• 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.

• Journal of Society of Preventive Korean Medicine
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• v.8 no.2
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• pp.65-80
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• 2004

Objectives : CRATAEGII FRUCTUS(山査) is known as the substance which delays aging by the antioxidant effects. The purpose of this study is to investigate the effects of CRATAEGII FRUCTUS(山査) on antioxidant enzyme activities such as Thiobarbituric acid reactive substance(TBARS), Superoxide dismutase(SOD), Catalase(CAT), Glutathione peroxidase (GSH-px) in rat erythrocytes and blood plasma. Methods : Sprague-Dawley rats were divided into 3 groups, Normal group (supplied enough water and feeds only, Normal Group), D-galatose administered group(injected D-galatose 50mg/kg, 1time/day for 6 weeks, Control Group) and CRATAEGII FRUCTUS(山査) administered group (D-galactose 50mg/kg and CRATAEGII FRUCTUS(山査) extracts 85.0mg/200g 1time/day for 6 weeks, SS Group). Rats were sacrificed and TBARS, SOD, CAT, GSH-px, neutral fat and cholesterol were measured in rat erythrocytes and blood plasma. Results : There was no significant difference in the level of TBARS in the blood plasma between each experimental group. Red blood cell SOD activities were significantly different in each group. They were significantly decreased in the Control group compared to those of Normal and there was an increasing phenomenon in the SS group compared to the Control group. There was a significant difference in the activities of the red blood cell - glutathione peroxides in each group. There was a significant increase in the SS group compared to the Control group. Red blood cell catalase activities was no significant difference in each group. Plasma total lipid concentration was significantly different in each group. It was significantly increased in the Control group compared with the Normal group and it was decreasing in the SS group compared to the control group. Plasma triglyceride was not significantly different in each group. Plasma total cholesterol and Plasma HDL -cholesterol concentrations in the blood plasma were not significantly different in each group. Conclusions : According to the above results, it is considered that CRATAEGII FRUCTUS(山査) is effective in inhibiting lipid peroxides and increasing the activities of antioxidative(anti aging) enzyme in D-galactose induced aging rat.

• Journal of Life Science
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• v.20 no.11
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• pp.1595-1602
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• 2010

Oxidation of low density lipoprotein (LDL) has been recognized as an important role in the initiation and progression of atherosclerosis. In this study, effects of allylmercaptan, a major metabolite compound of garlic, was studied on endothelial cell injury induced by oxidized low density lipoprotein (ox-LDL). The antioxidative activity of allylmercaptan was investigated by monitoring a thiobarbituric acid substance (TBARS). Allylmercaptan inhibited LDL oxidation induced by $Cu^{2+}$ at concentrations of 0.1, 1 and 10 mM in a dose dependent manner. Lactate dehydrogenase (LDH) release, as an index of cell injury, and intracellular glutathione levels were determined. Pulmonary artery endothelial cells were preincubated with allylmercaptan at $37^{\circ}C$ and 5% $CO_2$ for 24 hr, washed, and then exposed to 0.1 mg/ml oxidized LDL for 24 hr. Preincubation of endothelial cells with allylmercaptan significantly prevented the LDH release and depletion of GSH. Peroxides were measured directly in 24 well plates using a fluorometric assay. Allylmercaptan inhibited release of peroxides induced by ox-LDL in pulmonary artery endothelial cells. In a free system, allylmercaptan was shown to scavenge hydrogen peroxide. The data indicate that allylmercaptan can protect pulmonary artery endothelial cells from injury caused by oxidized LDL, and suggest that allylmercaptan may be useful for the prevention of atherosclerosis.

• Toxicological Research
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• v.29 no.3
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• pp.187-193
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• 2013

The effects of toluene in dimethylformamide (DMF)-induced hepatotoxicity were investigated with respect to the induction of cytochrome P-450 (CYP) and the activities of related enzymes. The rats were treated intraperitoneally with the organic solvents in olive oil (Single treatment groups: 450 [D1], 900 [D2], 1,800 [D3] mg DMF, and 346 mg toluene [T] per kg of body weight; Combined treatment groups: D1+T, D2+T, and D3+T) once a day for three days, while the control group received just the olive oil. Each group consisted of 4 rats. The activities of the xenobiotic metabolic enzymes and the hepatic morphology were assessed. The immunoblots indicated that the expression of CYP2E1 was considerably enhanced depending on the dosage of DMF and the CYP2E1 blot densities were significantly increased after treatment with both DMF and toluene, compared to treatment with DMF alone. The activities of glutathione-S-transferase and glutathione peroxidase were either decreased or remained unaltered after treatment with DMF and toluene, whereas the lipid peroxide levels were increased with increasing dosage of DMF and toluene. The liver tissue in the D3 group (1,800 mg/kg of DMF) showed signs of microvacuolation in the central vein region and a large necrotic zone around the central vein, in rats treated with both DMF (1,800 mg/kg) and toluene (D3T). These results suggest that the expression of CYP2E1 is induced by DMF and enhanced by toluene. These changes may have facilitated the accelerated formation of N-methylformamide (NMF) from toluene, and the generated NMF may directly induce liver damage.

• Journal of Life Science
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• v.9 no.4
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• pp.466-472
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• 1999

These studies were designed to investigate the effects of pine (Pinus densiflora Sieb et Zucc.) needle extract (PNE) on oxygen radicals and their scavenger enzymes in liver membranes of Sprague-Dawley (SD) rats as a study on investigation of anti-aging effect and determination of chemical structures of PNE through the animal experiments. Male SD rats were fed basic diets (control group) and experimental diets (0.5% and 1.0%-PNE group) for 6 weeks. There were no significant differences in hydroxyl radical (·OH) formations of liver mitochondria and microsomes in 0.5%-PNE group, while ·OH formations were significantly decreased (10% and 18%, respectively) in liver mitochondria and microsomes of 1.0%-PNE group compared with control group. Microsomal hydrogen peroxides and cytosolic superoxide radicals were remarkably decreased (20% and 20∼25%, respectively) in 0.5% and 1.0%-PNE groups compared with control group. Mn-SOD activities in mitochondria were significantly increased about 10% in 1.0%-PNE group, while Mn-SOD activities in mocrosomes were remarkably increased (16∼20%) in 0.5% and 1.0%-PNE groups compared with control group. There were no significant differences in Cu, Zn-SOD activities of liver cytosol in 0.5% and 1.0%-PNE groups, while glutathione peroxidase (GSHPx) and catalase (CAT) activities were significantly decreased (28∼30% and 15∼30%, respectively) in liver cytosols of 0.5% and 1.0%-PNE groups compared with control group. These results suggest that these PNE may play a effective role in a attenuating a oxygen radical formations and increasing a scavenger enzyme activities.

• Journal of Nutrition and Health
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• v.36 no.7
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• pp.675-683
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• 2003

This study investigated the effect of dietary $\beta$-carotene supplementation on lipid peroxidation and anti oxidative enzyme activity as indices of oxidative stress in diabetic rats. Fifty Sprague-Dawley male rats aging 7 weeks were used as experimental animals, which were divided into the non-diabetic control group and the diabetic group. The diabetic group received an intraperitoneal injection with streptozotocin to induce diabetes. Then the diabetic rats were divided into four dietary groups which contained different amounts of $\beta$-carotene; 0%, 0.002%, 0.02%, or 0.2% of the diet. The diabetic rats were fed the experimental diets and the non-diabetic rats were fed the basal diet without $\beta$-carotene supplementation for 2 weeks and then sacrificed. The diabetic group had a significantly higher blood glucose level than the non-diabetic group. However, blood glucose level were not significantly changed by the level of dietary $\beta$-carotene supplementation. Compared to the non-diabetic control group, the diabetic control group indicated a significant increase of plasma thiobarbituric acid reactive substance (TBARS). Liver TBARS level also tended to be higher in diabetic control group, although it was not significant. The $\beta$-carotene supplementation did not reduce plasma TBARS level. However, Liver TBARS level was significantly decreased when 0.02% or more $\beta$-carotene was supplemented in the diet. The liver lipofuscin level in the diabetic control group was higher than in the non-diabetic control group, but the effect of $\beta$-carotene supplementation did not show any differences. Superoxide dismutase activity was significantly lower in the diabetic group, but it was increased in groups receiving 0.02% or more $\beta$-carotene. Compared to the non-diabetic control group, lower activities of catalase and glutathione peroxidase were observed in the diabetic control group, although it was not significant. Catalase and glutathione peroxidase activities tended to increase as the levels of $\beta$-carotene supplementation increased, although it was not statistically significant. Therefore, it seems that dietary $\beta$-carotene supplementation might reduce diabetic complications by partly decreasing the lipid peroxidation and increasing the activity of antioxidative enzyme in diabetes.

• Biomolecules & Therapeutics
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• v.14 no.4
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• pp.226-234
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• 2006

Disturbance of antioxidant system is very common in chronic alcoholics and herbal or natural products with antioxidant activity have been used for its treatment. This study was to investigate the effect of Vitis vinifera extract(V), Schisandra chinensis extract(S), Taraxacum officinale extract(T), Gardenia jasminoides extract(G), Angelica acutiloba extract(A) and Paeonia japonica extract(P), and their combinations on the antioxidant and ethanol oxidation system. Male Sprague-Dawley rats were subjected to Lieber-DeCarli ethanol liquid diet(ED) and were then given different herbal extract mixtures for 6 weeks including VST(V 100+S 150+T 150mg/kg/day), VSG(V 100+S 150+G 150mg/kg/day), VTG(V 100+T 150+G 150mg/kg/day), and VAP(V 100+A 150+P 150mg/kg/day). When the activity of alcohol dehydrogenase(ADH) and acetaldehyde dehydrogenase(ALDH) were compared between ED only group and herbal extracts treatment group, the differences were statistically significant. Phase I and II(glutathione-S-transferase, phenol sulfatransferase) enzyme activities were found to be significantly higher in the VAT treatment group compared to the ED group. Herbal extracts not only repressed the ethanol-induced elevation of malondialdehyde level, but also protected against ethanol-induced decrease in glutathione content, glutathione reductase, glutathione peroxidase, catalase and superoxide dismutase activities. The administration of the herbal extracts was found to be effective in eliminating lipid-peroxides induced by long-term consumption of alcohol by activating various enzyme systems and physiological active compound formation system. After a chronic consumption of alcohol, Angelica Radix protected the liver via activating the ethanol-metabolism enzyme system, and Paeoniae Radix via activating the ethanol-metabolism enzyme and the phase I, II-metabolism enzyme system. Taraxaci Herba was also effective in liver protection via activating the ethanol-metabolism enzyme system and the phase I, II-metabolism enzyme system, Gardeniae Fructus via activating the phase II-metabolism enzyme system and the anti-oxidation system enzyme, and Schisandra Fructus and a grapestone via activating the anti-oxidation system. Our data suggest that these herbal extracts may be useful as a health functional food or new drug candidate for fatty liver and hepatotoxicity induced by chronic alcohol consumption.

• The Korean Journal of Physiology and Pharmacology
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• v.26 no.4
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• pp.263-275
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• 2022

There is a paucity of detailed data related to the effect of senescence on the mitochondrial antioxidant capacity and redox state of senescent human cells. Activities of TCA cycle enzymes, respiratory chain complexes, hydrogen peroxide (H₂O₂), superoxide anions (SA), lipid peroxides (LPO), protein carbonyl content (PCC), thioredoxin reductase 2 (TrxR2), superoxide dismutase 2 (SOD2), glutathione peroxidase 1 (GPx1), glutathione reductase (GR), reduced glutathione (GSH), and oxidized glutathione (GSSG), along with levels of nicotinamide cofactors and ATP content were measured in young and senescent human foreskin fibroblasts. Primary and senescent cultures were biochemically identified by monitoring the augmented cellular activities of key glycolytic enzymes including phosphofructokinase, lactate dehydrogenase, and glycogen phosphorylase, and accumulation of H₂O₂, SA, LPO, PCC, and GSSG. Citrate synthase, aconitase, α-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, isocitrate dehydrogenase, and complex I-III, II-III, and IV activities were significantly diminished in P25 and P35 cells compared to P5 cells. This was accompanied by significant accumulation of mitochondrial H₂O₂, SA, LPO, and PCC, along with increased transcriptional and enzymatic activities of TrxR2, SOD2, GPx1, and GR. Notably, the GSH/GSSG ratio was significantly reduced whereas NAD⁺/NADH and NADP⁺/NADPH ratios were significantly elevated. Metabolic exhaustion was also evident in senescent cells underscored by the severely diminished ATP/ADP ratio. Profound oxidative stress may contribute, at least in part, to senescence pointing at a potential protective role of antioxidants in aging-associated disease.

• 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.

• Journal of Microbiology and Biotechnology
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• v.21 no.4
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• pp.400-404
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• 2011

Indomethacin is a nonsteroid anti-inflammatory agent that is known to induce severe gastric mucosal lesions. In this study, we investigated the effect of selenium on gastric mucosal lesions in rats. To confirm the curative effect of selenium against indomethacin-induced gastric ulcers, gastric ulcers were induced by oral administration of 25 mg/kg indomethacin, and then different doses (10, 50, and 100 ${\mu}g$/kg of body weight) of selenium or vehicle were treated by oral gavage for 3 days. Oral administration of indomethacin clearly increased the gastric ulcer area in the stomach, whereas selenium applied for 3 days significantly decreased the gastric ulcer area in a dose-dependent manner. In addition, selenium markedly reduced the increase of lipid peroxidation induced by indomethacin in the gastric mucosa and increased activities of radical scavenging enzymes such as superoxide dismutase, catalase, and glutathione peroxidase in a dose-dependent manner. These results reveal that selenium can heal indomethacin-induced gastric ulcers through elimination of the lipid peroxides and activation of radical scavenging enzymes.