구강외과 환자의 합병증과 예방법

강정훈 단국대학교 치과대학 예방치과 1990 예방치과 세미나집 Vol.4 No.-

Aggregation of α-Synuclein Induced by Oxidized Catecholamines as a Potential Mechanism of Lewy Body

강정훈,Kyung Sik Kim 대한화학회 2005 Bulletin of the Korean Chemical Society Vol.26 No.8

Lewy bodies (LBs) are neuronal inclusions that are closely related to Parkinson's disease (PD). The filamentous component of LB from patients with PD contains biochemically altered -synuclein. We have investigated the effect of the oxidized products of catecholamines on the modification of -synuclein. When -synuclein was incubated with the oxidized 3,4-dihydroxyphenylalanine (L-DOPA) or dopamine, the protein was induced to be aggregated. The oxidized catecholamine-mediated -synuclein aggregation was enhanced by copper ion. Radical scavengers, azide and N-acetyl cysteine significantly prevented the oxidized catecholamine-mediated -synuclein aggregation. The results suggest that free radical may play a role in -synuclein aggregation. Exposure of -synuclein to the oxidized products of catecholamines led to the formation of dityrosine. Antioxidant dipeptides carnosine, homocarnosine and anserine significantly protected -synuclein from the aggregation induced by the oxidized products of catecholamines.

고품질 원유의 생산, 이용을 위한 원유 위생

강정훈,김진석,이원창 한국수의공중보건학회 1999 예방수의학회지 Vol.23 No.1

Protection by Carnosine and Homocarnosine against L-DOPA-Fe(III)-Mediated DNA Cleavage

강정훈 대한화학회 2005 Bulletin of the Korean Chemical Society Vol.26 No.8

It has been proposed that oxidation of L-3,4-dihydroxyphenylalanine (DOPA) may contribute to the pathogenesis of neurodegenerative disease. In this study, L-DOPA-Fe(III)-mediated DNA cleavage and the protection by carnosine and homocarnosine against this reaction were investigated. When plasmid DNA was incubated with L-DOPA in the presence of Fe(III), DNA strand was cleaved. Radical scavengers and catalase significantly inhibited the DNA breakage. These results suggest that H2O2 may be generated from the oxidation of DOPA and then Fe3+ likely participates in a Fenton’s type reaction to produce hydroxyl radicals, which may cause DNA cleavage. Carnosine and homocarnosine have been proposed to act as anti-oxidants in vivo. The protective effects of carnosine and homocarnosine against L-DOPA-Fe(III)-mediated DNA cleavage have been studied. Carnosine and homocarnosine significantly inhibited DNA cleavage. These compounds also inhibited the production of hydroxyl radicals in L-DOPA/Fe3+ system. The results suggest that carnosine and homocarnosine act as hydroxyl radical scavenger to protect DNA cleavage. It is proposed that carnosine and homocarnosine might be explored as potential therapeutic agents for pathologies that involve damage of DNA by oxidation of DOPA.

Protection by Histidine Dipeptides against Acrolein-induced Neurofilament-L Aggregation

강정훈 대한화학회 2008 Bulletin of the Korean Chemical Society Vol.29 No.9

The endogenous dipeptides, carnosine and related compounds, are the naturally occurring dipeptides with multiple neuroprotective properties. We have examined the protective effects of carnosine, homocarnosine and anserine on the aggregation of neurofilament-L (NF-L) induced by neurotoxin, acrolein. When NF-L was incubated with acrolein in the presence of carnosine, homocarnosine or anserine, protein aggregation was inhibited in a concentration-dependent manner. These compounds inhibited the formation of protein carbonyl compounds and dityrosine in acrolein-mediated NF-L aggregates. The aggregates of NF-L displayed thioflavin T reactivity, reminiscent of amyloid. This thioflavin T reactivity was inhibited by carnosine and related compounds. This effect was associated with decreased formation of oxidatively modified proteins. Our results suggested that carnosine and related compounds might have protective effects to brain proteins under pathophysiological conditions leading to degenerative damage such as neurodegenerative disorders.

Oxidative Modification of Ferritin Induced by Salsolinol, Catechol Neurotoxin

강정훈 대한화학회 2008 Bulletin of the Korean Chemical Society Vol.29 No.12

Previous evidences suggest that oxidative alteration of ferritin has been linked to the pathogenesis of Parkinson disease (PD). We have investigated the modification of ferritin induced by salsolinol (SAL), endogenous neurotoxin. When ferritin was incubated with SAL, the aggregation of protein increased with the SAL concentration. SAL also led to the release of iron from ferritin in a SAL concentration-dependent manner. Free radical scavengers and iron specific chelator inhibited the SAL-mediated ferritin modification. Exposure of ferritin to SAL led to the generation of protein carbonyl compounds and the formation of dityrosine. The present results indicate that free radicals may play a role in the modification and iron releasing of ferritin by SAL. It is suggested that oxidative damage of ferritin by SAL might induce the increase of iron content in cells and subsequently led to the deleterious condition. This mechanism, in part, may provide an explanation for the deterioration of organs under neurodegenerative disorder such as PD.

Oxidative Damage of DNA Induced by Ferritin and Hydrogen Peroxide

강정훈 대한화학회 2010 Bulletin of the Korean Chemical Society Vol.31 No.10

Excess free iron generates oxidative stress that may contribute to the pathogenesis of various causes of neurodegenerative diseases. Previous studies have shown that one of the primary causes of increased brain iron may be the release of excess iron from intracellular iron storage molecules. In this study, we attempted to characterize the oxidative damage of DNA induced by the reaction of ferritin with H2O2. When DNA was incubated with ferritin and H2O2,DNA strand breakage increased in a time-dependent manner. Hydroxyl radical scavengers strongly inhibited the ferritin/H2O2 system-induced DNA cleavage. We investigated the generation of hydroxyl radical in the reaction of ferritin with H2O2 using a chromogen, 2,2'-azinobis-(2-ethylbenzthiazoline-6-sulfonate) (ABTS), which reacted with ·OH to form ABTS+•. The initial rate of ABTS+• formation increased as a function of incubation time. These results suggest that DNA strand breakage is mediated in the reaction of ferritin with H2O2 via the generation of hydroxyl radicals. The iron-specific chelator, deferoxamine, also inhibited DNA cleavage. Spectrophotometric study using a color reagent showed that the release of iron from H2O2-treated ferritin increased in a time-dependent manner. Ferritin enhanced mutation of the lacZ' gene in the presence of H2O2 when measured as a loss of α-complementation. These results indicate that ferritin/H2O2 system-mediated DNA cleavage and mutation may be attributable to hydroxyl radical generation via a Fenton-like reaction of free iron ions released from oxidatively damaged ferritin.

The Reaction of Salsolinol with Ferritin Induces DNA Strand Breakage

강정훈 대한화학회 2008 Bulletin of the Korean Chemical Society Vol.29 No.12

Iron released from ferritin may trigger oxidative stress leading to progressive degeneration of brains from patients with neurodegenerative diseases. Previous studies have shown that oxidative damage of proteins and DNA was induced by catechol neurotoxin such as salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline). In the present study, we have investigated oxidative damage of DNA induced by the reaction of salsolinol with ferritin. When DNA was incubated with ferritin and salsolinol, DNA strand breakage increased in a time-dependent manner. Hydroxyl radical scavengers, such as azide, mannitol and dimethyl sulfoxide, effectively inhibited the salsolinol/ferritin system-mediated DNA cleavage, whereas Cu,Zn-superoxide dismutase did not suppress DNA cleavage. Catalase significantly inhibited the salsolinol/ferritin system-mediated DNA cleavage. Iron specific chelator, deferoxamine, also inhibited DNA cleavage. Spectrophotometric study using a color reagent showed that the release of iron from salsolinol-treated ferritin was increased in a time dependent manner. These results suggest that DNA strand breakage is mediated in the reaction of salsolinol with ferritin via the generation of hydroxyl radicals by the Fenton-like reaction of free iron ions released from oxidatively damaged ferritin.

Oxidative Modification of Neurofilament-L Induced by Endogenous Neurotoxin, Salsolinol

강정훈 대한화학회 2011 Bulletin of the Korean Chemical Society Vol.32 No.9

The endogenous neurotoxin, 1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol), has been considered a potential causative factor for the pathogenesis of Parkinson’s disease (PD). In this study, we examined oxidative modification of neurofilament-L (NF-L) induced by salsolinol. When disassembled NF-L was incubated with salsolinol, the aggregation of protein was increased with the concentration of sasolinol. The formation of carbonyl compound was obtained in salsolinol-mediated NF-L aggregates. This process was protected by free radical scavengers, such as N-acetyl-L-cysteine and glutathione. These results suggest that the aggregation of NF-L is mediated by salsolinol via the generation of free radicals. We also investigated the effects of copper ion on salsolinol-mediated NF-L modification. In the presence of copper ions, salsolinol enhanced the modification of NF-L. We suggest that salsolinol might be related to abnormal aggregation of NF-L which may be involved in the pathogenesis of neurodegenerative diseases and related disorders.

도시정부의 정치과정 연구 : 서울특별시의 청계천복원사업을 둘러싼 이익집단정치를 중심으로 Focusing on the Interest Groups Involved in the Restoration Project of Cheonggyecheon in Seoul

강정훈 한국도시연구소 2004 도시연구 Vol.- No.9