• Title/Summary/Keyword: GSH peroxidase

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Anti-Oxidant Efficiency and Memchanisms of Phytochemicals from Traditional Herbal Medicine (한약재-식물성천연화학물질의 항산화 효능 및 기전)

  • Kim, Jong-Bong
    • 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.

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Protective Effect of Astaxanthin Produced by Xanthophyllomyces dendrorhous Mutant on Indomethacin-Induced Gastric Mucosal Injury in Rats

  • Kim, Jeong-Hwan;Choi, Seok-Keun;Lim, Wang-Jin;Chang, Hyo-Ihl
    • Journal of Microbiology and Biotechnology
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    • v.14 no.5
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    • pp.996-1003
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    • 2004
  • Nonsteroidal anti-inflammatory drugs such as indomethacin induce severe gastric mucosal damage in humans and rodents. In the present study, the in vivo protective effect of astaxanthin on indomethacin-induced gastric lesions in rats was investigated. The test groups were injected with indomethacin (25 mg/kg) after the oral administration of astaxanthin (25 mg/kg) for 1, 2, and 3 days, while the control group was treated only with indomethacin. Thiobarbituric acid reactive substances in the gastric mucosa, as an index of lipid peroxidation, increased significantly after indomethacin administration and this increase was inhibited by oral administration of astaxanthin. In addition, pretreatment with astaxanthin resulted in a significant increase of the activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-px). Histologic examination clearly revealed acute gastric mucosal lesions induced by indomethacin in the stomach of the control group, but were not observed in that of the test group. These results indicate that astaxanthin activates SOD, catalase, and GSH-px, and removes the lipid peroxides and free radicals induced by indomethacin. It is evident that astaxanthin acts as a free radical quencher and antioxidant, and is an effective molecule in the remedy of gastric mucosal lesions.

New evidences of neurotoxicity of aroclor 1254 in mice brain: potential of coenzyme q10 in abating the detrimental outcomes

  • Majumdar, Anuradha;Nirwane, Abhijit;Kamble, Rahul
    • Environmental Analysis Health and Toxicology
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    • v.29
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    • pp.1.1-1.7
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    • 2014
  • Objectives The present subacute study was designed to evaluate the effect of coenzyme Q 10 (CoQ10) in the 28 days aroclor 1254 exposure induced oxidative stress in mice brain. Methods Biochemical estimations of brain lipid peroxidation (LPO), reduced glutathione (GSH), and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and acetyl cholinesterase (AChE), and histopathological investigations of brain tissue were carried out. Results Oral exposure of aroclor 1254 (5 mg/kg) led to significant decrease in levels of GSH, and activities of SOD, CAT, GPx, and AChE, and increase in LPO. These aberrations were restored by CoQ10 (10 mg/kg, intraperitoneal injection [IP]). This protection offered was comparable to that of L-deprenyl (1 mg/kg, IP) which served as a reference standard. Conclusions Aroclor 1254 exposure hampers the activities of various antioxidant enzymes and induces oxidative stress in the brains of Swiss albino mice. Supplementation of CoQ10 abrogates these deleterious effects of aroclor 1254. CoQ10 also apparently enhanced acetyl cholinesterase activity which reflects its influence on the cholinergic system.

Effects of Excess Vitamin C Feeding on Blood and Liver Lipid and its Peroxidation Levels, and Platelet Thromboxane $A_2$Formation in Rats (비타민 C의 만성적 과량투여가 흰쥐의 혈액과 간의 지질성상, 과산화상태 및 혈소판 Thromboxane $A_2$ 생성에 미치는 영향)

  • 이정원
    • Journal of Nutrition and Health
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    • v.30 no.6
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    • pp.639-647
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    • 1997
  • The effect of excess L-ascorbic acid(AsA) in blood, liver lipid levels and peroxidation status were investigate . Ten Sprague-Dawley male rats weighing 150-200g were fed 300mg AsA/100g body weight/day, mixed into ground chow diet, for 4 weeks. And another set of then rats were fed only chow diet as the control. Average body weight gain was slightly lowered by AsA feeding without food intake change. The AsA group showed higher AsA levels in plasma and liver than the control group. In addition, the AsA group showed a higher plasma TBARS value. Liver TBARS seemed to be elevated in the AsA, but not significantly. The hemolysis of red cells tended to increase with excess AsA, accompanied by a raised GSH-Px activity and lowered total GSH levels. Plasma HDL-Chol level was increased while the levels of total Chol, LDL-plus VLDL-Chol , and triglyceride were unchanged . Atherogenic index decreased. Hepatic TG levels were also decreased, but the total amount of Chol increased slightly . Platelet TXA$_2$ production was inhibited by excess AsA feeding. Above results indicafe that oral feeding of excess AsA may be beneficial in reducing the risk of atherosclerosis ; however such practice may be detrimental for tissue lipid peroxidation and weight gain.

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Effects of Small Molecular Antioxidants on Cerulein-induced Acute Pancreatitis in Rat

  • Choi, Joo-Young;Kim, Kyung-Hwan
    • The Korean Journal of Physiology and Pharmacology
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    • v.2 no.5
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    • pp.629-635
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    • 1998
  • It has been suggested that oxygen free radicals are involved in the initiation process of acute pancreatitis, although its pathogenesis is not clear. This study evaluates the roles of oxygen radicals and the effects of small molecular antioxidants (rebamipide, N-acetyl-cysteine, allopurinol, ${\beta}-carotene)$ on the development of cerulein-induced acute pancreatitis. Acute edematous pancreatitis was induced by the intravenous infusion of cerulein at supramaximal dose of 10 ${\mu}g/kg/hour$ for 3.5 hours. The effects of antioxidants, rebamipide (100 mg/kg, i.p.), N-acetyl-cysteine (200 mg/kg, i.v.), allopurinol (20 mg/kg/hour), ${\beta}-carotene$ (50 mg/kg, i.p.), were examined. Cerulein administration resulted in a significant increase in serum amylase activity and pancreatic malondialdehyde (MDA), but not glutathione peroxidase (GSHpx). The glutathione (GSH) content in pancreatic tissue decreased dramatically. Pretreatment of N-acetyl-cysteine significantly decreased the cerulein-induced hyperamylasemia and maintained GSH content in pancreas, but MDA was slightly decreased. In addition, N-acetyl-cysteine ameliorated histological damage. Allopurinol and ${\beta}-carotene$ attenuated cerulein-induced hyperamylasemia, but histologically there was no difference from control. These results indicate that oxygen free radicals play an important role in the initiation of experimental acute pancreatitis. N-acetyl-cysteine is an effective antioxidant that ameliorates the cerulein-induced acute pancreatitis, and the possible therapeutic application of antioxidants against acute pancreatitis needs a further evaluation.

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Inhibitory Effect of Angelica keiskei Koidz Green Juice on the Liver Damage in CCl4-Treated Rats (신선초 녹즙이 사염화탄소 투여에 의한 흰쥐의 간 손상에 미치는 영향)

  • 이명렬;정희경;박평심;허남칠;김성오;김경수
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.27 no.3
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    • pp.531-536
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    • 1998
  • To investigate effects of Angelica keiskei Koidz green juice on the liver damage of CCl4-treated tats, Sprague-Dawley male rats weighing 80~100g were divided into 4 groups of control group(CON), Angelica keiskei Koidz green juice-treated group(ANJ), CCl4-treated group(CCL) and Angelica keiskei Kodiz green juice and CCl4-treated group(ACL). Each group was sacrified after feeding for 4 weeks and examined the activities of transminase (sGOT, sGPT), superoxide dismutase (SOD), catalase and glutathione peroxidase(GSH-Px), and contents of lipid peroxide and glutathione in liver. The activities of sGOT and sGPT, and content of lipid peroxide after CCl4 treatment were markedly increased, compared to CON, but those levels were significantly decreased by the pretreatment of Angelica keiskei Koidz green juice as compared to CCL. The activities of SOD, catalase and GSH-Px were elevated by CCl4-treatment as compared to control group, and concomitant treatment of Angelical keiskei Koidz and CCl4 decreased those levels significantly except the activity of catalase. The hepatic content of glutathione was decreased by CCl4 and increased more abundant by Angelica keiskei Koidz administration than CCl4 treated group. These results suggest that Angelica keiskei Koidz green juice is believed to have a possible protective effect for the carbon tetrachloride-induced hepatotoxicity in rats.

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Mechanism of Lung Damage Induced by Cyclohexane in Rats (Cyclohexane에 의한 랫드의 폐손상 기전)

  • 전태원;윤종국
    • Toxicological Research
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    • v.18 no.2
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    • pp.159-165
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    • 2002
  • Recently, we reported (korean J. Biomed. Lab. Sci., 6(4): 245-251, 2000) that cyclohexane (l.56 g/kg of body wt., i.p.) administration led to lung injury in rats. However the detailed mechanism remain to be elucidated. This study was designed to clarify the mechanism of lung damage induced by cyclohexane in rats. First, lung damage was assessed by quantifying bronchoalveolar lavage fluid (BAL) protein content as well us by histopathological examination. Second, activities of serum xanthine oxidase (XO), pulmonary XO and oxygen free radical scavenging enzymes. XO tope conversion (O/D + O, %) ratio and content of reduced glutathione (GSH) were determined. In the histopathological findings, the vasodilation, local edema and hemorrhage were demonstrated in alveoli of lung. And vascular lumens filled with lipid droplets, increased macrophages in luminal margin and increased fibroblast-like interstitial cells in interstitial space were observed in electron micrographs. The introperitoneal treatment of cyclohexane dramatically increased BAL protein by 21-fold compared with control. Cyclohexane administration to rats led to a significant rise of serum and pulmonary XO activities and O/D + O ratio by 47%,30% and 24%, respectively, compared witれ control. Furthermore, activities of pulmonary oxygen free radical scavenging enzymes such as superoxide dismutase, glutathione peroxidase and glutathione S-transferase, and GSH content were not found to be statistically different between control and cyclohexane-treated rats. These results indicate that intraperitoneal injection of cyclohexane to rats may induce the lipid embolism in pulmonary blood vessel and lead to the hypoxia with the ensuing of oxygen free radical generation, and which may be responsible for the pulmonary injury.

Interactions between Oxidative Stress, Lipid Profile and Antioxidants in Breast Cancer: A Case Control Study

  • Gupta, Rakesh Kumar;Patel, Amit Kumar;Kumari, Rajni;Chugh, Seema;Shrivastav, Chitrangada;Mehra, Siddharth;Sharma, Ajay Narayan
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.12
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    • pp.6295-6298
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    • 2012
  • Oxidant/antioxidant balance has been suggested as an important factor for initiation and progression of cancer. The objective of this study was to determine changes in the levels of malondialdehyde (MDA), nitric oxide (NO), total cholesterol, triglycerides, LDL-cholesterol, HDL-cholesterol, total antioxidant capacity (TAC), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) activities in serum samples of breast cancer patients (n=30) and healthy subjects (n=100). MDA and NO levels were found to be increased in breast cancer patients compared to the healthy subject group (p<0.05). Total cholesterol and triglycerides were elevated; and HDL-cholesterol level was found to be decreased in the cancer patients as compared to the healthy subjects (p<0.05). Compared to the healthy group, both serum TAC levels (p<0.001) and activity of SOD and GSH-Px (p=0.05) were found to be decreased in the breast cancer patients as compared to the healthy controls. Considering the data presented in this study, we suggest that free radicals induce lipid eroxidation and peroxidation of unsaturated fatty acid with decreased activity of enzymatic antioxidants in breast cancer.

EFFECTS OF GINSENOSIDE $Rb_2$ ON THE ANTIOXIDANTS IN SENESCENCE - ACCELERATED MICE(SAM - R/1)

  • Chung H.Y.;Kim K.W.;Oura H.;Yokozawa T.
    • Proceedings of the Ginseng society Conference
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    • 1993.09a
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    • pp.30-32
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    • 1993
  • In biological system, there are enzymes such as superoxide dismutase(SOD), catalase and glutathione(GSH) peroxidase which scavenge reactive oxygen species as well as antioxidants such as ceruloplasmin, albumin and nonprotein-bound SH including GSH related to defense mechanism. In the present study, the protective effects of ginsenoside $Rb_2$ against oxidative stress were investigated in the SAM-R/1 mice. Treatment with ginsenoside $Rb_2$ significantly increased Cu, Zn-SOD and Mn-SOD in the liver. Ginsenoside $Rb_2$ tended to increase hepatic catalase activity and significantly increased serum albumin and nonprotein-bound SH levels in the liver. But treatment with ginsenoside $Rb_2$ showed a significant decrease in hepatic malondialdehyde(MDA) levels compared to control group. Furthermore, we compared the effects in the hepatic SOD, MDA and serum albumin. These findings suggest that the increase of antioxidants by ginsenoside $Rb_2$ results in the protective effects against reactive oxygen species.

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Radioprotective Effect of Ascorbate in the Liver of ${\gamma}-Irradiated$ Mice (Ascorbate의 방사선 보호효과에 관한 연구)

  • Kim, Dong-Yun;Park, Young-Soon
    • Journal of radiological science and technology
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    • v.23 no.1
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    • pp.81-89
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    • 2000
  • In the present study, to determine whether the ascorbate protect against radiation damage and the possible relationship among the radioprotective effects and antioxidant actions, the effects of ascorbate(240 mg/kg, i.p) pretreatment of mice on the survival ratio, splenic weight, major antioxidant enzymes(SOD, catalase and glutathione peroxidase) activities, glutathione contents and lipid peroxidation in the liver were examined for 2 weeks after whole-body ${\gamma}-irradiation$(6.5 Gy). The 30-day survival ratio Increased from 10% to 47% for mice treated with ascorbate. The ascorbate decreased the extent of loss in splenic weight and stimulated recovery of splenic weight in irradiated mice(p<0.01). On the day of 14 after ${\gamma-irradiation}$, the ascorbate pretreatment produced a slight increase of antioxidant enzymes activities and significantly increased reduced glutathione(GSH) contents(P<0.05) in the liver compared with non-treated group. Pretreatment with the ascorbate significantly decreased GSSG/total GSH ratio(p<0.05) without the change of GSSG in the liver and inhibited the radiation-induced increase in the hepatic malondialdehyde levels(p<0.05). In these results, we found that its radioprotective effect by protecting antioxidant enzyme activities and glutathione contents from radiation induced a decrease, and thereby suppressing lipid peroxidation which is induced by free radicals.

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