• Molecules and Cells
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• v.21 no.2
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• pp.276-283
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• 2006

The potent environmental contaminant, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), induces thymus atrophy in experimental animals. However, its mechanism of action is not fully understood. To gain insight into its immunosuppressive effect, Balb/c mice were intraperitoneally injected with TCDD ($30{\mu}g/kg$ body weight) and genes regulated by TCDD were identified using cDNA arrays [Park and Lee (2002)]. One of the regulated genes was that for plasma glutathione peroxidase (pGPx). Upon TCDD injection, pGPx mRNA levels in the thymus increased, in parallel with increases in GPx activity and the frequency of anti-human pGPx antibody-reactive cells. pGPX mRNA levels were also moderately up-regulated in the testis and spleen. This is the first report that a particular isotype of the glutathione peroxidase family is regulated by TCDD at both mRNA and protein levels. pGPx is expressed in various tissues in contact with body fluids, and detoxifies hydrogen peroxides and lipid hydroperoxides. It will be of interest to assess the role of pGPx in TCDD-induced thymic atrophy.

• BMB Reports
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• v.44 no.8
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• pp.497-505
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• 2011

Reactive oxygen species (ROS), which include superoxide anions and peroxides, induce oxidative stress, contributing to the initiation and progression of cardiovascular diseases involving atherosclerosis. The endogenous and exogenous factors hypercholesterolemia, hyperglycemia, hypertension, and shear stress induce various enzyme systems such as nicotinamide adenine dinucleotide (phosphate) oxidase, xanthine oxidase, and lipoxygenase in vascular and immune cells, which generate ROS. Besides inducing oxidative stress, ROS mediate signaling pathways involved in monocyte adhesion and infiltration, platelet activation, and smooth muscle cell migration. A number of antioxidant enzymes (e.g., superoxide dismutases, catalase, glutathione peroxidases, and peroxiredoxins) regulate ROS in vascular and immune cells. Atherosclerosis results from a local imbalance between ROS production and these antioxidant enzymes. In this review, we will discuss 1) oxidative stress and atherosclerosis, 2) ROS-dependent atherogenic signaling in endothelial cells, macrophages, and vascular smooth muscle cells, 3) roles of peroxidases in atherosclerosis, and 4) antioxidant drugs and therapeutic perspectives.

• Archives of Pharmacal Research
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• v.21 no.3
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• pp.236-240
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• 1998

The effect of thyroid hormones on the hepatic xanthine oxidase activity was studied in rats after the intraperitoneal injections of comthyroid (triiodotyronine:thyroxine=1:4) at 0.3 mg/kg for 3 consecutive days. The aim of this study was to understand the precise mechanism of hyperthyroidism induced by oxidative stress. The concentration of lipid peroxides determined indirectly by the measurement of thiobarbituric acid reactants was increased in comthyroid treated rats. The hepatic glutathione content was decreased in comthyroid injected rat compared to the euthyroid state. It was also observed that the increment of xanthine oxidase activity has a profound role in oxygen radicals generation system in comthyroid treated rat. These findings suggest that the enhanced xanthine oxidase activity and depleting glutathione content in comthyroid treated rats result in pathophysiological oxidative stress including an increment of hepatic lipid peroxidation.

• KOREAN JOURNAL OF CROP SCIENCE
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• v.49 no.2
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• pp.116-120
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• 2004

In order to investigate low molecular antioxidants synthesized by enhanced UV-B radiation, we used the seedlings of two rice varieties. Woonjangbyeo, UV-tolerant, and Hwajoongbyeo, UV-susceptible, were subjected under supplemental UV-B irradiation. When rice seedlings were irradiated with UV light for short period, biosynthesis of total phenolic compound, ascorbate and glutathione were momently reduced. With an increase of UV-B radiation, however, those were slightly synthesized. The content of lipid peroxides in UV-challenged rice leaves was considerably increased after 12 hrs of UV-B treatment. Lipoxygenase activity under supplemental UV-B radiation was differently responded on rice varieties.

• Journal of Nutrition and Health
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• v.38 no.5
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• pp.364-372
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• 2005

This study is designed to examine the effects of dietary supplementation with vitamin E and dehydroepiandrosterone (DHEA) on the formation of preneoplastic lesions in diethylnitrosamine (DEN) induced rat hepatocarcinogenesis. All Weaning male Sprague-Dawley rats were initiated by a single dose of DEN (200mg/kg body weight), subjected to two­thirds partial hepatectomy 3 weeks later and were sacrificed 8 weeks after DEN initiation. Two weeks after initiation, rats were fed Purina purified rodent diet 5053 (Ralston Purina Rat chow, USA) with $1.5\%$ (15,000 IU/kg diet) vitamin E, $0.5\%$ DHEA and both of those supplemented diet for 6 weeks. Placental glutathione S-transferase (GST-P) positive foci, the activities of catalase, total-glutathione peroxidase (GPx) , glutathione reductase (GR), glutathione S-transferase (GST) and thiobarbituric acid reactive substances (TBARS) contents were decreased significantly by vitaimin E supplement. On the other hand GST-P positive foci number, Cu/Zn-superoxide dismutase (SOD) and glucose 6-phosphatase (G6Pase) activities weren't changed by vitamin E supplement. It might suggest that protective effect of vitamin E against hepatocarcinogens is not involved in the formation of the GST-P positive foci but related to the expansion of that. It seemed that vitamin E supplement helped endogenous defense system in carcinogenesis by decreasing TBARS contents, $H_2O_2$, organic peroxides. Therefore, vitamin E seemed to protect cell from free radical damage in carcinogenesis. By DHEA supplement liver weight and liver/body ratio were increased, the area and number of GST-P positive foci, the activities of catalase, GR, total GPx, GST and the TBARS contents were decreased significantly. On the other hand Cu/Zn-SOD and G6Pase activities weren't changed by DHEA supplement. In hepatocarcinogenesis the activities of antioxidant enzymes weren't increased by DHEA supplement. DHEA did not increase the oxidative stress, while DHEA seems to have anticarcinogenic effect in rats hepatocarcinogenesis.

• Journal of Nutrition and Health
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• v.31 no.6
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• pp.1014-1023
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• 1998

The influences of fish oil and different levels of vitamin I supplement on hepatocellular chemical carcinogenesis have been studied. Male Sprague-Dawley rats received diethylnitrosamine (DEN)(200mg/kg body weight) and were subjected to two-thirds partial hepatectomy to induce murine chemical hepatocarcinogenic procedure. Placental glutathione S-transferase(GST-P) positive foci area, antioxidant enzymes(Cu/Zn-superoxide dismutase(SOD), catalase, glutathione reductase (GR), total- glutathione peroxidase (TGPx), glutathione S -transferase (GST)), glucose 6-phosphatase (G6Pase) activities, and lipid peroxidation of microsomes(thiobarbituric acid reactive substances (TBARS)) were measured. Experimental animals were fed 15% corn or fish oil with 0, 40, 1,000, 10,000IU vitamin E /kg diet for 8 weeks. Vitamin E supplements decreased the area of GST-P positive foci in both groups. The higher the vitamin E levels, the smaller the area of GST-P positive foci were noticed. Compared to 0 IU vitamin E, 40 IU in corn oil and 1,000 IU in fish oil groups were effective in decreasing G57-P positive foci area. Fish oil groups tended to have smaller area of GST-P positive foci. fish oil groups showed lower body weight, lower activities of Cu/Zn-SOD and TGPx, higher TBARS contents, higher activities of GST, catalase, G6Pase, GR and higher liver/body ratio than corn oil groups. As the level of vitamin I increased, GST-P positive foci count, catalase activities, and TBARS tended to decrease. G6Pase activities tended to increase in both groups. At higher vitamin E levels, GST activities tended to decrease in fish oil groups. These results suggest that vitamin I has suppressive offects on hepatocellular chemical carcinogenesis probably through antioxidant eH:cts decreasing TBARS contents, $H_2O$$_2$, and organic peroxides. fish oil tended to have greated suppressive offects than corn oil on hepatocellular carcinogenesis. (Korean J Nutrition 31(6) : 1014-1023, 1998)

• Journal of Society of Preventive Korean Medicine
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• v.12 no.1
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• pp.103-118
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• 2008

Antioxidants are compounds that protect cells against the damaging effects of reactive oxygen species (ROS). Some ROS, such as superoxide and hydrogen peroxide, are normally produced in cells as by-products of biochemical reactions or as signaling molecules. When ROS-generating reactions are activated excessively, pathological quantities of ROS are released to create an imbalance between antioxidants and ROS, called as oxidative stress. Oxidative stress, which may result in cellular damage, has been linked to cardiovascular disease, diabetes, cancer, and other degenerative conditions. In humans the first line of antioxidant defence are the antioxidant enzymes, especially SOD, glutathione peroxidase (GPX), and to a lesser extent catalase, as well as the tripeptide glutathione(GSH). These enzymes will help destroy ROS(reactive oxygen species) such as hydroxyl radical, $H_2O_2$ and lipid peroxides, while GSH protects against oxidized protein. Many herbal medicines possess antioxidant properties. Herbal antioxidants may protect against these diseases by contributing to the total antioxidant defense system of the human body. Here, many herbal medicines including Ginseng, Licorice, Ligusticum Chuanxiong, Ginkgo biloba and many others was reviewed in terms of anti-oxidant efficiency related to their components.

• Journal of the Korean Dietetic Association
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• v.4 no.2
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• pp.168-177
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• 1998

It has been reported that cigarette smoking increases free radical generation, which can also increase lipid peroxides and deplete antioxidants. The purpose of this study was to determine whether cigarette smoking and other lifestyle choices may affect serum lipid peroxide concentrations, serum antioxidant concentrations such as tocopherol and vitamin C, and serum antioxidant enzyme activity such as glutathione peroxidase and superoxide dismutase. Dietary intakes were assessed by 24-hour recall and survey questionnaires from 48 male non-smokers and 52 male smokers. Overnight fasting blood was collected and measured for individual antioxidant status. The daily vitamin C intakes of smokers tended to be lower than those of non-smokers, and the intakes of both groups were under the Recommended Daily Allowance (RDA). Vitamin E intake was sufficient for smokers and non-smokers. Serum lipid peroxide concentrations were no difference among all subjects. The serum $\alpha$-tocopherol concentrations of all subjects were in a normal range, and they were highest in mild smokers (p<0.05). Mean serum vitamin C levels were lowest in heavy smokers (p<0.05). The activities of serum glutathione peroxidase and superoxide dismutase were not significantly different in smokes and non-smokers. In conclusion, smoking did not increase oxidative stress in heathy young men. However, it is desirable for heavy smokers to consume more vitamin C than the RDA sine their serum vitamin C concentrations are relatively low.

• Preventive Nutrition and Food Science
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• v.13 no.3
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• pp.139-145
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• 2008

We located a group of healthy young males (aged $20{\sim}30$) who had been taking a high dose (more than 5 g) of vitamin C daily for more than one year. We observed that this vitamin C group had plasma levels of vitamin C that were more than three times that of the control group. The control group had not taken any additional vitamin C except for that included in their diets. But the vitamin C group showed significantly lower amounts of Cu/ZnSOD, catalase and glutathione-s-transferase and lower activities of glutathione peroxidase and glutathione reductase in erythrocyte lysates than the control group. However, there was no difference in the plasma levels of lipid peroxides between the two groups. These results suggest that vitamin C offsets its own contribution to anti-oxidant activity by repressing the expression of anti-oxidant enzymes and also excludes the possibility that vitamin C acts as a pro-oxidant in vivo.

• Molecules and Cells
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• v.39 no.1
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• pp.20-25
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• 2016

Photosynthesis is a highly robust process allowing for rapid adjustment to changing environmental conditions. The efficient acclimation depends on balanced redox metabolism and control of reactive oxygen species release which triggers signaling cascades and potentially detrimental oxidation reactions. Thiol peroxidases of the peroxiredoxin and glutathione peroxidase type, and ascorbate peroxidases are the main peroxide detoxifying enzymes of the chloroplast. They use different electron donors and are linked to distinct redox networks. In addition, the peroxiredoxins serve functions in redox regulation and retrograde signaling. The complexity of plastid peroxidases is discussed in context of suborganellar localization, substrate preference, metabolic coupling, protein abundance, activity regulation, interactions, signaling functions, and the conditional requirement for high antioxidant capacity. Thus the review provides an opinion on the advantage of linking detoxification of peroxides to different enzymatic systems and implementing mechanisms for their inactivation to enforce signal propagation within and from the chloroplast.