• Journal of Veterinary Clinics
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• v.27 no.2
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• pp.130-135
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• 2010

Malassezia (M.) is a member of normal mycobiota in warm-blooded vertebrates. Increased humidity is likely to be crucial in this infection. We studied the proportion of the species infected in dog during summer of Korea. Fifty samples were analyzed by PCR-RFLP and direct sequencing from June 2006 to October 2006. The study showed that lipid-dependent species was main pathogen (M. furfur; 86%, M. obtusa; 10%) while M. pachydermatis (4%) has only small portion. This result suggests that Malassezia infection has endemic characters that can be affected by the climate (temperature and humidity) in dogs.

• Journal of Microbiology and Biotechnology
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• v.33 no.8
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• pp.992-997
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• 2023

Ferroptosis is a new kind of programmed cell death of which occurrence in microorganisms is not clearly verified. The elevated level of reactive oxygen species (ROS) influences cellular metabolisms through highly reactive hydroxyl radical formation under the iron-dependent Fenton reaction. Iron contributes to ROS production and acts as a cofactor for lipoxygenase to catalyze poly unsaturated fatty acid (PUFA) oxidation, exerting oxidative damage in cells. While ferroptosis is known to take place only in mammalian cells, recent studies discovered the possible ferroptosis-like death in few specific microorganisms. Capacity of integrating PUFA into intracellular membrane phospholipid has been considered as a key factor in bacterial or fungal ferroptosis-like death. Vibrio species in bacteria and Saccharomyces cerevisiae in fungi exhibited certain characteristics. Therefore, this review focus on introducing the occurrence of ferroptosis-like death in microorganisms and investigating the mode of action underlying the cells based on contribution of lipid peroxidation and iron-dependent reaction.

• The Journal of Korean Medicine
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• v.28 no.1 s.69
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• pp.148-158
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• 2007

Objective : The objective of this study was to investigate the antioxidant effects of Mori Folium extract. Methods Total antioxidant status was examined by total antioxidant capacity(TAC) and total antioxidant response(TAR) against potent free radical reactions. The effect of Mori Folium extract was examined by measuring total phenolic content, concentration at which 1,1-dipheny1-2-picrylhydrazyl(DPPH) radical scavenging activity was inhibited, inhibitory effect on lipid peroxidation, and the effect on reactive oxygen species(ROS) generation. Results : 1. TAC and TAR of Mori Folium extract at the concentration of 5 mg/ml were 1.61 and 1.24 mM Trolox equivalents, respectively. 2. Total phenolic content of Mori Folium extract at the concentration of 5 mg/Ml was 1.70 mM gallic acid equivalent. 3. Concentration of Mori Folium extract at which DPPH radical scavenging activity was inhibited by 50% was 2.29 m9/m4 as compared to 100% by Pyrogallol solution as a reference. 4. The inhibitory effect of the extract on lipid peroxidation was examined using rat liver mitochondria induced by FeSO$_4$/ascorbic acid. Mori Folium extract at the concentration of 10 mg/ml significantly decreased thiobarbituric acid reactive substances(TBARS) concentration. The extract prevented lipid peroxidation in a dose-dependent 5. The effect of Mori Folium extract on reactive oxygen species(ROS) generation was examined using a celt-free system induced by hydrogen peroxide FeSO$_4$. Addition of 1 mg/ml of Mori Folium extract significantly reduced dichlorofluorescein(DCf) fluorescence. The extract caused concentration-dependent attenuation of the increase in DCF fluorescence, indicating that the extract significantly prevented ROS generation in vitro. Conclusion ; The antioxidant effects of Mori Folium extract seem to be due, at least in part, to the prevention offree radical-induced oxidation, fllowed by inhibition of lipid peroxidation.

• Journal of Yeungnam Medical Science
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• v.34 no.2
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• pp.174-181
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• 2017

Ferroptosis is a newly recognized type of cell death that results from iron-dependent lipid peroxidation and is different from other types of cell death, such as apoptosis, necrosis, and autophagic cell death. This type of cell death is characterized by mitochondrial shrinkage with an increased mitochondrial membrane density and outer mitochondrial membrane rupture. Ferroptosis can be induced by a loss of activity of system $X_c{^-}$ and the inhibition of glutathione peroxidase 4, followed by the accumulation of lipid reactive oxygen species (ROS). In addition, inactivation of the mevalonate and transsulfuration pathways is involved in the induction of ferroptosis. Moreover, nicotinamide adenine dinucleotide phosphate oxidase and p53 promote ferroptosis by increasing ROS production, while heat shock protein beta-1 and nuclear factor erythroid 2-related factor 2 inhibit ferroptosis by reducing iron uptake. This article outlines the molecular mechanisms and signaling pathways of ferroptosis regulation, and explains the roles of ferroptosis in human disease.

• BMB Reports
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• v.46 no.11
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• pp.555-560
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• 2013

Acrolein is the most reactive aldehydic product of lipid peroxidation and is found to be elevated in the brain when oxidative stress is high. The effects of acrolein on the structure and function of human Cu,Zn-superoxide dismutase (SOD) were examined. When Cu,Zn-SOD was incubated with acrolein, the covalent crosslinking of the protein was increased, and the loss of enzymatic activity was increased in a dose-dependent manner. Reactive oxygen species (ROS) scavengers and copper chelators inhibited the acrolein-mediated Cu,Zn-SOD modification and the formation of carbonyl compound. The present study shows that ROS may play a critical role in acrolein-induced Cu,Zn-SOD modification and inactivation. When Cu,Zn-SOD that has been exposed to acrolein was subsequently analyzed by amino acid analysis, serine, histidine, arginine, threonine and lysine residues were particularly sensitive. It is suggested that the modification and inactivation of Cu,Zn-SOD by acrolein could be produced by more oxidative cell environments.

• Biomedical Science Letters
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• v.8 no.4
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• pp.251-256
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• 2002

This study was undertaken to determine the underlying mechanisms of reactive oxygen species-induced cell injury in renal epithelial cells and whether there is a difference in the role of lipid peroxidation between freshly isolated renal cells and cultured renal cells. Rabbit renal cortical slices were used as a model of freshly isolated cells and opossum kidney (OK) cells as a model of cultured cells. Cell injury was estimated by measuring lactate dehydrogenase (LDH) release in renal cortical slices and frypan blue exclusion in OK cells. $H_2O$$_2$ was used as a drug model of reactive oxygen species. $H_2O$$_2$ induced cell injury in a dose-dependent manner in both cell types. However, renal cortical slices were resistant to $H_2O$$_2$ approximately 50-fold than OK cells. $H_2O$$_2$-induced cell injury was prevented by thiols (glutathione and dithiothreitol) and iron chelators (deferoxamine and phenanthroline) in both cell types. $H_2O$$_2$-induced cell injury in renal cortical slices was completely prevented by antioxidants N,N-diphenyl-p -phenylenediamine and Trolox, but the cell injury was not affected by these antioxidants in OK cells. $H_2O$$_2$ increased lipid peroxidation in both cell types, which was completely inhibited by the antioxidants. These results suggest that $H_2O$$_2$ induces cell injury through a lipid peroxidation-dependent mechanism in freshly isolated renal cells, but via a mechanism independent of lipid peronidation in cultured cells.

• The Journal of Korean Medicine
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• v.28 no.1 s.69
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• pp.137-147
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• 2007

Objective : The objective of this study was to investigate the antioxidative effects of Carthami Flos extract. Methods : Total antioxidant status was examined by total antioxidant capacity(TAC) and total antioxidant response(TAR) against potent free radical reactions. The effect of Carthami Flos extract was examined far details of total phenolic content concentration at which 1,1-dipheny1-2-picrylhydrazyl(DPPH) radical scavenging activity was inhibited, the inhibitory effect on lipid peroxidation, and the effect on reactive oxygen species(ROS) generation. Results : TAC of Carthami Flos extract at the concentration of 5 mg/ml was 1.84 mM Trolox equivalent. 2. TAR of Carthami Flos extract, on the other hand, couldn't be determined due to interference from unidentified compounds. 3. Total phenolic content of Carthami Flos extract at the concentration of 5 mg/ml was 2.01 mM gallic acid equivalent. 4. Concentration of Carthami Flos extract at which DPPH radical scavenging activity was inhibited by 50% was 6.43 mg/ml as compared to 100% by Pyrogallol solution as a reference. 5. The inhibitory effect of the extract on lipid peroxidation was examined using rat liver mitochondria induced by FeS04/ascorbic acid. Carthami Flos extract at the concentration of 10 ms/ml slightly but significantly decreased TBARS concentration. The extract continued to prevent lipid peroxidation in a dose-dependent manner. 6. The effect of Carthami Flos extract on reactive oxygen species(ROS) generation was examined using a cell-free system induced by hydrogen peroxide/FeS04. Addition of 1 mg/ml of Carthami Flos extract significantly reduced dichlorofluorescein(DCF) fluorescence. Carthami Flos extract caused concentration-dependent attenuation of the increase in DCF fluorescence, indicating that the ektract significantly prevented ROS generation in vitro. Conclusion: : Antioxidant efffcts of Carffami ffor extract seem to be due, at least in part, to the prevention offree radical-induced oxidation, fellowed by inhibition of lipid peroxidation.

• Environmental Analysis Health and Toxicology
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• v.15 no.4
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• pp.147-155
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• 2000

In order to evaluate anti -oxidant activities and protective effect against oxidatve damage, DPPH radical scavenging activity and lipid peroxidation inhibitory activity were measured among methanol extracts prepared from natural medicinal plants. Fourteen natural medicinal plants which were reported to have anti -oxidative or anti-inflammatory effects were selected based on our previous report. In addition to the total methanol extracts, n-hexane, dichloromethane, ethylacetate, n-butanol and water fractions were prepared from each total extract. DPPH radical scavenging assay was performed against 14 total extracts and all samples showed dose-dependent activities in various extent. Among those, 6 samples, methanol extracts of Euryale ferox, paeonia suffruticosa, Areca catechu var. dulcissima, Cinnamomun cassia, Alpinia katsumadai and Betula platyphlla var. japonica showed IC$\sub$50/ value lower than 6.0 $\mu\textrm{g}$/ml. The highest DPPH radical scavenging activity was found in ethylacetate fraction of paeonia suffruticosa with IC$\sub$50/ value of 1.1 $\mu\textrm{g}$/ml. Analysis of lipid peroxidation inhibitory activity on hydrogen peroxide-induced oxidative damage in Chinese hamster lung fibroblast (V79-4) cells revealed that the highest inhibitory effect was observed in methanol extract of Betula platyhpylla var. japonica. Lipid peroxidation inhibitory activity was observed as a dose-dependent manner in all samples used in this study. Among fraction samples, ethylacetate fraction of Alpinia katsumadai had the strongest inhibitory activity with IC$\sub$50/ value of 0.9 $\mu\textrm{g}$/ml.

• Journal of Pharmacopuncture
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• v.10 no.3
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• pp.53-62
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• 2007

Objective The objective of this study was to investigate the antioxidative effects of Puerariae Radix extract. Method Total antioxidant capacity (TAC), Total antioxidant response (TAR), Total phenolic content, Reactive oxygen species (ROS), 1,1-Diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging activities, lipid peroxidation were examined. Result Total antioxidant status was examined by total antioxidant capacity(TAC) and total antioxidant response(TAR) against potent free radical reactions. TAC and TAR of Puerariae Radix extract at the concentration of 5 mg/ml were 2.02 and 1.50 mM Trolox equivalents, respectively. Total phenolic content of Puerariae Radix extract at the concentration of 5 mg/ml was 2.29 mM gallic acid equivalent. Concentration of Puerariae Radix extract at which DPPH radical scavenging activity was inhibited by 50% was 5.91 mg/ml as compared to 100% by pyrogallol solution as a reference. The inhibitory effect of the extract on lipid peroxidation was examined using rat liver mitochondria induced by FeSO4/ascorbic acid. Puerariae Radix extract at the concentration of 1 mg/ml slightly but significantly decreased TBARS concentration. The extract further prevented lipid peroxidation in a dose-dependent manner. The effect of Puerariae Radix extract on reactive oxygen species (ROS) generation was examined using cell-free system induced by hydrogen peroxide/FeSO4. Addition of 1 mg/ml of Puerariae Radix extract significantly reduced dichloroflurescein (DCF) fluorescence. The extract caused concentration-dependent attenuation of the increase in DCF fluorescence, indicating that the extract significantly prevented ROS generation in vitro. Thus antioxidant effects of Puerariae Radix extract seem to be due to, at least in part, the prevention from free radicals-induced oxidation, followed by inhibition of lipid peroxidation. Conclusion As a result, Puerariae Radix seems to have antioxitative effect and antioxidant compount.

• Korean Journal of Plant Resources
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• v.19 no.6
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• pp.649-654
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• 2006

The objective of present study was to investigate the anti oxidative and hepatoprotective effects of tomato extracts. Total antioxidant capacity and total antioxidant response were 5.5 and $19.8{\mu}g$ Trolox equivalent per mg of tomato extract, respectively. DPPH radical scavenging activity of tomato extracts ($10mg\;ml^{-1}$) was 70% as compared to 100% by pyrogallol solution as a reference. The effect of the tomato extracts on lipid peroxidation was examined using rat liver mitochondria induced by iron/ascorbate. Tomato extracts at the concentration of $0.5mg\;ml^{-1}$ significantly decreased TBARS concentration. Tomato extracts prevented lipid peroxidation in a dose-dependent manner. The effect of the tomato extracts on reactive oxygen species (ROS) generation was examined using cell-free system induced by $H_2O_2/FeSO_4$. Addition of $1mg\;ml^{-1}$ of tomato extracts significantly reduced dichlorofluorescein (DCF) fluorescence. Tomato extracts caused concentration-dependent attenuation of the increase in DCF fluorescence, indicating that tomato extracts significantly prevented ROS generation in vitro. The effect of tomato extracts on cell viability and proliferation was examined using hepatocyte culture. Primary cultures of rat hepatocytes were incubated with 1mM tert-butyl hydroperoxide (t-BHP) for 90 min in the presence or absence of tomato extracts. MTT values by addition of tomato extracts at the concentration of 2, 10, and $20mg\;ml^{-1}$ in the presence of t-BHP were 13, 33 and 48%, respectively, compared to 100% as control. Tomato extracts increased cell viability in a dose-dependent manner. These results demonstrate that tomato extracts suppressed lipid peroxidation and t-BHP-induced hepatotoxicity and scavenged ROS generation. Thus antioxidant and hepatoprotective effects of tomato extracts seem to be due to, at least in part, the prevention from free radicals-induced oxidation, followed by inhibition of lipid peroxidation.