation. Indeed, peroxiredoxins are evolutionarily conserved peroxidases able to reduce, with high rate constants, hydrogen peroxide, alkyl hydroperoxides and peroxynitrite which are generated during inflammation. In this minireview, we point out different possible roles of peroxiredoxins during inflammatory processes such as cytoprotective enzymes against oxidative stress, modulators of redox signaling, and extracellular pathogen- or damage-associated molecular patterns. A better understanding of peroxiredoxin functions in inflammation could lead to the discovery of new therapeutic targets.