• Proceedings of the Korean Society of Sericultural Science Conference
• /
• 2003.10a
• /
• pp.112-113
• /
• 2003

Kynurenic acid (KYNA), tryptophan metabolite is known to have cell protective effect against various insults in the brain. But so far, the protective mechanism is largely unknown. In this study, we investigated how the KYNA exerts protective effect against 6-OHDA, a causative molecule of Parkinsonian syndrome, using SH-SY5Y cells. (omitted)

• 대한예방의학회:학술대회논문집
• /
• 2005.10a
• /
• pp.406-406
• /
• 2005

• 대한예방의학회:학술대회논문집
• /
• 2005.10a
• /
• pp.432-432
• /
• 2005

• Proceedings of the Korean Society of Tribologists and Lubrication Engineers Conference
• /
• 2002.05a
• /
• pp.88-95
• /
• 2002

Fretting of fuel rod cladding material, Zircaloy-4 Tube, in PWR nuclear power plants must be reduced and avoided. Nowadays the introduction of surface treatments or coatings is expected to bean ideal solution to fretting damage since fretting is closely related to wear, corrosion and fatigue. Therefore, in this study the fretting wear experiment was peformed using TiAIN coated Zircaloy-4 tube as the fuel rod cladding and uncoated Zircaioy-4 tube as one of grids, especially concentrating on the sliding component. Fretting wear resistance of TiAIN coated Zircaloy-4 tubes was improved compared with that of TiN coated tubes and uncoated tubes and the fretting wear mechanisms were delamination and plastic flow following by brittle fracture at lower slip amplitude but severe oxidation and spallation of oxidative layer at higher slip amplitude.

• BMB Reports
• /
• v.32 no.5
• /
• pp.440-444
• /
• 1999

Membrane lipid peroxidation processes yield reactive aldehydes that may react with copper,zinc superoxide dismutase (Cu,Zn SOD), one of the key antioxidant enzymes against oxidative stress. We investigated this possibility and found that exposing Cu,Zn SOD to malondialdehyde (MDA) or 4-hydroxynonenal (HNE) caused the loss of dismutase activity, cross-linking of peptides, and an increase in protein oxidation, reflected by the increased level of carbonyl groups. When Cu,Zn SOD that had been exposed to MDA or HNE was subsequently analyzed by amino acid analysis, histidine content was found to be significantly lost. Both MDA-and HNE-treated Cu,Zn SOD were resistant to proteolysis, which may imply that damaged proteins exist in vivo for a longer period of time than the native enzyme. The lipid peroxidation-mediated damage to Cu,Zn SOD may result in the perturbation of cellular antioxidant defense mechanisms, and subsequently lead to a pro-oxidant condition.

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2001.05a
• /
• pp.146-146
• /
• 2001

Gastroesophageal reflux disease (GERD) is multifactorial in etiology and is characterized by movement of acid and other noxious substances from the stomach into the esophagus. The most severe histologic consequence of chronic gastroesophgeal reflux is Barrett's esophagus, which has been considered as a premalignant condition often leading to the formation of adenocarcinoma of esophagus.(omitted)

• Proceedings of the Korean Society of Applied Pharmacology
• /
• 1997.04a
• /
• pp.105-105
• /
• 1997

Reactive oxygen species(ROS)에 의한 세포독성이나 DNA손상은 노화와 암에 밀접한 관련이 있다. 본연구에서는 ROS중 hydroxyl radical 생성에 관여되는 $H_2O$$_2$에 의해 유도되는 산화적 세포독성이나 DNA손상에 억제적으로 작용할 수 있는 천연물을 창출하기 위한 연구를 하였다. 인삼(Panax Ginseng)C.A. Meyer의 석유에텔의 추출물(GPE)과 일부분획성분(P2)에 대하여 in vitro에서 지질과산화억제효과 및 프리라디칼소거효과를 시험하고 CHL Cell에서의 $H_2O$$_2$ 유도 세포독성과 산화적 DNA손상에 미치는 영향을 연구하였다. 한편 이들 물질을 기존의 항산화제인 ascorbic acid, dl-$\alpha$-tocopheorl 및 $\beta$-carotene등과 비교하였다.

• Proceedings of the KSAR Conference
• /
• 2002.06a
• /
• pp.63-63
• /
• 2002

Peroxiredoxin (Prx) has been known to play an important role in the protection against oxidative damage of reactive oxygen species (ROS). Recent reports implied that the ROS may be closely related with the reproductive system. To define the possible roles of Prx family in reproduction, the expression profiles were investigated in reproductive organs of four murine strains. (omitted)

• Asian-Australasian Journal of Animal Sciences
• /
• v.11 no.3
• /
• pp.265-267
• /
• 1998

Cattle in Alaska seemed to be tolerant to low blood selenium (Se) although arctic winter energy demands might exacerbate oxidative damage to tissues lacking protection by Se. The thermogenic properities of brown adipose tissue (BAT) and the long cold adaptation period for Alaskan cattle indicates that they might develop BAT. Eighteen mature beef cows with whole blood Se of< 19 ppb were used to examine possible relation-ships among Se deficiency, tissue lesions, and observable BAT. All cows were wintered on a diet low in Se and nine cows were given supplemental Se provided by intraruminal bolus. Blood Se was elevated (p < .05) from November through February by supplemental Se, but body weight and back fat thickness were unaffected (p < .10). Tissues were taken from two Se deficient cows, two cows supplemented with Se, and two cows given large doses of Se (300 mg by injection) four weeks before slaughter. Histopathological examination of 187 samples of fat (7 to 55 from each cow) showed no observable amount of BAT. Examination of other tissues showed no lesions attributable to Se deficiency.

• The Korean Journal of Physiology and Pharmacology
• /
• v.1 no.2
• /
• pp.221-224
• /
• 1997

Effects of melatonin on hepatic glutathione-peroxidase (GSH-Px) and glutathione-reductase (GSH-reductase) activities were studied in Sprague-Dawley (SD) rats administered i.p. (10 mg/kg body weight) with melatonin during 15 days. The activity of cytosolic GSH-reductase in the liver was not changed by melatonin. However, melatonin injection increased significantly the activity of liver cytosolic GSH-Px activity compared with those in saline-treated rats. At the same time, plasma GSH-Px was also increased significantly in melatonin-treated rats. Since GSH-Px, a major antioxidative enzyme, removes $H_2O_2$ and lipid peroxides which are formed during lipid peroxidation from cellular membrane, such elevation of heptatic GSH-Px activity may contribute to the improvement of antioxidative effects under oxidative damage in the liver.