• Bulletin of the Korean Chemical Society
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• v.28 no.1
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• pp.77-80
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• 2007

As neurofilament proteins are major cytoskeletal components of neuron, abnormality of neurofilament is proposed in brain with neurodegenerative disorders such as Parkinson's disease (PD). Since oxidative stress might play a critical role in altering normal brain proteins, we investigated the oxidative modification of neurofilament-L (NF-L) induced by the reaction of cytochrome c with H2O2. When NF-L was incubated with cytochrome c and H2O2, the protein aggregation was increased in cytochrome c and H2O2 concentrationsdependent manner. Radical scavengers, azide, formate and N-acetyl cysteine, prevented the aggregation of NFL induced by the cytochrome c/H2O2 system. The formations of carbonyl group and dityrosine were obtained in cytochrome c/H2O2-mediated NF-L aggregates. Iron specific chelator, desferoxamine, prevented the cytochrome c/H2O2 system-mediated NF-L aggregation. These results suggest that the cytochrome c/H2O2 system may be related to abnormal aggregation of NF-L which may be involved in the pathogenesis of PD and related disorders.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2018.04a
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• pp.68-68
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• 2018

In this study, we investigated whether S. baicalensis rhizome ethanol extract (SBRE) has antioxidant capacities against oxidative stress induced cellular damage in the HaCaT keratinocytes. Our results revealed that treatment with SBRE prior to hydrogen peroxide ($H_2O_2$) exposure significantly increased the HaCaT cell viability. SBRE also effectively attenuated $H_2O_2$ induced comet tail formation, and inhibited the $H_2O_2$ induced phosphorylation levels of the histone ${\gamma}H2AX$, as well as the number of apoptotic bodies and Annexin V positive cells. In addition, SBRE exhibited scavenging activity against intracellular ROS generation and restored the mitochondria membrane potential loss induced by $H_2O_2$. Moreover, $H_2O_2$ enhanced the cleavage of caspase-3 and degradation of poly (ADP-ribose)-polymerase as well as DNA fragmentation; however, these events were almost totally reversed by pretreatment with SBRE. Furthermore, SBRE increased the levels of HO-1 associated with the induction of Nrf2. Therefore, we believed that SBRE may potentially serve as an agent for the treatment and prevention of neurodegenerative diseases caused by oxidative stress.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.3
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• pp.127-132
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• 2010

Reactive oxygen species (ROS), which include hydrogen peroxide ($H_2O_2$), the superoxide anion (${O_2}^-{\cdot}$), and the hydroxyl radical ($OH{\cdot}$), are generated as by-products of oxidative metabolism in cells. The cerebral cortex has been found to be particularly vulnerable to production of ROS associated with conditions such as ischemia-reperfusion, Parkinson's disease, and aging. To investigate the effect of ROS on inhibitory GABAergic synaptic transmission, we examined the electrophysiological mechanisms of the modulatory effect of $H_2O_2$ on GABAergic miniature inhibitory postsynaptic current (mIPSCs) in mechanically isolated rat cerebral cortical neurons retaining intact synaptic boutons. The membrane potential was voltage-clamped at -60 mV and mIPSCs were recorded and analyzed. Superfusion of 1-mM $H_2O_2$ gradually potentiated mIPSCs. This potentiating effect of $H_2O_2$ was blocked by the pretreatment with either 10,000-unit/mL catalase or $300-{\mu}M$ N-acetyl-cysteine. The potentiating effect of $H_2O_2$ was occluded by an adenylate cyclase activator, forskolin, and was blocked by a protein kinase A inhibitor, N -(2-[p-bromocinnamylamino] ethyl)-5-isoquinolinesulfonamide hydrochloride. This study indicates that oxidative stress may potentiate presynaptic GABA release through the mechanism of cAMP-dependent protein kinase A (PKA)-dependent pathways, which may result in the inhibition of the cerebral cortex neuronal activity.

• Journal of Microbiology and Biotechnology
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• v.28 no.1
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• pp.145-156
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• 2018

Most eukaryotic peroxiredoxins (Prxs) are readily inactivated by a high concentration of hydrogen peroxide ($H_2O_2$) during catalysis owing to their "GGLG" and "YF" motifs. However, such oxidative stress sensitive motifs were not found in the previously identified filamentous fungal Prxs. Additionally, the information on filamentous fungal Prxs is limited and fragmentary. Herein, we cloned and gained insight into Aspergillus nidulans Prx (An.PrxA) in the aspects of protein properties, catalysis characteristics, and especially $H_2O_2$ tolerability. Our results indicated that An.PrxA belongs to the newly defined family of typical 2-Cys Prxs with a marked characteristic that the "resolving" cysteine ($C_R$) is invertedly located preceding the "peroxidatic" cysteine ($C_P$) in amino acid sequences. The inverted arrangement of $C_R$ and $C_P$ can only be found among some yeast, bacterial, and filamentous fungal deduced Prxs. The most surprising characteristic of An.PrxA is its extraordinary ability to resist inactivation by extremely high concentrations of $H_2O_2$, even that approaching 600 mM. By screening the $H_2O_2$-inactivation effects on the components of Prx systems, including Trx, Trx reductase (TrxR), and Prx, we ultimately determined that it is the robust filamentous fungal TrxR rather than Trx and Prx that is responsible for the extreme $H_2O_2$ tolerence of the An.PrxA system. This is the first investigation on the effect of the electron donor partner in the $H_2O_2$ tolerability of the Prx system.

• Biomolecules & Therapeutics
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• v.24 no.3
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• pp.338-345
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• 2016

Neurodegenerative diseases are often associated with oxidative damage in neuronal cells. This study was conducted to investigate the neuro-protective effect of methanolic (MeOH) extract of Perilla frutescens var. japonica and its one of the major compounds, rosmarinic acid, under oxidative stress induced by hydrogen peroxide ($H_2O_2$) in C6 glial cells. Exposure of C6 glial cells to $H_2O_2$ enhanced oxidative damage as measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and thiobarbituric acid-reactive substance assays. The MeOH extract and rosmarinic acid prevented oxidative stress by increasing cell viability and inhibiting cellular lipid peroxidation. In addition, the MeOH extract and rosmarinic acid reduced $H_2O_2-indcued$ expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the transcriptional level. Moreover, iNOS and COX-2 protein expression was down-regulated in $H_2O_2-indcued$ C6 glial cells treated with the MeOH extract and rosmarinic acid. These findings suggest that P. frutescens var. japonica and rosmarinic acid could prevent the progression of neurodegenerative diseases through attenuation of neuronal oxidative stress.

• Plant Biotechnology Reports
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• v.5 no.3
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• pp.225-234
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• 2011

Arabidopsis mutants with T-DNA insertion in seven calmodulin genes (CAM) were used to determine the specific role of CAM in the tolerance of plants to oxidative stress induced by paraquat and hydrogen peroxide ($H_2O_2$) treatments. Arabidopsis calmodulin mutants (cam) were screened for seedling growth, seed germination, induced oxidative damage, and levels of ${\gamma}$-aminobutyric acid (GABA) shunt metabolites. Only the cam5-4 and cam6-1 mutants exhibited an increased sensitivity to paraquat and $H_2O_2$ during seed germination and seedling growth. In response to treatments with $3{\mu}M$ paraquat and 1 mM $H_2O_2$, only the cam5-4, cam6-1 mutants showed significant changes in malonaldehyde (MDA) levels in root and shoot tissues, with highly increased levels of MDA. In terms of the GABA shunt metabolites, GABA was significantly elevated in root and shoot tissues in response to the paraquat treatments in comparison to alanine and glutamate, while the levels of all shunt metabolites increased in root tissue but not in the shoot tissue following the $H_2O_2$ treatments. GABA, alanine and glutamate levels were significantly increased in root and shoot of the cam1, cam4, cam5-4, and cam6-1 mutants in response to paraquat (0.5, 1 and $3{\mu}M$), while they were increased only in the root tissue of the cam1, cam4, cam5-4, and cam6-1 mutants in response to $H_2O_2$ (200 and $500{\mu}M$, 1 mM). These data show that the cam5-4 and cam6-1 mutants were sensitive to the induced oxidative stress treatments in terms of seed germination, seedling growth, and oxidative damage. The accumulation of GABA shunt metabolites as a consequence of the induced oxidative stress treatments (paraquat and $H_2O_2$ treatments) suggests that the GABA shunt pathway and the accumulation of GABA metabolites may contribute in antioxidant machinery associated with reactive oxygen species and in the acquisition of tolerance in response to induced oxidative stress in Arabidopsis seedlings.

• Korean Journal of Food Science and Technology
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• v.44 no.1
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• pp.82-88
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• 2012

Chrysanthemum indicum L. (Asteraceae) is a traditional herbal medicine that has been used for the treatment of inflammation, hypertension, and respiratory diseases due to its strong antagonistic activity against inflammatory cytokines. The effects of Chrysanthemum indicum L. Extract (CIE) for increasing cell growth, alkaline phosphatase (ALP) activity, and collagen content were totally inhibited, suggesting that the effect of CIE might be partly involved with estrogen activity. Furthermore, the protective effects of CIE on the response of osteoblasts to oxidative stress were evaluated. Osteoblastic MC3T3-E1 cells were incubated with hydrogen peroxide and/or CIE, and markers of osteoblast function and oxidative damage were examined. CIE significantly increased cell survival, ALP activity, and calcium deposition, and decreased the production of Reactive Oxygen Species (ROS) and Tumor Necrosis Factor-${\alpha}$ (TNF-${\alpha}$) in osteoblasts. Taken together, these results indicate that the enhancement of osteoblast function by CIE may prevent osteoporosis and inflammatory bone diseases.

• Microbiology and Biotechnology Letters
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• v.49 no.2
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• pp.138-147
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• 2021

The overproduction of reactive nitrogen species (RNS) and reactive oxygen species (ROS) causes oxidative damage to neuronal cells, leading to the progression of neurodegenerative diseases. In this study, we determined the nitric oxide radical (NO), hydroxyl radical (·OH), and superoxide anion radical (O₂^-) scavenging activities of apigenin. Our results showed that apigenin exhibited remarkable, concentration-dependent ·OH, O₂^-, and NO radical scavenging activities. Particularly, apigenin indicated the strongest ·OH radical scavenging activity with 93.38% in the concentration of 100 µM. Furthermore, we also investigated the protective effects of apigenin against hydrogen peroxide (H₂O₂)-induced oxidative stress in SH-SY5Y cells. The H₂O₂ treatment resulted in a significant decrease in cell viability, as well as an increase in lactate dehydrogenase (LDH) release and ROS production compared with the H₂O₂-nontreated SH-SY5Y cells. However, the cell viability significantly increased in the apigenin-treated group, as well as inhibited ROS generation and LDH release compared with the H₂O₂-induced control group. To elucidate the protective mechanisms of apigenin against oxidative stress in SH-SY5Y, we analyzed the apoptosis-related protein expression. The apigenin treatment resulted in the downregulated expression of apoptosis-related protein markers, such as cytochrome C, cleaved caspase-3, poly (ADP)-ribose polymerase (PARP), and B-cell lymphoma 2-associated X (Bax), as well as the upregulated expression of anti-apoptosis markers such as B-cell lymphoma 2 (Bcl-2). In this study, we report that apigenin exhibits a neuroprotective effect against oxidative stress in SH-SY5Y cells. These results suggest that apigenin may be considered as a potential agent for neurodegenerative disease prevention.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.1
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• pp.51-55
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• 2004

Sopungsungi-won has been used as a traditional medicine for diabetes and it has been proved to be a potential remedy for type 2 diabetes mellitus. We previously reported that water extract of Sopungsungi-won exhibits anti-diabetic effects both in vivo and in vitro experiments. In the present study, we have chosen to examined anti-apoptotic effect of Rheum undulatum, which is the main component of Sopungsungi-won, on pancreatic ${\beta}-cells$, HIT-T15, against hydrogen peroxide $(H_2O_2)$. oxidative stress. To investigate the anti-apoptotic effect of Rheum undulatum water extract (RUWE) against $H_2O_2-induced$ apoptosis in pancreatic ${\beta}-cell$ line of hamster, HIT-T15, MTT assay, DAPI staining, TUNEL assay, RT-PCR and caspase-3 enzyme assay were performed. The morphological analysis demonstrated that cells treated with $H_2O_2$ exhibited classical apoptotic features, while such changes was reduced in cells pre-treated with RUWE. In addition, RUWE pre-treated cells prior to $H_2O_2$ treatment induced increase of levels of bcl-2 expression and decrease of caspase-3 enzyme activity compared to cells treated with $H_2O_2$ only. These results provide the possibility of usage of RU in patients with progressively deteriorated diabetes.

• Proceedings of the Korea Technical Association of the Pulp and Paper Industry Conference
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• 2000.11a
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• pp.15-21
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• 2000

In chlorine dioxide delignification and bleaching the formation of chlorate is undesirable because it does not react with lignin and is harmful to the environment. Chlorate is mainly formed from the in-situ generated hypochlorus acid which is also the main reason for AOX formation. In previous literature scavengers of hypochlorous acid such as sulfamic aicd, DMSO, and hydrogen peroxide have been added to bleaching stages to reduce AOX formation but less attention has been paid to chlorate reduction. This paper thus focuses on the reduction of chlorate content caused by the following additives, sulfamic acid, DMSO, hydrogen peroxide, and oxalic acid. The results show that only sulfamic acid and DMSO reduce chlorate formation under our chlorine dioxide prebleaching conditions. Results by UV spectroscopy and pH adjustment show that scavengers react with hypochlorous acid much faster than with chlorine. Hydrogen peroxide and oxalic acid react with HClO/$Cl_2$much slower than DMSO and sulfamic acid do. The reason for the ineffectiveness of hydrogen peroxide and oxalic acid is ascribed to their slow reaction rates with HClO compared to that of chlorate formation. The fact that only 30-35% of the chlorate can be reduced by sulfamic acid and DMSO when charged in same mole ratio to chlorine dioxide, suggested that the reaction rate of DMSO and sulfamic acid with hypochlorous aicd are of the same magnitude as that of chlorate formation.