• Journal of Environmental Health Sciences
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• v.19 no.2
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• pp.69-77
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• 1993

In the present study, the comparison of liver damage in carbon tetrachloride (CCl$_4$)-treated rats with that those pretreated with ethanol and an effect of liver injury on the serum and liver xanthine oxidase (XOD) activity were evaluated. The increasing rate of liver weight per body wt., the levels of serum alanine aminotransferase, and the decreasing rate of hepatic glucose-6-phosphatase activity and the protein contents in the liver cell were higher in carbon tetrachloride-treated animals pretreated with ethanol than the carbon tetrachloride-treated group. Especially, the histopathological findings also showed more severe liver damage in the ethanol-pretreated rats than the rats treated with carbon tetrachloride only. In such a experimental condition the xanthine oxidase activity of serum and liver both of carbon tetrachloride-treated rats and those pretreated with ethanol were higher than that of each control group. And the increasing rate of xanthine oxidase enzyme activity to the control group was higher in carbon tetrachloride-treated group pretreated with ethanol than those treated with CCl$_4$. In addition, the heptic uricase activity and the serum levels of uric acid were more increased in carbon tetrachloride-treated group pretreated with ethanol than those in the CCl$_4$-treated rats. On the other hand, there were no statistical differences in hepatic catalase and glutathione S-transferase activities between the CCl$_4$-treated rats and those pretreated with ethanol. In conclusion, it is assumed that the more severe liver damage in ethanol pretreated rats would be due to oxygen free radical produced by the xanthine oxidase system.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.3
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• pp.269-278
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• 2014

Various antiepileptic drugs (AEDs) especially enzyme-inducing AEDs might be associated with increased vascular risk, through impairment of the endogenous antioxidative ability which may trigger oxygen-dependent tissue injury. Lamotrigine (LTG) a non-enzyme-inducing AED has scarce information regarding its effects on oxidative stress. The present study aimed to study the possible modulation of vascular risk factors of epileptogenesis by LTG, in a rat model of kindling seizure induced by pentylenetetrazole (PTZ). Four groups of male Wister rats were used; vehicle control group, PTZ group (alternate day PTZ, 30 mg/kg, i.p), LTG/PTZ group (LTG 20 mg/kg/day p.o and alternate day PTZ) and LTG group. The study period was 5 weeks. Lipoproteins and total homocysteine (tHcy), malondialdehyde (MDA) and reduced glutathione (GSH) were measured. Aortic endothelial function study and histopathological examination of the rats' brains, aortas and coronaries were conducted. Serum total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C), tHcy, MDA, GSH levels were significantly higher in epileptic rats than normal controls rats. A decrease in HDL-cholesterol with high atherosclerotic index was also demonstrated. The administration of LTG improved the PTZ-kindled seizures. It produced a significant decrease in TC, TG and LDL-cholesterol, MDA, aortic GSH and increase in HDL-cholesterol with no significant effect on serum GSH and tHcy levels. LTG improved endothelium-dependent relaxation, decreased hippocampal neurodegenerative changes and atherosclerotic changes of aortas and coronaries. LTG decreased seizures severity, hippocampal damage and improved vascular risk markers in this rat model of kindling seizures.

• Biomolecules & Therapeutics
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• v.6 no.3
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• pp.247-255
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• 1998

Carbon tetrachloride (CCI$_4$) induces the hepatotoxicity due to the reactive free radicals generated by cytochrome P-450 (CYP-450) enzyme, which result in destabilization of cellular membrane. Diltiazem, a calcium channel blocking agent, has been known to suppress the CYP-450 enzyme activities. To study the effect of diltiazem in $CCl_4$-treated rats, we measured the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and glutathione S-transferase (GST), contents of bilirubin, albumin, total protein, cholesterol, triglyceride, blood urea nitrogen, creatinine malondialdehyde and calcium. Also we conducted liver histopathologic examinations. Diltiazem, when administered 1 hour prior to CCI$_4$ treaeent, significantly reduced the activities of ALT and AST, the contents of microsomal malondialdehyde and calcium in liver and microsome as compared with those of $CCl_4$-treated rats. In addition, histopathologic examination showed that diltiazem prevented the development of centrilobular necrosis induced by CCI$_4$ in liver tissue. Our results suggested that diltiazem could inhibit the formation of free radicals and the influx of calcium. Therefore diltiazem may be applied to suppress the liver damage caused by $CCl_4$.

• Biomolecules & Therapeutics
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• v.20 no.5
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• pp.492-498
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• 2012

Phytochemicals have been known to exhibit potent antioxidant activity. This study examined cytoprotective effects of phytochemicals including quercetin, catechin, caffeic acid, and phytic acid against oxidative damage in SK-Hep-1 cells induced by the oxidative and non-oxidative metabolism of ethanol. Exposure of the cells to excess ethanol resulted in a significant increase in cytotoxicity, reactive oxygen species (ROS) production, lipid hydroperoxide (LPO), and antioxidant enzyme activity. Excess ethanol also caused a reduction in mitochondrial membrane potential (MMP) and the quantity of reduced glutathione (GSH). Co-treatment of cells with ethanol and quercetin, catechin, caffeic acid and phytic acid significantly inhibited oxidative ethanol metabolism-induced cytotoxicity by blocking ROS production. When the cells were treated with ethanol after pretreatment of 4-methylpyrazole (4-MP), increased cytotoxicity, ROS production, antioxidant enzyme activity, and loss of MMP were observed. The addition of quercetin, catechin, caffeic acid and phytic acid to these cells showed suppression of non-oxidative ethanol metabolism-induced cytotoxicity, similar to oxidative ethanol metabolism. These results suggest that quercetin, catechin, caffeic acid and phytic acid have protective effects against ethanol metabolism-induced oxidative insult in SK-Hep-1 cells by blocking ROS production and elevating antioxidant potentials.

• Biomolecules & Therapeutics
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• v.20 no.2
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• pp.201-206
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• 2012

Ultraviolet (UV) A penetrates deeply into the skin and induces the generation of reactive oxygen species (ROS) causing damage to fibroblasts, which leads to aging of the skin. However, the body has developed an antioxidant defence system against the harmful effects of ROS. Enzymes such as superoxide dismutase (SOD) and catalase (CAT) play critical roles on the removal of excess ROS in living organisms. In this study, the antioxidant activities of anthocyanins (cyanidin 3-galactoside and cyanidin 3-lathyroside) from Acanthopanax divaricatus var. albeofructus (ADA) fruits were investigated by xylenol orange, thiobarbituric acid reactive substances (TBARS), and antioxidant enzyme assay. As a result, generation of $H_2O_2$ and lipid peroxide induced by UVA-irradiation in human dermal fibroblast (HDF-N) cells was reduced by treatment of anthocyanins. Also, augmented enzyme (SOD and CAT) activities were observed in UVA-irradiated cells when treated with anthocyanin. In conclusion, the results obtained show that anthocyanins from ADA fruits are potential candidates for the protection of fibroblast against the damaging effects of UVA irradiation. Furthermore, anthocyanin may be a good candidate for antioxidant agent development.

• Journal of Radiation Industry
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• v.8 no.1
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• pp.35-42
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• 2014

This study was conducted to analyze the protective capacity of cyanidin-3-glucoside (C3G), which is rich in mulberry and blackberry as an anthocyanin pigment. In this study, we found that treatment with C3G significantly reduced ROS production in hydrogen peroxide $(H_2O_2)-treated$ HepG2 cells in a dose-dependent manner. In addition, treatment with C3G significantly increased the cell viability in a dose-dependent manner in $H_2O_2-treated$ HepG2 cells. Moreover, treatment with C3G dose-dependently decreased the release of LDH and activation of caspase-3 in HepG2 cells treated with $H_2O_2$. Furthermore, the DNA damage in $H_2O_2-treated$ HepG2 cells was decreased by C3G treatment when compared with the control group in a dose-dependent manner. Additionally, treatment with C3G recovered the activity of antioxidant enzymes such as superoxide dismutase and catalase in $H_2O_2-treated$ HepG2 cells. To summarize, these results suggest that C3G protects cells from $H_2O_2-induced$ oxidative damage by activating antioxidant enzymes.

• Korean Journal of Acupuncture
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• v.29 no.1
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• pp.131-141
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• 2012

Objectives : This study was performed to investigate the effect of invasive laser acupuncture treatment at Liver Brook (LR2) acupoint and Liver Sea (LR8) acupoint on liver damage induced by D-galactosamine (D-GalN) in rats Methods : Liver damage was induced by D-GalN. The experimental rats were divided into two groups (control group, Low Level Laser Treatment (LLLT) group). Control groups were classified into small groups. Intact group had no liver damage and no treatment. D-GalN group was induced liver damage induced by D-GalN and not treated. LLLT group were induced liver damage induced by D-GalN and then treated at the LR2 or LR8 acupoint with 532, 658, 904 nm invasive laser acupuncture. The treatment was carried out three days at a time for 15days at both acupoints. To examine mechanism of the effect of invasive laser acupuncture, we measured the contents of ASP, ALT, ALP, TBIL in serum, CBC in blood and SOD in liver tissue. Results : The change of body weight increased in all groups. That change was AST and ALP, the AST activity decreased significantly compared with the control groups and decreased by 532 nm and 904 nm both LLLT groups. But ALP increased at LR8 acupoint by 658 nm. TBIL level significantly decreased in all LLLT groups. The SOD of LLLT groups increased in the liver tissue of rats compared to the control groups. SOD activity indicated that LLLT can help cellular defense mechanism by preventing scavenging hydrogen peroxide. In the change of WBC, it was increased in D-GalN Control group compared to intact group and LLLT groups. Conclusions : These results suggested that invasive laser acupuncture treatment at LR2 or LR8 acupoint reduced activation of hepatic enzyme and damage of liver tissue. Thus, the effect of invasive laser acupuncture was nearly identical to the way of the traditional acupuncture for the treatment of hepatocytotoxicity.

• Journal of Nutrition and Health
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• v.44 no.5
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• pp.366-377
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• 2011

Glutathione S-transferase (GST) is a multigene family of phase II detoxifying enzymes that metabolize a wide range of exogenous and endogenous electrophilic compounds. GSTM1 and GSTT1 gene polymorphisms may account for inter-individual variability in coping with oxidative stress. We investigated the relationships between the level of lymphocyte DNA and antioxidative parameters and the effect on GST genotypes. GSTM1 and GSTT1 were characterized in 301 young healthy Korean adults and compared with oxidative stress parameters such as the level of lymphocyte DNA, plasma antioxidant vitamins, and erythrocyte antioxidant enzymes in smokers and non smokers. GST genotype, degree of DNA damage in lymphocytes, erythrocyte activities of superoxide dismutase, catalase, and glutathione peroxidase (GSH-Px), and plasma concentrations of total radical-trapping antioxidant potential (TRAP), vitamin C, ${\alpha}$- and ${\gamma}$-tocopherol, ${\alpha}$- and ${\beta}$-carotene, and cryptoxanthin were analyzed. Lymphocyte DNA damage assessed by the comet assay was higher in smokers than that in non-smokers, but the levels of plasma vitamin C, ${\beta}$-carotene, TRAP, erythrocyte catalase, and GSH-Px were lower than those of non-smokers (p < 0.05). Lymphocyte DNA damage was higher in subjects with the GSTM1- or GSTT1-present genotype than those with the GSTM1-present or GSTT1- genotype. No difference in erythrocyte antioxidant enzyme activities, plasma TRAP, or vitamin levels was observed in subjects with the GSTM1 or GSTT1 genotypes, except ${\beta}$-carotene. Significant negative correlations were observed between lymphocyte DNA damage and plasma levels of TRAP and erythrocyte activities of catalase and GSH-Px after adjusting for smoking pack-years. Negative correlations were observed between plasma vitamin C and lymphocyte DNA damage only in individuals with the GSTM1-present or GSTT1- genotype. The interesting finding was the significant positive correlations between lymphocyte DNA damage and plasma levels of ${\alpha}$-carotene, ${\beta}$-carotene, and cryptoxanthin. In conclusion, the GSTM1- and GSTT1-present genotypes as well as smoking aggravated antioxidant status through lymphocyte DNA damage. This finding confirms that GST polymorphisms could be important determinants of antioxidant status in young smoking and non-smoking adults. Consequently, the protective effect of supplemental antioxidants on DNA damage in individuals carrying the GSTM1- or GSTT1-present genotypes might show significantly higher values than expected.

• Biomedical Science Letters
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• v.12 no.3
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• pp.281-287
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• 2006

Cigarette smoke causes atypical structure of pulmonary and oxidative damage. Therefore, we carried out to determine if exposure to cigarette smoke alters pulmonary structure and anti-oxidant related enzyme in a animal model, when natural product extracts using by Nebulizer. The rat were divided into four groups: $H_2O-treated$ (Control), natural product (Camellia sinensis) extracts-treated (CS), natural product extracts-treated with cigarette smoke-exposed (CS+SM) and cigarette smoke-expose (SM). All groups are similar to Control group in weight, but SM group is lower than the other groups. Microscopic image of the pulmonary structure in SM group showed deleterious alterations in the morphology, but the other groups are maintained in normal structure. In anti-oxidant related enzymes, SOD (superoxide dismutase) and catalase, SM group represents the lowest enzyme activity among all groups. But G6PD (glucose-6-phosphate dehydrogenase) and LPO (lipid peroxidation) is SM group represents the highest enzyme activity among all groups. These result indicate that the natural product extracts is an efficient tissue protective substance against smoke-induced lung injury.

• Journal of the Korean Society of Food Science and Nutrition
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• v.12 no.2
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• pp.84-92
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• 1983

In order to investigate the effect of autoxidized oil on the enzyme activity in the mouse liver, we administered the fixed dosage of autoxidized methyl linoleate (AOML) to mice once per day for 20 days by using stomach tube and investigated the enzyme activity with the histochemical staining method and biochemical analysis. The following results were obtained: The POV, COV and TBA value in the liver of AOML group were significantly increased than those of normal group. The phospholipid, triglyceride and total cholesterol in the liver of AOML group were slightly increased than those of normal group. The activities of acid phosphatase and alkaline phosphatase in the liver of AOML group were increased than those of normal group but ATPase activity was decreased in the AOML group. The decrease of RNA, accumulation of fat and damage of liver cells were observed as the morphological changes in the liver of AOML group. From the results obtained we conclude that the autoxidized methyl linoleate influenced upon the various enzyme activity and the morphological changes in the mouse liver.