• KOREAN JOURNAL OF CROP SCIENCE
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• v.48
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• pp.13-23
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• 2003

The trace mineral, selenium (Se), is an essential nutrient of fundamental importance to human health. It is also very toxic and can cause Se poisoning (selenosis) in human and animals when its intake exceeds a suitable amount. Se functions within mammalian systems primarily in the form of solenoprotein. About 35 selenoproteins have been identified, though many have not yet been fully elucidated. Selenoproteins contain Se as selenocyseine (Sec) and perform variety of structural and enzymic roles; the enzymic roles are best-known as the antioxidants for hydrogen peroxides and lipid peroxides, and the catalysts for production of activity thyroid hormone. Glutathione peroxidases ($\textrm{GP}_X$) among the selenoproteins prevent the generation of free radicals and decrease the risk of oxidative damage to tissues, as does thioredoxin reductase (TR). TR also provides reducing power for several biochemical processes. Selenoproteins P and W are involved with oxidant defense in plasma and muscle, respectively, A selenoprotein is also required for sperm motility and may reduce the risk of miscarriage. Some epidemiological studies have revealed an inverse correlation between Se status and cardiovascular disease, and there is considerable evidence 1mm population com-parison data and animal studies that Se is anticarcinogenic. It is also suggested that Se should be needed for the proper functioning of the immune system, and appear to be a key nutrient in counteracting the development of virulence and inhibiting HIV progression to AIDS. As research continues, the role of selenium in the etiology of chronic diseases like appropriate medical nutrition therapy can be delivered and its effectiveness assessed. Se status in individuals is affected by diet and the availability of the Se. The Se content of plants is affected by the content and availability of the element in the soil in which they are grown, and so greatly varies from country to country, while the Se composition of meat reflects the feeding patterns of livestock. This paper provides an overview on Se as an essential trace mineral for human.

• Journal of Nutrition and Health
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• v.37 no.9
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• pp.771-779
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• 2004

This study was performed to investigate the effect of dietary $\beta$-carotene supplementation on lipid metabolism and antioxidant enzyme activities in hyperlipidemic rats. Fifty Sprague-Dawley male rats aging 7 weeks were fed the control diet (CD,5% corn oil) and the high fat diet (HFD,15% beef tallow +1% cholesterol) for 4 weeks and then 0.02% $\beta$-carotene was supplemented to CD and HFD group for 8 more weeks. Serum lipid compositions, lipid peroxides and antioxidative enzymes in liver were analyzed at 4, 8 and 12week of the experiment. Serum levels of total lipid, total cholesterol, triglyceride, LDL-cholesterol, VLDL-cholesterol were higher in HFD groups than in CD groups (p < 0.001), Serum levels of HDL-cholesterol were higher in CD groups than in HFD groups (p < 0.01) . The effect of $\beta$-carotene supplementation was not significant in all groups but tended to be lower in total lipid, total cholesterol and Triglyceride. Thiobarbituric acid reactive substances (TBARS) levels in plasma and liver were showed significantly higher in HFD groups (p < 0.001, p < 0.05). The effects of $\beta$-carotene supplementation on the level of plasma and liver TBARS were not found except HFD groups at 12 week. Liver conjugated diene levels in HFD groups were higher than in CD groups (p < 0.01), but the effect of $\beta$-carotene supplementation did not show any differences. Liver lipofuscin levels were not significantly different among all groups. The activities of superoxide dismutase (SOD) and catalase were significantly lower in HFD groups at 8 week (p < 0.001) but were not significantly different at 4 and 12week. The activity of SOD in $\beta$-carotene supplemented HFD group was significantly higher at 8 week (p < 0.01). Glutathione peroxidase (GSH-Px) activity was significantly lower in HFD groups (p < 0.01) and was significantly increased in groups supplemented $\beta$-carotene (p < 0.05). It is suggested that $\beta$-carotene supplementation partly decreases the serum lipid and lipid peroxide levels and increases the activities of antioxidant enzymes in hyperlipidemic rats.

• Environmental Analysis Health and Toxicology
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• v.14 no.3
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• pp.87-93
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• 1999

Antioxidative and scavenging effects were investigated by using two hyaroxycinnamic acids (caffeetannins). such as caffeic acid and chlorogenic acid, on oxidative stress and hepatotoxicity that induced by paraquat. The results are summerized as follows: 1. To assess radical scavenging ability, reduction concentration (IC$\sub$50/) of 1.1 diphenyl-2-dipicrylhydrazine (DPPH) were measured. IC$\sub$50/ values of caffeic acid and chlorogenic acid were 29.7 ${\pm}$0.6 ${\mu}$M and 26.0${\pm}$0.5 ${\mu}$M respectively. Their radical scavenging activities showed concentration-dependent manner. 2. In H$_2$O$_2$-induced hemolysis assay to rat blood, caffeic acid and chlorogenic acid led to different effects, whose hemolysis inhibition ratios at 100 ${\mu}$M were 45.2${\pm}$7.1% and 11.6${\pm}$3.1% respectively 3. In hypoxanthine-xanthine oxidase system producing superoxide anion, caffeic acid and chlorogenic acid showed different inhibitory activities of xanthine oxidase showing 36.8${\pm}$4.3% and 5.4${\pm}$2.3% respectively. 4. To microsomal NADPH dependent cytochrome p-450 reductase in rat liver, paraquat consumed NADPH at a dose-dependent manner from 0 to 1 ${\mu}$M paraquat concentration. Caffeic acid and chlorogenic acid blocked NADPH consumption rates at concentration-dependent manner and inhibition ratios at 100 ${\mu}$M were 67.6% and 59.2% respectively. 5. Administration (30mg/kg, iv) of paraquat to rats caused the marked elevation of glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and lipid peroxides (LPO) in the serum and lipid peroxides in the microsome as compared to the control group. Serum GOT, GPT, LDH, ALP and LPO and liver microsomal LPO were reduced significantly by caffeic acid (50mg/kg), chlorogenic acid (25mg/kg) and silymarin (150 mg/kg) as compared to the paraquat group. From these results, caffeic acid and chlorogenic acid exerted their antioxidative agents by removing reactive oxygen substance (ROS) and scavenging effects by inhibiting ROS generating enzyme. As a general, two hydroxyeinnamic acids showed the useful compounds for scavenger and reducer on the paraquat induced hepatotoxicity.

• Nutrition Research and Practice
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• v.6 no.1
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• pp.3-8
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• 2012

Polyphenol-rich grape seeds have a beneficial effect on human health. The present study was performed to investigate the effects of grape seeds on antioxidant activities in rats. Male Sprague-Dawley rats were randomly divided into a control diet group (C), a high-fat diet group (HF), a 5% grape seed-supplemented control diet group (G), and a 5% grape seed-supplemented high-fat diet group (HG). Dietary supplementation with grape seeds reduced serum concentrations of lipid peroxides compared with those in the C and HF groups. The hepatic level of lipid peroxides decreased significantly in the grape seed groups compared with that in the C and HF groups. Superoxide dismutase activity in the G group increased significantly compared with that in the C group. Catalase activity tended to be higher by feeding grape seeds. The grape seed diet increased glutathione peroxidase activity in the C group. Glutathione-S-transferase activity increased significantly in the G group compared with that in the C group. Hepatic content of total glutathione increased significantly in the HG group but decreased significantly in the HF group. The ratio of reduced glutathione and oxidized glutathione increased by feeding the grape seed diet. Total vitamin A concentration was significantly higher in HG group than in other groups. Liver tocopherol content of the G and HG groups was significantly higher than that of the control groups. These results suggest that dietary supplementation with grape seeds is beneficial for suppressing lipid peroxidation in high fat-fed rats.

• Journal of the Korean Applied Science and Technology
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• v.13 no.2
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• pp.55-65
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• 1996

The antioxidant effects of freeze-drying acorn were examined to find how much the freeze-drying acorn can reduce peroxidized corn oil poisoning, which influenced cholesterol, triglyceride, phospholipids, lipidperoxides, GOT(glutamate oxaloacetate transaminase), GPT(glutamate pyruvate transaminase) in serum, and cholesterol, triglyceride, lipidperoxides, fatty acid of phospholipids, SOD(superoxide dismutase), catalase in liver. In this experiment, male rats of Sprague-Dawley strain were used. The rats were divided into 6 groups, which were fed differently for 5 weeks : basal diet, 10% peroxidized corn oil added to basal diet, 1% acorn flour and 10% peroxidized corn oil added to basal diet, 5% acorn flour and 10% peroxidized corn oil added to basal diet, 10% acorn flour and 10% peroxidized corn oil added to basal diet, and 0.25% tannic acid and 10% peroxidized corn oil added to basal diet. The results were as follows : It was found that the peroxidized corn oil-fed 5 weeks induced the elevation of cholesterol, triglycerides, lipid peroxides, GOT, GPT in serum, and cholesterol, triglycerides, lipid peroxides in liver as compared to the basal diet-fed rats, but the acorn flour-fed rats reduced the elevation of these components. In addition, saturated fatty acid in rat liver phospholipids induced the elevation by feeding of peroxidized corn oil and, on the other hand, the acorn flour-fed rats reduced the elevation of saturated fatty acids. The acorn flour-fed rats reduced the activity of SOD in liver while they enhanced the activity of catalase in liver as compared with the peroxidized corn oil-fed rats.

• Nutritional Sciences
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• v.9 no.1
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• pp.9-13
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• 2006

The differential effects of various fatty acids such as n-3 and n-6 types or degrees of unsaturation on the CYP2E1 induction and the production of lipid peroxidation (LPO) were investigated. The CYP2E1-transduced human hepatoma HepG2 cells (E47) were cultured in RPMI 1640 media containing different concentrations of various fatty acids up to 48 h incubation compared to 04 cells and CYP2E1-null cells. Treated fatty acids were linoleic acid (LA:n-6, C18:2), arachidonic acid (AA:n-6, C20:4) and docosahexaenoic acid (DHA:n-3, C22:6). The cell survival rate was decreased corresponding to the degree of unsaturation (LA>AA $\cong$DHA) and to LPO production in E47 and 04 cells. The four or five unsaturation degree of fatty acids, AA and DHA, caused time- and dose-dependent cell death in E47 cells but not as much as in C34 (without CYP2E1), suggesting an important role of CYP2E1 in the DHA mediated damage. In the levels of lipid peroxides (LPO), AA also elevated LPO by 3- and 5- fold compared to DHA or LA treated E47 cells. However, AA did not increase LPO until 48 h incubation in C34 cells. In conclusion, the polyunsaturated fatty acids induced CYP2E1 induction might be changed by the elevated levels of lipid peroxide (LPO) and oxidative stress through the connection of CYP2E1 and degrees of unsaturated fatty acids.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2001.11a
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• pp.94-94
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• 2001

Prostaglandin endoperoxide H synthase (PGHS) catalyzes the committed step in prostaglandins and thromboxane A$_2$-- oxygenation of arachidonic acid to the hydroperoxy endoperoxide PGG$_2$, followed by reduction PGG$_2$to the alcohol PGH$_2$. The two reactions by PGHS -- cyclooxygenase and peroxidase -- occur at distinct but structurally and functionally interconnected sites. The peroxidase reaction occurs at a heme-containing active site located near the protein surface. The cyclooxygenase reaction occurs in a hydrophobic channel in the core of the enzyme. Initially a peroxide reacts with the heme group, yielding Compound I and an alcohol derived from the oxidizing peroxide. Compound I next undergoes an intramolecular reduction by a single electron traveling from Tyr385 along the peptide chain to the proximal heme ligand, His388, and finally to the heme group. Following the binding of arachidonic acid, Tyr385 tyrosyl radical initiates the cyclooxygenase reaction by abstracting the 13-pro(5) hydrogen atom to give an arachidonyl radical, which sequentially reacts with two molecules of oxygen to yield PGG$_2$. In order to characterize PGHS peroxidase active site, we examined various lipid peroxides with purified recombinant ovine PGHS proteins and determined the rate constants. The results have shown that twenty-carbon unsaturated fatty acid hydroperoxides have similar efficiency in peroxidation by PGHS, irrespective of either the location of hydroperoxy group or the number of double bonds. It was also confirmed by the subsequent study with PGHS peroxidase active site mutants.

• BMB Reports
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• v.36 no.6
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• pp.593-596
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• 2003

The effects of $N{\omega}$-nitro-L-arginine methylester (L-NAME) and L-arginine on cardiotoxicity that is induced by doxorubicin (Dox) were investigated. A single dose of Dox 15 mg/kg i.p. induced cardiotoxicity, manifested biochemically by a significant elevation of serum creatine phosphokinase (CPK) activity [EC 2.7.3.2]. Moreover, cardiotoxicity was further confirmed by a significant increase in lipid peroxides, measured as malon-di-aldehyde (MDA) in cardiac tissue homogenates. The administration of L-NAME 4 mg/kg/d p.o. in drinking water 5 days before and 3 days after the Dox injection significantly ameliorated the cardiotoxic effects of Dox, judged by the improvement in both serum CPK activity and lipid peroxides in the cardiac tissue homogenates. On the other hand, the administration of L-arginine 70 mg/kg/d p.o. did not protect the cardiac tissues against the toxicity that was induced by the Dox treatment. The findings of this study suggest that L-NAME can attenuate the cardiac dysfunction that is produced by the Dox treatment via the mechanism(s), which may involve the inhibition of the nitric oxide (NO) formation. L-NAME may, therefore, be a beneficial remedy for cardiotoxicity that is induced by Dox and can then be used to improve the therapeutic index of Dox.

• Journal of Nutrition and Health
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• v.32 no.3
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• pp.230-238
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• 1999

The present study was conducted to investigate te effect of sea tangle and hypoglycemic agent(Metformin) on lipid peroxidation and antioxidants levels in normal and diabetic rats. Male Sprague-Dawley rats were fed AIN-76 based experimental diets containing 5% (w/w) cellulose or 15%(w/w) sea tangle for 3 weeks, and then rats of diabetic groups were rendered diabetic by intramuscular injection of streptozotocin(STZ, 45mg/kg BW). After induction of diabetes Metformin(350mg/kg BW) was given once a day using a feeding tube for 5 days. Blood glucose level in diabetic rats fed sea tangle was significantly lower than that of diabetic rats fed cellulose. Metformin feeding resulted in further lowering blood glucose. Plasma and liver microsomal levels of lipid peroxides were increased significantly in diabetic rats as compared to normal rats, and the plasma level tended to be decreased by sea tangle feeding. Plasma level of retinol was reduced by STZ treatment, but it was increased by Metformin feeding in diabetic rats fed sea tangle. The liver contents of retinyl plamitate were reduced in diabetic rats but recovered by sea tangle feeding to some extent. Liver contents of total vitamin A were increased significantly by sea tangle in diabetic rats. Although difference in either plasma or liver level of $\alpha$-tocopherol by diet and STZ treatment was not significant, $\alpha$-tocopherol levels were the highest in the group with simultaneous feeding of sea tangle and metformin. Liver contents of zinc and copper were not influenced by either STZ treatment or sea tangle feeding. The present study indicates that the lowering blood glucose level could be attained by simultaneous trial of sea tangle diet and hypoglycemic agent and the increased oxidative stress caused by STZz treatment could be relieved by sea tangle feeding.

• Korean Journal of Pharmacognosy
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• v.27 no.3
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• pp.159-166
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• 1996

To evaluate hepatoprotective effects of G009, an hepatoprotective agent which was extracted from the mycelia of Ganoderma lucidum IY009, we were, studied using $CCl_4$-and galactosamine-induced hepatotoxicity in rats. The ratio of liver weight to body weight, the value of glutamic oxaloacetic transaminase(GOT) and glutamic pyruvic transaminase (GPT) activities, the change of a lipids in serum, and the inhibitory activity of malondialdehyde (MDA) formation in serum and liver homogenate were determined in rats. G009 was not significantly changed of the ratio of liver weight to body weight and the content of lipids in serum, but reduced the serum GOT and GPT values in $CCl_4$-and galactosamine-induced hepatotoxicity in rat. Especially, protective effect of G009 on rat hepatic injuries induced by galactosamine was significantly appeared. $CCl_4$ increased markedly the formation of lipid peroxides in the liver homogenate, and serum. The increase of lipid peroxides by $CCl_4$-induced hepatotoxicity was markedly reduced by the treatment with G009. These results suggest that the hepatoprotective effects of G009 may be correlated with its anti-lipid peroxidative activity, therefore, it may be potential agent for hepatic disease.