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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.
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.
Acrolein, A Reactive Product of Lipid Peroxidation, Induces Oxidative Modification of Cytochrome c
강정훈 대한화학회 2013 Bulletin of the Korean Chemical Society Vol.34 No.11
Acrolein (ACR) is a well-known carbonyl toxin produced by lipid peroxidation of polyunsaturated fatty acids, which is involved in the pathogenesis of neurodegenerative disorders such as Alzheimer’s disease (AD). In Alzheimer's brain, ACR was found to be elevated in hippocampus and temporal cortex where oxidative stress is high. In this study, we evaluated oxidative modification of cytochrome c occurring after incubation with ACR. When cytochrome c was incubated with ACR, protein aggregation increased in a dose-dependent manner. The formation of carbonyl compounds and the release of iron were obtained in ACR-treated cytochrome c. Reactive oxygen species scavengers and iron specific chelator inhibited the ACR-mediated cytochrome c modification and carbonyl compound formation. Our data demonstrate that oxidative damage of cytochrome c by ACR might induce disruption of cyotochrome c structure and iron mishandling as a contributing factor to the pathology of AD.
Oxidative Modification of Cytochrome c by Tetrahydropapaveroline, an Isoquinoline-Derived Neurotoxin
강정훈 대한화학회 2013 Bulletin of the Korean Chemical Society Vol.34 No.2
Tetrahyropapaveroline (THP) is compound derived from dopamine metabolism and is capable of causing dopaminergic neurodegenerative disorder, such as Parkinson’s disease (PD). The aim of this study was to evaluate the potential of THP to cause oxidative damage on the structure of cytochrome c (cyt c). Our data showed that THP led to protein aggregation and the formation of carbonyl compound in protein aggregates. THP also induced the release of iron from cyt c. Reactive oxygen species (ROS) scavengers and iron specific chelator inhibited the THP-mediated cyt c modification and carbonyl compound formation. The results of this study show that ROS may play a critical role in THP-induced cyt c modification and iron releasing of cyt c. When cyt c that has been exposed to THP was subsequently analyzed by amino acid analysis, lysine, histidine and methionine residues were particularly sensitive. It is suggested that oxidative damage of cyt c by THP might induce the increase of iron content in cells and subsequently led to the deleterious condition. This mechanism is associated with the deterioration of organs under neurodegenerative disorder such as PD.
강정훈,임신재,손승훈,김규정,황현수 한국산림과학회 2013 Forest Science And Technology Vol.9 No.3
The goal of this study was to gain an understanding of small mammal populations in thinned and clearcut stands in Japanese larch (Larix leptolepis) plantations on Mt. Maehwasan, Hongcheon, Korea. Foliage profiles, diameter at breast height distribution, coverage of ground, and volume of coarse woody debris were significantly different between thinned and clearcut stands. Total number of captured small mammals, number of captured striped field mice, and mean striped field mouse population densities obtained from Jolly–Seber estimates were higher in clearcut stands. Coverage of ground,volume of coarse woody debris, and number of downed trees were critical variables for abundance of small mammals in this study. Our results suggest that retention of coarse woody debris and downed trees prevent reduction of small mammal populations after forest practices in Japanese larch plantations.
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.