• Journal of the Korean Society of Food Science and Nutrition
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• v.23 no.6
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• pp.899-907
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• 1994

Accumulation of peroxidized lipid, fed or injected in the body of rats was investigated and the effect of peroxidized lipid on the antioxidative system was studied also. Three groups each having six of Sprague-dawley rats were raised for 8 weeks. the peroxide value(POV) of diet fed to the control and the peroxidized group was 5.47 and 22.14meq/kg , respectively. Injected group was given the control diet and peroxidized linoleic acid(POV 31.81meq/kg) was injected into the peritoneal area three times a week. The POV, MDA, and protein carbonyl values of the peroxidized and the injected group (experimental groups) were significantly higher (p<0.05) than those of the control group. Cu, Zn-SOD and M-SOD activity of the experimentla groups increased 1.6 times that of control group at 4 th week. and decreased by 60% of their activityafter 8 weeks of feeding (p<0.05) . Catalase activity, glutathione and Vt, E contents of the experimental groups were significantly lower (p<0.05) than those of the control group during 8 weeks. The accumulation of peroxidcized lipid in liver were ovserved both in the fed or the injected group. The increased of enzyme activity of the experimental group during 4 weeks suggests ianadaptation of antioxidative system to get rid of the peroxidized lipid. Decrease of enzyme activity and glutathione observed as the peroxidized lipid lipid accumulation proceeded further, however, seems to indicate the oxdiative damage of enzyme and protein . Determination of the protein carbonyl content may be used as a method for measuring the oxidative damaging effect of peroxidized lipid.

• Environmental Analysis Health and Toxicology
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• v.28
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• pp.16.1-16.8
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• 2013

Objectives Fish vitellogenin (VTG) is produced in the female liver during oogenesis through the estradiol cycle and produced in the male liver by endocrine disrupting chemicals (EDCs) such as alkylphenols. In this study, we propose that the VTG concentration in the pale chub could be detected using monoclonal antibodies and polyclonal antibodies against vitellin (Vn) in a VTG enzyme-linked immunosorbent assay (ELISA) system. Methods Monoclonal antibodies and polyclonal antibodies were produced using the Vn extracted from the matured ovum of the ovary. The VTG was extracted from the plasma of the male pale chub. The Vn and VTG were confirmed by measuring the molecular weight of their proteins using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and the specificity of the antibodies was checked through western blotting methods. The assay system was validated with respect to optimal assay concentrations, specificity, recovery, and intra- and inter-assay variations. Results The Vn consisted of two protein bands with apparent molecular weights of 64 and 37 kDa. The SDS-PAGE indicated protein weights of 146 and 77 kDa in the VTG. The assay range was 15.6 ng/mL to 2,000 ng/mL, and the value of the intra- and inter-assay variations were within 10.0% and 14.7%, respectively. The recovery rate was $99.5{\pm}5.5%$. Conclusions A sandwich ELISA was developed that could be used to qualify the VTG of pale chub in screening for EDCs. Pale chub is an ideal species for observing estrogen activity in the environment because of its extensive habitat and extensive food chain. The ELISA developed here would be more favorable than those for other species for determining the effect of long-term food chain accumulation of EDCs in aquatic environments.

• The Korean Journal of Zoology
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• v.27 no.4
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• pp.221-230
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• 1984

The activities of aminopyrine demethylase which is marker enzyme of the microsomal drug-metabolizing system, NADPH-cytochrome a reductase and glutathione peroxidase were measured during the course of liver regeneration after about seventy percent hepatectomy in Wistar rats. In addition, the extent of lipid peroxidation and contents of cytochrome P-450 were also measured. Partial hepatectomy produced a significant depression in aminopyrine demethylase, to reach a minium about 24 hours after operation, but this activity was increased to normal value during regeneration. On the other hand, in sham-operated animals, this showed no change. All the activities of NADPH-chrome P-450 contents of liver microsomes were rapidly decreased at the early stage of regeneration. These values returned to normal after 7 days. By contrast, the activity of glutathione peroxidase was nearly unchanged. According to these results, at the early stage of regeneration, the decrease of cytochrome P-450 and NADPH-cytochrome c reductase activity lead to decrease of lipid peroxidation and drug metabolizing enzyme activity. But these phenomena were not detected after 7 days of regeneration.

• Journal of Korean Physical Therapy Science
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• v.8 no.1
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• pp.923-934
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• 2001

In order to investigate a pathogenesis of liver damage induced by skin burn, thermal injury was induced by scald burn on entirely dorsal surface in rats (total body surface area 30%) except for inhalated injury. At 5 and 24 h after scald bum, biochemical assay and morphological changes in skin tissue, serum and liver tissue were examined. The effects of bum injury on the levels of glutathione, lipid peroxide and on the activities of oxygen free radical generating and scavenging enzymes have been determined in association with observing of histologic and ultrastructural changes, measuring the protein concentration in plasma, and counting the number of intravascular polymorphonuclear leukocytes. The activity of xanthine oxidase, an enzyme of oxygen free radical generating system. was elevated (p<0.01) in serum, but not in skin and in liver tissue. Futhermore, thermal injury decreased not only the protein concentration in plasma but also the number of leukocytes, that indicates induction of edema formation with protein exudation and inflammation by neutrophil infiltration into the internal organs. These data suggest that acute dermal scald burn injury leads to liver damage, that is related to elevation of xanthine oxidase activity in serum. Xanthine oxidase may be a key role in the pathogenesis of liver damage induced by skin burn.

• Advances in Traditional Medicine
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• v.7 no.3
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• pp.311-320
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• 2007

The present study was designed to estimate the protective effect of (-) epigallocatechin gallate (EGCG) on ethanol-induced liver injury in rats. Chronic ethanol administration (6 g/kg/day ${\times}$ 60 days) caused liver damage that was manifested by the elevation of markers of liver dysfunction - aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, bilirubin and ${\gamma}$-glutamyl transferase in plasma and reduction in liver glycogen. The activities of alcohol metabolizing enzymes such as alcohol dehydrogenase and aldehyde dehydrogenase were found to be altered in alcohol-treated group. Ethanol administration resulted in the induction of cytochrome p450 and cytochrome-$b_{5}$ activities and reduction of cytochrome-c reductase and glutathione-S-transferase, a phase II drug metabolizing enzyme. Further, ethanol reduced the viability of isolated hepatocytes (ex vivo) as assessed by trypan blue exclusion test and induced hepatocyte apoptosis as assessed by propidium iodide staining. Treatment of alcoholic rats with EGCG restored the levels of markers of liver injury and mitigated the alterations in alcohol metabolizing and drug metabolizing enzymes and cyt-c-reductase. Increased hepatocyte viability and reduced apoptotic nuclei were observed in alcohol + EGCG-treated rats. These findings suggest that EGCG acts as a hepatoprotective agent against alcoholic liver injury.

• Toxicological Research
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• v.19 no.2
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• pp.105-114
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• 2003

TO evaluate an effect of cyclohexane treatment on the degree of liver damage, rats were induced liver damage with 10 or 17 times $CCl_4$ injection (0.1 m1/100 g body wt., 50% $CCl_4$ dis-solved in olive oil) at intervals of every other day. Cyclohexane (1.56 g/kg body wt., i.p.) was administrated to the animals at 48 hours after the last pretreatment of $CCl_4$ . Rats were sacrificed at 4 hours after injection of cyclohexane. On the basis of histopathological findings, liver weight/body weight (LW/ BW, %), activities of serum alanine aminotransferase (ALT), xanthine oxidase (XO) and akaline phosphatase (ALP), and contents of liver protein and manlondialdehyde (MDA), $CCl_4$ -pretreatment induced liver damage. And $CCl_4$ 17 times treated group showed more severe liver damage than $CCl_4$ 10 times treated group. Administration of one dose of cyclohexane to $CCl_4$ 10 times treated animals resulted in the enhanced liver damage; liver necrosis with proliferation of fibroblast and bile duct abnormality, and increase in hepatic MDA content and the activities of serum ALP and ALT, But the enhanced liver damage was not found in $CCl_4$ 17 times treated animals. Serum cyclohexanone concentrations at 4 or 8 hours after injection of cyclohexane were higher in all liver damaged groups than normal group and were somewhat higher In $CCl_4$ 17 times treated animals than $CCl_4$ 10 times treated ones. Among the oxygen free radical metabolizing enzymes, hepatic cytochrome P45O dependent aniline hydroxylase (CYPdAH) activity in cyclohexane metabolizing enzyme system was meaningfully increased by the injection of cyclohexane to the liver damaged rats, with increased Vmax and high affinity to aniline. LW/BW (%) and activities of serum XO and ALT were more significantly increased in liver damaged groups than normal group by administration of cyclohexanone. In conclusion, it is assumed that an enhancement of liver damage by injection of one dose of cyclohexane to liver damaged animals might be caused by oxygen free radicals and cyclohexanone.

• Herbal Formula Science
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• v.10 no.2
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• pp.85-95
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• 2002

Objectives: In traditional medicine, Wolgukwhan has been used for the treatment of digestive system disease, such as indigestion, brash, ructation, nausea and vomiting. This study was purposed to investigate the effects of Wolgukwhan methnol extract (WGWM) on oxidative liver cell injury. Methods: In vivo assay, we administerated acetaminophen(500mg/kg, i.p.) to starved mice 24hrs after pretreatment of WGWM for 6days. In the liver homogenates, lipid peroxide and glutathione(GSH) levels were measured. In addition, activities of hepatic enzyme, such as catalase, glutathione peroxidase(GPX), glutathione S-transferase(GST) were measured in the hepatic mitochondrial and cytosolic fractions. Results: In vivo administeration of WGWM showed effective inhibition of acetaminophen induced lipid peroxidation and elevations of glutathione level. The acetaminophen treatment resulted in a decrease of catalase, GPX and GST activities. By contrast, WGWM pretreatment increased compare to those of untreated groups. Conclusions: These results suggested that WGWM might protect against lipid peroxidation by free radicals, destruction of hepatic cell membranes.

• Herbal Formula Science
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• v.11 no.2
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• pp.135-146
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• 2003

Objectives : Wolguk-whan has been used as a prescription of natural drug for the treatment of stress digestive system disease. Recently, we reported that Wolguk-whan methnol extract (WGWM) exerted a significant protective effect against oxidative damage to the liver of ICR mice. This study was purposed to investigate the effects of Wolguk-whan water extract (WGWW) on liver injury induced by oxidative stress. Methods : In order to investigate the effects of WGWW on acute liver injury, ICR mice were pretreated with WGWW for 6days, starved for 24hrs, and administerated acetamirtophen(500mg/kg, i.p.). In the liver homogenates, lipid peroxide and glutathione(GSH) levels were measured. In addition, activities of hepatic enzyme, such as catalase, glutathione peroxidase(GSH-Px), glutathione S-transferase(GST) were measured in the hepatic mitochondrial and cytosolic fractions. Results : In vivo administeration of WGWW showed effective inhibition of acetaminophen induced lipid peroxidation, and showed elevations of GSH level, catalase, GSH-Px, GST activities. Conclusions : These results suggested that WGWW might suppress the formation of oxidative metabolites, and prevent acetaminophen induced hepatotoxicity.

• Journal of the Korean Society of Food Science and Nutrition
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• v.22 no.6
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• pp.678-684
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• 1993

To evaluate the role of xanthine oxidase in liver damage by CCl4, a group of rats were fed tungstate for a month, which suppressed the activities of xanthine oxidase in serum and liver. Control group of rats were fed standard diet without tungstate. Liver damage was induced both in tungstate fed and control groups by two intraperitoneal injections of CCl4 at the level of 0.1ml/100g body weight at intervals of 24 hours. Increases in the levels of serum alanine aminotransferase by CCl4 were significantly smaller in tungstate fed rats than in control rats. Concomitantly, histopathologic changes were less in tungstate fed rats than in control ones. In rats either treated with CCl4 or not, hepatic type O xanthine oxidase activities were remarkably reduced by tungstate feeding. Hepatic aniline hydroxylase activities were higher in rats fed tungstate than control rats when animals were not treated with CCl4, but the enzyme activities were lower in tungstate fed rats than control when they were treated with CCl4. Neither tungstate feeding nor CCl4 treatment caused any significant changes in hepatic glutathione contents, and activities of hepatic glutathione S-transferase, glutathione peroxidase and superoxide dismutase. It is concluded xanthine oxidase reaction augment CCl4 induced liver damage via oxygen free radical system.

• Toxicological Research
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• v.11 no.2
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• pp.247-252
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• 1995

To evaluate the effect of xanthine oxidase on liver injury by $CCl_4$, liver damage was induced both in allopurinol pretreated rats (500 mg/kg. ip) and control group by twice intraperitoneal injection of $CCl_4$ (0.1 ml/100 g body wt. 50% in olive oil) at interval of one day. Increases in the levels of serum alanine aminotransferase and liver weight/body weight (%) by $CCl_4$ were significantly smaller inallopurinol pretreated rats than in control whereas the hepatic microsomal glucose-6-pholphatase activities were significantly higher in allopurinol pretreated rats than control group by $CCl_4$ treatment. These results indicates that allopurinol pretreatment may reduce the liver damage in $CCl_4$ intoxicated rats. In rats either with $CCl_4$or not, hepatic type O xanthine oxidase activities were significantly reduced by allopurinol pretreatment and the increasing rate of these enzymes to each control was remarkably lower in allopurinol pretreated rats than control. Liver cytosolic protein contents and aniline hydroxylase, aminopyrine demethylase activities were higher in allopurinol pretreated rats than coirol rats when animals were treated with $CCl_4$. On the other hand, neither allopurinol pretreated nor $CCl_4$ treatment caused any significant changes in hepatic superoxide dismutase and catalase activities. Hepatic glutathione contents were higher in $CCl_4$-treated rats than control, but no significant changes were found in both between the allopurinol treated rats and $CCl_4$-treated rats pretreated with allopurinol, and glutathione and glutathione S-transferase activities were significantly reduced in $CCl_4$-treated rats than control whereas these enzyme activities showed on significant change in both between allopurinel treated and $CCl_4$-treated rats pretreated with allopurinol. It is concluded that xanthine oxidase reaction system augment $CCl_4$ induced liver injury via even oxygen free radical system.