• Safety and Health at Work
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• v.4 no.4
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• pp.177-186
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• 2013

The use of nanoparticles (NPs) in industry is increasing, bringing with it a number of adverse health effects on workers. Like other chemical carcinogens, NPs can cause cancer via oxidative DNA damage. Of all the molecules vulnerable to oxidative modification by NPs, DNA has received the greatest attention, and biomarkers of exposure and effect are nearing validation. This review concentrates on studies published between 2000 and 2012 that attempted to detect oxidative DNA damage in humans, laboratory animals, and cell lines. It is important to review these studies to improve the current understanding of the oxidative DNA damage caused by NP exposure in the workplace. In addition to examining studies on oxidative damage, this review briefly describes NPs, giving some examples of their adverse effects, and reviews occupational exposure assessments and approaches to minimizing exposure (e.g., personal protective equipment and engineering controls such as fume hoods). Current recommendations to minimize exposure are largely based on common sense, analogy to ultrafine material toxicity, and general health and safety recommendations.

• Korean journal of food and cookery science
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• v.28 no.3
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• pp.311-318
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• 2012

The correlation between osteoporosis and reactive oxygen species (ROS)-induced oxidative stress was investigated. Thus, interest in food and plants with antioxidant effects that can reduce damage caused by ROS during bone metabolism is heightening. In this study, the antioxidant effect of Taraxacum mongolicum on proliferation and differentiation of MC3T3-E1 cells under H2O2-induced oxidative stress was studied to investigate its protective effect against oxidative stress and its availability as an antioxidant material related to bone diseases. As a result, total polyphenol and total flavonoid contents of T. mongolicum were 33.65 mg/g and 4.45 mg/g, respectively. The T. mongolicum extract increased proliferation of both MC3T3-E1 cells and differentiated osteoblasts under $H_2O_2$-induced oxidative stress conditions. In addition, two differentiation markers, alkaline phosphatase activity and mineralization level in the T. mongolicum extract, tended to increase. These results indicate that T. mongolicum extract suppressed the damage to osteoblasts under oxidative stress and that it is potential antioxidant materials for preventing bone diseases.

• Korean Journal of Agricultural Science
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• v.38 no.4
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• pp.717-722
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• 2011

In this study, we investigated the antioxidant activity of hesperidin and hesperetin, which are the active compounds from Citrus junos, in the cellular system. Under cellular model of oxidative damage using LLC-$PK_1$ renal epithelial cell, the oxidative damage induced by 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH) led to the loss of cell viability, while treatment of hesperidin and hesperetin increased significantly the cell viability as dose-dependent manner. In addition, NO-induced cellular oxidative damage by sodium nitroprusside were significantly recovered by the treatment of hesperidin and hesperetin, showing the increase of cell viability. But hesperidin and hesperetin showed no significant protective effect on $O_2{^-}$-induced cellular oxidative damage. The present study indicates that hesperidin and hesperetin protect against free radical, especially AAPH-induced peroxyl radical. In particular, hesperetin has stronger protective effect against oxidative stress than hesperidin.

• Biomedical Science Letters
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• v.17 no.1
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• pp.69-77
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• 2011

In this study, we evaluated the protective effects of supercritical extracts and two step ethanol extracts after supercritical extraction from Schizandra chinensis on antioxidant activities and oxidative DNA and cell damages. Supercritical extracts removed DPPH (1,1-diphenyl-2-picryldrazyl) radical by 85.5% at 200 ${\mu}g$/ml, but showed low activities of scavenging and chelating the hydroxyl radical and ferrous iron. However, two step ethanol extracts showed low activities of scavenging the DPPH radical, but removed the hydroxyl radical by 86% at 200 ${\mu}g$/ml. In addition, we tested the activities of extracts for reducing hydroxyl radical-induced DNA and cell damage. Two step ethanol extracts showed protective effect against the oxidative DNA damage by reducing DNA segmentation, inhibiting DNA migration and decreasing the expression of phospho-H2AX. Also, two step ethanol extracts showed protective effect against the oxidative cell damage by inhibiting lipid peroxidation and increasing the expression of p21 protein. Taken together, we suggest that two step ethanol extracts from S. chinensis have a role as useful inhibitors against oxidative damages.

• Korean Journal of Plant Resources
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• v.22 no.6
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• pp.498-505
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• 2009

The plant Agastache rugosa Kuntze has various physiological and pharmacological activities. Especially, it has been regarded as a valuable source for the treatment of anti-inflammatory and oxidative stress-induced disorders. However, little has been known about the functional role of it on oxidative damage in mammalian cells by ROS. In this study, we investigated the DPPH radical, hydroxyl radical, hydrogen peroxide and intracellular ROS scavenging capacity, and $Fe^{2+}$ chelating activity of the extracts from Agastache rugosa. In addition, we evaluated whether the extract can be capable of reducing $H_2O_2$-induced DNA and cell damage in NIH 3T3 cells. These extracts showed a dose-dependent free radical scavenging capacity and a protective effect on DNA damage and the lipid peroxidation causing the cell damage by $H_2O_2$. Therefore, these results suggest that Agastache rugosa is useful as a herbal medicine for the chemoprevention against oxidative carcinogenesis.

• YAKHAK HOEJI
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• v.47 no.6
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• pp.369-375
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• 2003

Xiaoshuan Zaizao Wan (XZW) has been used in China to improve hemiplegia, deviation of eye and mouth, and dysphasia due to cerebral thrombosis. To characterize pharmacological actions of XZW, we evaluated its effects on neuronal cell damage induced in primary cultured rat cortical cells by various oxidative insults, glutamate or N-methyl-D-aspartate (NMDA), and $\beta$-amyloid fragment ($A_{\beta(25-35)}$). XZW was found to inhibit the oxidative neuronal damage induced by $H_2O_2$, xanthine/xanthine oxidase, or $Fe^{2+}$/ascorbic acid. It also attenuated the excitotoxic damage induced by glutamate or NMDA. The NMDA-induced neurotoxicity was more effectively inhibited than the glutamate-induced toxicity. In addition, we found that XZW protected neurons against the $A_{\beta(25-35)}$-induced toxicity. Moreover; XZW exhibited dramatic inhibition of lipid peroxidation in rat brain homogenates and mild 1,1-diphenyl-2-picrylhydrazyl radical scavenging activity. Taken together; these results demonstrate that XZW exerts neuroprotective effects against oxidative, excitotoxic, or $A_{\beta(25-35)}$-induced neuronal damage. These findings may provide pharmacological basis for its clinical usage treating the sequelae caused by cerebral thrombosis. Furthermore, XZW may exert beneficial effects on Alzheimer's disease and other oxidative stress-related neurodegenerative disorders.

• Nutrition Research and Practice
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• v.9 no.2
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• pp.123-128
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• 2015

BACKGROUND/OBJECTIVES: Natural products or active components with a protective effect against oxidative stress have attracted significant attention for prevention and treatment of degenerative disease. Oligonol is a low molecular weight polyphenol containing catechin-type monomers and oligomers derived from Litchi chinensis Sonn. We investigated the protective effect and its related mechanism of oligonol against oxidative stress. MATERIALS/METHODS: Oxidative stress in C6 glial cells was induced by hydrogen peroxide ($H_2O_2$) and the protective effects of oligonol on cell viability, nitric oxide (NO) and reactive oxygen species (ROS) synthesis, and mRNA expression related to oxidative stress were determined. RESULTS: Treatment with oligonol inhibited NO and ROS formation under cellular oxidative stress in C6 glial cells. In addition, it recovered cell viability in a dose dependent-manner. Treatment with oligonol also resulted in down-regulated mRNA expression related to oxidative stress, nuclear factor kappa-B (NF-${\kappa}B$) p65, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS), compared with the control group treated with $H_2O_2$. In particular, expression of NF-${\kappa}B$ p65, COX-2, and iNOS was effectively reduced to the normal level by treatment with $10{\mu}g/mL$ and $25{\mu}g/mL$ of oligonol. CONCLUSIONS: These results indicate that oligonol has protective activity against oxidative stress-induced inflammation. Oligonol might be a promising agent for treatment of degenerative diseases through inhibition of ROS formation and NF-${\kappa}B$ pathway gene expression.

• Preventive Nutrition and Food Science
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• v.18 no.1
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• pp.11-17
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• 2013

Dysfunction of endothelial cells is considered a major cause of vascular complications in diabetes. In the present study, we investigated the protective effect of Padina arborescens extract against high glucose-induced oxidative damage in human umbilical vein endothelial cells (HUVECs). High-concentration of glucose (30 mM) treatment induced cytotoxicity whereas Padina arborescens extract protected the cells from high glucose-induced damage and significantly restored cell viability. In addition, lipid peroxidation, intracellular reactive oxygen species (ROS), and nitric oxide (NO) levels induced by high glucose treatment were effectively inhibited by treatment of Padina arborescens extract in a dose-dependent manner. High glucose treatment also induced the overexpressions of inducible nitric oxide synthase (iNOS), cyclooxygenase- 2 (COX-2) and NF-${\kappa}B$ proteins in HUVECs, but Padina arborescens extract treatment reduced the over-expressions of these proteins. These findings indicate the potential benefits of Padina arborescens extract as a valuable source in reducing the oxidative damage induced by high glucose.

• Biomedical Science Letters
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• v.20 no.2
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• pp.56-61
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• 2014

This study attempted to confirm the antioxidative potential of luteolin against tert-butyl hydroperoxide (t-BHP) induced oxidative damage and to investigate its molecular mechanism related to glutathione (GSH)-dependent enzymes in HepG2 cells. Treatment with luteolin resulted in attenuation of t-BHP induced generation of reactive oxygen species (ROS) and oxidative stress-mediated cell death. In addition, accelerated expression of GSH-dependent antioxidative enzymes, glutathione peroxidase (GPx) and glutathione reductase (GR), and heme oxygenase (HO)-1, as well as strengthened GSH content was induced by treatment with luteolin, which was in accordance with increased nuclear translocation of nuclear factor-erythroid 2 p45-related factor 2 (Nrf2), a transcription factor for phase 2 enzymes, in a dose-dependent manner. These results suggest that the cytoprotective potential of luteolin against oxidative damage can be attributed to fortified GSH-mediated antioxidative pathway and HO-1 expression through regulation of Nrf2 in HepG2 cells.

• International Journal of Oral Biology
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• v.36 no.3
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• pp.149-154
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• 2011

In the present study, total methanol extracts prepared from Alpinia katsumadai showed significant protective effects against the oxidative stress induced by hydrogen peroxide, UV-C or ${\gamma}$-ray irradiation. These protective effects were substantially increased by treatment with 20~100 ${\mu}g$/ml of the extract. The A. katsumadai total methanol preparation was further fractionated into n-hexane, dichloromethane, ethylacetate, n-butanol and water fractions. Among these five fractions, the ethylacetate and butanol fractions of A. katsumadai showed the strongest protective effects against oxidative stress induced by UV-C and ${\gamma}$-ray irradiation. These fractions also showed high DPPH radical scavenging and lipid peroxidation inhibitory activities. In addition, both fractions displayed cell proliferation activation effects, as evidenced by significant increases in colony formation. Our current data thus suggest that the mechanisms underlying the protective effects of A. katsumadai against oxidative damage may include radical scavenging, protection against cell membrane damage and stimulation of cell proliferation.