• 제목/요약/키워드: Oxidative damage

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Mitochondrial DNA Mutation and Oxidative Stress

  • Kim, Tae-Ho;Kim, Hans-H.;Joo, Hyun
    • Interdisciplinary Bio Central
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    • 제3권4호
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    • pp.16.1-16.8
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    • 2011
  • Defects in mitochondrial DNA (mtDNA) cause many human diseases and are critical factors that contribute to aging. The mechanisms of maternally-inherited mtDNA mutations are well studied. However, the role of acquired mutations during the aging process is still poorly understood. The most plausible mechanism is that increased reactive oxygen species (ROS) may affect the opening of mitochondrial voltage dependent anion channel (VDAC) and thus results in damage to mtDNA. This review focuses on recent trends in mtDNA research and the mutations that appear to be associated with increased ROS.

Protective Effects of Histidine Dipeptides on the Modification of Neurofilament-L by the Cytochrome c/Hydrogen Peroxide System

  • Kim, Nam-Hoon;Kang, Jung-Hoon
    • BMB Reports
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    • 제40권1호
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    • pp.125-129
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    • 2007
  • Neurofilament-L (NF-L) is a major element of the neuronal cytoskeleton and is essential for neuronal survival. Moreover, abnormalities in NF-L result in neurodegenerative disorders. Carnosine and the related endogeneous histidine dipeptides prevent protein modifications such as oxidation and glycation. In the present study, we investigated whether histidine dipeptides, carnosine, homocarnosine, or anserine protect NF-L against oxidative modification during reaction between cytochrome c and $H_2O_2$. Carnosine, homocarnosine and anserine all prevented cytochrome c/$H_2O_2$-mediated NF-L aggregation. In addition, these compounds also effectively inhibited the formation of dityrosine, and this inhibition was found to be associated with the reduced formations of oxidatively modified proteins. Our results suggest that carnosine and histidine dipeptides have antioxidant effects on brain proteins under pathophysiological conditions leading to degenerative damage, such as, those caused by neurodegenerative disorders.

Oxidative damage of DNA induced by the reaction of methylglyoxal with lysine in the presence of ferritin

  • An, Sung Ho;Kang, Jung Hoon
    • BMB Reports
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    • 제46권4호
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    • pp.225-229
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    • 2013
  • Methylglyoxal (MG) is an endogenous metabolite which is present in increased concentrations in diabetics and reacts with amino acids to form advanced glycation end products. In this study, we investigated whether ferritin enhances DNA cleavage by the reaction of MG with lysine. When plasmid DNA was incubated with MG and lysine in the presence of ferritin, DNA strand breakage was increased in a dose-dependent manner. The ferritin/MG/lysine system-mediated DNA cleavage was significantly inhibited by reactive oxygen species (ROS) scavengers. These results indicated that ROS might participate in the ferritin/MG/lysine system-mediated DNA cleavage. Incubation of ferritin with MG and lysine resulted in a time-dependent release of iron ions from the protein molecules. Our data suggest that DNA cleavage caused by the ferritin/MG/lysine system via the generation of ROS by the Fenton-like reaction of free iron ions released from oxidatively damaged ferritin.

Protective Effect of Celecoxib, a Selective Cyclooxygenase-2 Inhibitor, Against Beta-Amyloid-Induced Apoptosis: Possible Involvement of Proinflammatory Signals in Beta-Amyloid-Mediated Cell Death

  • Jang, Jung-Hee;Surh, Young-Joon
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2003년도 추계학술대회
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    • pp.139-140
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    • 2003
  • Inflammatory as well as oxidative tissue damage has been implicated in pathophysiology of Alzheimer's disease (AD), and non-steroidal anti-inflammatory drugs have been reported to have beneficial effects in the treatment or prevention of AD. In the present study, we investigated the effect of celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, on inflammatory cell death induced by beta-amyloid, a neurotoxic peptide associated with senile plaques formed in the brains of patients with AD.(omitted)

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Resveratrol, an Antioxidant in Red Wine, Inhibits Metabolic Formation of Catechol Estrogens and Their Induction of Oxidative Dna Damage and Cell Death

  • Chen, Zhi-Hua;Hurh, Yeon-Jin;Na, Hye-Kyung;Kim, Do-Hee;Chun, Young-Jin;Kim, Dong-Hyun;Surh, Young-Joon
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2003년도 추계학술대회
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    • pp.182-182
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    • 2003
  • cResveratrol (3,5,4'-trihydroxystilbene), a naturally occurring phytoalexin present in grapes and other foods, has been well documented for chemopreventive effects in different systems based on its striking inhibition of diverse cellular events associated with tumor initiation, promotion and progression.(omitted)

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Tricyclic Antidepressants Amitriptyline and Desipramine Induced Neurotoxicity Associated with Parkinson's Disease

  • Lee, Min-yeong;Hong, Seokheon;Kim, Nahmhee;Shin, Ki Soon;Kang, Shin Jung
    • Molecules and Cells
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    • 제38권8호
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    • pp.734-740
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    • 2015
  • Recent studies report that a history of antidepressant use is strongly correlated with the occurrence of Parkinson' disease (PD). However, it remains unclear whether antidepressant use can be a causative factor for PD. In the present study, we examined whether tricyclic antidepressants amitriptyline and desipramine can induce dopaminergic cell damage, both in vitro and in vivo. We found that amitriptyline and desipramine induced mitochondria-mediated neurotoxicity and oxidative stress in SH-SY5Y cells. When injected into mice on a subchronic schedule, amitriptyline induced movement deficits in the pole test, which is known to detect nigrostriatal dysfunction. In addition, the number of tyrosine hydroxylase-positive neurons in the substantia nigra pars compacta was reduced in amitriptyline-injected mice. Our results suggest that amitriptyline and desipramine may induce PD-associated neurotoxicity.

Development of functional substances on Alzheimer's disease

  • 허호진
    • 식품저장과 가공산업
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    • 제6권2호
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    • pp.25-29
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    • 2007
  • Phytochemicals have long been known to hold a number of physiological benefits, including antioxidant, anticardiovascular activities and anticancer. The profitable effects of phytochemicals from food sources such as vegetables and fruits, with respect to neurodegeneration, are only beginning to receive increased attention. Alzheimer's disease(AD) is one of the major neurodegenerative diseases for which no treatment is available, and characterized by loss of cognitiion and memory. Many recent studies show that the brain of AD patient is subjected to increased oxidative stress resulting from free radical damage, and the resulting cellular malfunctions are widely believed to be responsible for neuronal degeneration in AD. In this study, the relative relation between D and phytochemicals were surveyed.

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Effect of Natural Compounds on Catechol Estrogen-Induced Carcinogenesis

  • Sung, Nam-Ji;Park, Sin-Aye
    • 대한의생명과학회지
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    • 제25권1호
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    • pp.1-6
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    • 2019
  • The hydroxylation of estradiol results in the formation of catechol estrogens such as 2-hydroxyestradiol ($2-OHE_2$) and 4-hydroxyestradiol ($4-OHE_2$). These catechol estrogens are further oxidized to quinone metabolites by peroxidases or cytochrome P450 (CYP450) enzymes. Catechol estrogens contribute to hormone-induced carcinogenesis by generating DNA adducts or reactive oxygen species (ROS). Interestingly, many of the natural products found in living organisms have been reported to show protective effects against carcinogenesis induced by catechol estrogens. Although some compounds have been reported to increase the activity of catechol estrogens via oxidation to quinone metabolites, many natural products decreased the activity of catechol estrogens by inhibiting DNA adduct formation, ROS production, or oxidative cell damage. Here we focus specifically on the chemopreventive effects of these natural compounds against carcinogenesis induced by catechol estrogens.

In vivo evidence for brain-to-blood efflux transport of taurine and regulation of this transport by tumor necrosis factor-$\alpha$ at the blood-brain barrier

  • Lee, Na-Young;Kang, Young-Sook
    • 대한약학회:학술대회논문집
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    • 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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    • pp.69.2-69.2
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    • 2003
  • The purpose of this study is to examine whether the efflux system for taurine from brain to blood is present on the blood-brain barrier (BBB) using the brain efflux index (BEl) method and taurine transport system is regulated by CNS cell damage with oxidative stress agent such as diethyl maleate (DEM) or tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) in vivo. [$^3$H]Taurine was microinjected into parietal cortex area 2 (Par2) of the rat brain, and was eliminated from the brain with efflux transport rate of 1.22 10$\^$-2//min, and the process is saturable with a $K_{m}$ of 43.5 ${\mu}$M. (omitted)

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