• Environmental Analysis Health and Toxicology
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• v.21 no.2 s.53
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• pp.165-172
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• 2006

The backs with a hair cut of 6-week-old healthy ICR male mice were once exposed to a dose of $400mJ/cm^2$ UVB. An acute dermal inflammation was observed, and the inflamed skins were almost completely cured after 6 days of the exposure. At 24 hours after exposure, the epidermal keratinocytes showed a cell-membrane damage with the destruction of intercellular junctions, agglutination of tonofilaments within the cytoplasm and nucleus damage. The activity of XO showed a significant increase (p<0.05) in up to 144 hours. The activities of CAT and SOD showed a significant decrease (p<0.05) in up to 96 hours, but they were not significantly different from the normal value at 144 hours. The GST activity was significantly decreased (p<0.01) in up to 96 hours, not so at 24 hours. However, that was not significantly different from the normal value at 144 hours. There was a significant decrease (p<0.01) in the contents of TBARS at 48 and 96 hours, without any significant difference at 144 hours. While the content of GSH was significantly lower (p<0.05) at 24 hours, that was not significantly different thereafter up to 144 hours from the normal value. Therefore, it is assumed that skin damage with a dose of $400mJ/cm^2$ UVB irradiation might be caused by the oxidative stress which was resulted from the unbalance of oxygen fret radical generating and scavenging enzymes.

• Environmental Analysis Health and Toxicology
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• v.24 no.4
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• pp.303-309
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• 2009

Hepatic antioxidant defense systems were examined in rats treated with tetrabromobisphenol-A (TBBPA), a brominated flame retardant, at the doses of 0, 250, 500 and 1,000 mg/kg for four weeks. Hepatic ratio of glutathione disulfide to glutathione (GSH) and levels of malondialdehyde, oxidative stress markers were not changed in rats treated with TBBPA. Hepatic expression of antioxidant enzymes including GSH peroxdiase-1 (GPX-1)/GSH reductase (GR), alpha-, mu- and pi-class glutathione-S-transferase (GST) and gamma-glutamylcysteine ligase catalytic subunit was determined using immunoblot analysis. Alpha-class GSTs, GPX-1 and GR levels were significantly decreased in rats treated with TBBPA at the dose of 500 or 1,000 mg/kg. These results show that TBBPA results in down-regulation of hepatic expression of antioxidant enzymes related with GSH, suggesting the liver in TBBPA-treated rats may be more sensitive to oxidants.

• Korean Journal of Agricultural Science
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• v.41 no.2
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• pp.75-83
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• 2014

Recently, a quick drop of air temperature in plastic film houses by adverse weather conditions leads to the occurrence of low temperature damages to growing crops. Chilling injury, defined as a variety of growth restriction occurring below the optimal temperature, is one of environmental factors strongly affecting crop growth and yield. Low temperature causes the restricted evapotranspiration, reduced mineral uptake (P > K > $NO_3{^-}$), and an increase in electrolyte leakage such as K. Despite being different with plant species, an accumulation of soluble carbohydrates such as glucose, fructose, sucrose and starch under chilling condition is well known. A variety of environmental stresses are known to cause oxidative damage to plants either directly or indirectly by triggering an increased level of production of reactive oxygen species (ROS), and, to combat the oxidative damage, plants have the antioxidant defense systems comprising of enzymes, SOD, POD, CAT, GPX and APX, and non-enzymes, ascorbate, gluthathione, ${\alpha}$-tocopherol, phenolic compounds, carotenoid and flavonoids. The aim of this review is to provide basic information to build chilling-indicators and optimal nutrition management under adverse temperature conditions as broadly considering mineral uptake, carbohydrate metabolism and antioxidative defense system.

• Journal of Environmental Science International
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• v.21 no.12
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• pp.1435-1447
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• 2012

The present study was conducted to determine the effect of hexaconazole (HEX), a triazole fungicide, on the growth, yield, photosynthetic response and antioxidant potential in cucumber (Cucumis sativus L.) plants subjected to UV-B stress. UV-B radiation and HEX were applied separately or in combination to cucumber seedlings. The growth parameters were significantly reduced under UV-B treatment, however, this growth inhibition was less in HEX treated plants. HEX caused noticeable changes in plant morphology such as reduced shoot length and leaf area, and increased leaf thickness. HEX was quite persistent in inhibiting shoot growth by causing a reduction in shoot fresh and dry weight. HEX noticeably recovered the UV-B induced inhibition of biomass production. Significant accumutation in anthocyanin and flavonoid pigments in the leaves occurred as a result of HEX or UV-B treatments. HEX permitted the survival of more green leaf tissue preventing chlorophyll content reduction and higher quantum yield for photosystemII under UV-B exposure. HEX treatment induced a transient rise in ABA levels in the leaves, and combined application of HEX and UV-B showed a significant enhancement of ABA content which activates $H_2O_2$ generation. UV-B exposure induced accumulation of $H_2O_2$ in the leaves, while HEX prevented UV-B induced increase in $H_2O_2$, indicating that HEX serves as an antioxidant agent able to scavenge $H_2O$ to protect cells from oxidative damage. An increase in the ascorbic acid was observed in the HEX treated cucumber leaves affecting many enzyme activities by removing $H_2O_2$ during photosynthetic processes. The activities of antioxidant enzymes including catalase(CAT), ascorbate peroxidase(APX), superoxide dismutase(SOD) and peroxidase(POD) in the leaves in the presence of HEX under UV-B stress were higher than those under UV-B stress alone. These findings suggest that HEX may participate in the enhanced tolerance to oxidative stress. From these results it can be concluded that HEX moderately ameliolate the effect of UV-B stress in cucumber by improving the components of antioxidant defense system.

• Preventive Nutrition and Food Science
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• v.13 no.4
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• pp.259-265
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• 2008

This study was designed to investigate the protective effect of fucoidan against AAPH-induced oxidative stress in LLC-PK1 cells (porcine kidney epithelial cells). Oxidative stress was induced by exposing of LLC-PK1 cells to the 1 mM 2,2'-azobis(2-amidino propane) dihydrochloride (AAPH) for 24 hr. Exposure of LLC-PK1 cells to 1 mM AAPH for 24 hr resulted in a significant (p<0.05) decrease in cell viability, but fucoidan treatment protected LLC-PK1 cells from AAPH-induced cell damage in a dose dependant manner. To investigate the protective action of fucoidan against AAPH-induced damage of LLC-PK1 cells, we measured the effects of fucoidan on lipid peroxidation and antioxidant enzymes activities of AAPH treated cells as well as scavenging activities on superoxide anion radical and hydroxyl radical. Fucoidan had protective effect against the AAPH-induced LLC-PK1 cellular damage and decreased lipid peroxidation and increased activities of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-px). Furthermore, fucoidan showed strong scavenging activity against superoxide anion radical. The $IC_{50}$ value of fucoidan was $48.37{\pm}1.54\;{\mu}g/mL$ for superoxide anion radical scavenging activity. The fucoidan also had high hydroxyl radical scavenging activity ($IC_{50}=32.03\;{\mu}g/mL$). These results indicate that fucoidan protects against AAPH-induced LLC-PK1 cell damage by inhibiting lipid peroxidation, increasing antioxidant enzyme activities and scavenging offree radicals.

• Toxicological Research
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• v.31 no.1
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• pp.17-23
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• 2015

Excessive manganese (Mn) in the brain promotes a variety of abnormal behaviors, including memory deficits, decreased motor skills and psychotic behavior resembling Parkinson's disease. Hereditary hemochromatosis (HH) is a prevalent genetic iron overload disorder worldwide. Dysfunction in HFE gene is the major cause of HH. Our previous study has demonstrated that olfactory Mn uptake is altered by HFE deficiency, suggesting that loss of HFE function could alter manganese-associated neurotoxicity. To test this hypothesis, Hfe-knockout ($Hfe^{-/-}$) and wild-type ($Hfe^{+/+}$) mice were intranasally-instilled with manganese chloride ($MnCl_2$ 5 mg/kg) or water daily for 3 weeks and examined for memory function. Olfactory Mn diminished both short-term recognition and spatial memory in $Hfe^{+/+}$ mice, as examined by novel object recognition task and Barnes maze test, respectively. Interestingly, $Hfe^{-/-}$ mice did not show impaired recognition memory caused by Mn exposure, suggesting a potential protective effect of Hfe deficiency against Mn-induced memory deficits. Since many of the neurotoxic effects of manganese are thought to result from increased oxidative stress, we quantified activities of anti-oxidant enzymes in the prefrontal cortex (PFC). Mn instillation decreased superoxide dismutase 1 (SOD1) activity in $Hfe^{+/+}$ mice, but not in $Hfe^{-/-}$ mice. In addition, Hfe deficiency up-regulated SOD1 and glutathione peroxidase activities. These results suggest a beneficial role of Hfe deficiency in attenuating Mn-induced oxidative stress in the PFC. Furthermore, Mn exposure reduced nicotinic acetylcholine receptor levels in the PFC, indicating that blunted acetylcholine signaling could contribute to impaired memory associated with intranasal manganese. Together, our model suggests that disrupted cholinergic system in the brain is involved in airborne Mn-induced memory deficits and loss of HFE function could in part prevent memory loss via a potential up-regulation of anti-oxidant enzymes in the PFC.

• Biomolecules & Therapeutics
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• v.26 no.2
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• pp.130-138
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• 2018

Quercetin and resveratrol are known to have beneficial effects on the diabetes and diabetic complication, however, the effects of combined treatment of these compounds on diabetes are not fully revealed. Therefore, the present study was designed to investigate the combined antidiabetic action of quercetin (QE) and resveratrol (RS) in streptozotocin (STZ)-induced diabetic rats. To test the effects of co-treated with these compounds on diabetes, serum glucose, insulin, lipid profiles, oxidative stress biomarkers, and ions were determined. Additionally, the activities of hepatic glucose metabolic enzymes and histological analyses of pancreatic tissues were evaluated. 50 male Sprague-Dawley rats were divided into five groups; normal control, 50 mg/kg STZ-induced diabetic, and three (30 mg/kg QE, 10 mg/kg RS, and combined) compound-treated diabetic groups. The elevated serum blood glucose levels, insulin levels, and dyslipidemia in diabetic rats were significantly improved by QE, RS, and combined treatments. Oxidative stress and tissue injury biomarkers were dramatically inhibited by these compounds. They also shown to improve the hematological parameters which were shown to the hyperlactatemia and ketoacidosis as main causes of diabetic complications. The compounds treatment maintained the activities of hepatic glucose metabolic enzymes and structure of pancreatic ${\beta}-cells$ from the diabetes, and it is noteworthy that cotreatment with QE and RS showed the most preventive effect on the diabetic rats. Therefore, our study suggests that cotreatment with QE and RS has beneficial effects against diabetes. We further suggest that cotreatment with QE and RS has the potential for use as an alternative therapeutic strategy for diabetes.

• Journal of Life Science
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• v.15 no.3 s.70
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• pp.382-386
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• 2005

To investigate the effects of simulated acid rain (SAR) on growth and biochemical defense responses of plant, garden balsam (Impatiens balsamina L.) was subjected to four levels of SAR based on pH (5.6, 4.0, 3.0, 2.0) and placed in the growth chambers for 2 weeks. SAR drastically inhibited both height and dry weight of garden balsam. The content of total carotenoid was tended to decrease, but the level of malondialdehyde was significantly increased by SAR. As the pH levels decreased from 5.6 to 2.0, the content of dehydroascorbate and oxidized glutathione of the plant were significantly increased. The enzyme (superoxide dismutase, ascorbate peroxidase etc.) activities of the plant affected by SAR were increased as the pH decreased. The results indicate that garden balsam may receive oxidative stresses by the application of SAR and by which the plant growth can be significantly retarded. A biochemical protective mechanism might be activated to nullify the oxidative stresses generated through SAR.

• Korean Journal of Weed Science
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• v.30 no.2
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• pp.135-142
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• 2010

To investigate the effects of ultraviolet(UV-B) on growth and biochemical defense responses of plant, garden balsam (Impatiens balsamina L.) was subjected to enhanced UV-B irradiation [daily dose: 0.02 (No UV-B) and 11.34 (enhanced UV-B) kJ $m^{-2}$ ; $UV-B_{BE}$] for 3 weeks. Enhanced UV-B drastically inhibited leaf area as well as dry weight of garden balsam. The content of malondialdehyde was significantly increased by about 50% after 3 weeks of UV-B irradiation. The ratios of dehydroascorbate/ascorbate and oxidized glutathione/reduced glutathione were also considerably increased by UV-B irradiation. Three major polyamines of garden balsam leaves: putrescine, spermidine and spermine were observed. All polyamine contents were increased with UV-B irradiation. The enzyme (superoxide dismutase, ascorbate peroxidase etc.) activities of garden balsam were increased by the UV-B enhancement. Based on the results, enhanced UV-B caused oxidative stress in garden balsam and biochemical protection responses might be activated to prevent from damaging effects of oxidative stress generated by UV-B irradiation.

• Journal of Microbiology and Biotechnology
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• v.23 no.3
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• pp.405-413
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• 2013

Monocyte chemotactic protein-3 (MCP-3), a chemokine that is in a superfamily of structurally related small chemotactic cytokines involved in leukocyte trafficking, is regarded as a key factor in atherogenesis. In this study, we examined the changes in atherogenic parameters including hepatic lipid accumulation and oxidative balance in MCP- 3-overexpressing transgenic mice (MCP-3 mice) under atherogenic conditions. To induce an extreme atherogenic condition, mice were fed a high-fat, high-cholesterol (HFHC) diet for 12 weeks. The body weight and food intake were not changed by MCP-3 overexpression in the aorta. On a HFHC diet, the MCP-3 mice had higher plasma levels of total cholesterol and a higher atherogenic index compared with wild-type mice, although there were no differences in the plasma HDL-cholesterol and triglyceride levels. Furthermore, an increase in lipid accumulation was observed in the aortas as well as the livers of the HFHC diet-fed MCP-3 mice compared with wild-type mice. The activities of antioxidant enzymes increased in the livers of the HFHC diet-fed MCP-3 mice, whereas supplementation with antioxidants, naringin and hesperidin, reversed the activities of the hepatic antioxidant enzymes in HFHC diet-fed MCP-3 mice, indicating that there might be more oxidative damage to the tissues in the HFHC diet-fed MCP-3 mice leading to progression towards atherosclerosis and hepatic steatosis. Microarray analyses of the aorta revealed atherosclerosis-, PPARs-, lipoprotein receptor, and apolipoprotein-related genes that were affected by the HFHC diet in MCP-3 mice. These findings suggest that aortic MCP-3 overexpression may contribute to the development of atherosclerosis and hepatic steatosis under atherogenic conditions.