• Biomedical Science Letters
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• v.5 no.2
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• pp.201-208
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• 1999

To evaluate an effect of growth periods on the bromobenzene-induced liver damage, bromobenzene was administrated to 5-week-old rats and 10-week-old rats pretreated with bromobenzene 5 times every other day for 10 days and then the animals were sacrificed. The results were obtained as follows; The increasing rate of serum levels of alanine aminotransferase, xanthine oxidase activity, hepatic lipid peroxide contents, liver weight per body weight (％) and decreasing rate of hepatic contents of protein to each control group were higher in 10-week-old rats than 5-week-old rats by the pretreatment of bromobenzene. According to the above results, 10-week-old rats indicated more severe liver injury than 5-week-old those in case of bromobenzene pretreatment. On the other hand, hepatic aniline hydroxylase activity was more increased in 10-week-old rats than 5-week-old rats both in control and bromobnezene pretreated rats where as the reverse in hepatic glutathione S-transferase. In case of hepatic GSH determination at the intervals of 2, 4, 8, 24 hours throughout 24 hr after administration of single dose of bromobenzene to 5-week-old and 10-week-old rats both in control and bromobnezene pretreated, the rate of GSH utilization was lower in 10-week-old rats than 5-week-old rats. In conclusion, from the above experimental, it is deduce that the 10-week-old rats showed more severe liver injury than 5-week-old rats by the bromobenzene treatment because the disposal ability of bromobenzene in liver was lower in 10-week-old rats than 5-week-old rats.

• 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.

• Food Science and Biotechnology
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• v.15 no.6
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• pp.833-837
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• 2006

To determine whether alcohol-treated rat liver cells can be protected by a static magnetic field (SMF), we analyzed the blood chemistry and histology of hepatic tissue removed from alcohol-exposed rats that had been exposed to a static magnetic field. The rats were exposed to a 0.3 tesla (3,000 gauss) magnetic field (MF) for 24 hr daily for 5 weeks with appropriate controls. Glutamic pyruvic transaminase activity and the triglyceride levels in animals exposed to the north (N) or south (S) pole of the MF decreased significantly (p<0.01 and p<0.05, respectively) compared with negative control animals with alcohol exposure. A histological examination of hepatic tissue revealed a moderate to severe accumulation of fat vacuoles of various sizes in the cytoplasm of the hepatocytes of animals in the negative control group throughout the study; whereas in groups exposed to the MF poles, fewer fat vacuoles were seen compared with the negative control group. Electron microscopic observations showed that exposure to the N or S pole protected organelles, including the nucleus, from damage during exposure to this toxic agent, as indicated by the fact that the nucleus and the mithochondria virtually retained their shape throughout this study. These results suggest that exposure to a SMF could be an excellent way of protecting against alcohol-induced damage to the rat liver cell.

• The Korean Journal of Nuclear Medicine
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• v.5 no.2
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• pp.19-40
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• 1971

Since the iron balance is maintained by regulated intestinal absorption rather than regulated excretion, there have been many reports concerning the factors which may influence the intestinal iron absorption. As the liver is the largest iron storage organ of the body, any hepatocellular damage may result in disturbances in iron metabolism, e,g., frequent co-existence of hemochromatosis and liver cirrhosis, or elevated serum iron level and increased iron absorption rate in patients with infectious hepatitis or cirrhosis. In one effort to demonstrate the influence of hepatocellular damage on intestinal iron absortion, the iron absorption rate was measured in the rabbits whose livers were injured by a single subcutaneous injection of carbon tetrachloride (doses ranging from 0.15 to 0.5cc per kg of body weight) or by a single irradiation of 2,000 to 16,000 rads with $^{60}Co$ on the liver locally. A single oral dose of $1{\mu}Ci\;of\;^{59}Fe$-citrate with 0.5mg of ferrous citrate was fed in the fasting state, 24 hours after hepatic damage had been induced, without any reducing or chelating agents, and stool was collected for one week thereafter. Serum iron levels, together with conventional liver function tests, were measured at 24, 48, 72, 120 and 168 hours after liver damage had been induced. All animals were sacrificed upon the completing of the one week's test period and tissue specimens were prepared for H-E and Gomori's iron stain. Following are the results. 1. Normal iron absorption rate of the rabbit was $41.72{\pm}3.61%$ when 0.5mg of iron was given in the fasting state, as measured by subtracting the amount recovered in stool collected for 7 days from the amount given. The test period of 7 days is adequate, for only 1% of the iron given was excreted thereafter. 2. The intestinal iron absorption rate and serum iron level were significantly increased when the animal was poisoned by a single subcutaneous injection of 0.15cc. per kg. of body weight of carbon tetrachloride or more, or the liver was irradiated with a single dose of 12,000 rads or more. The results of liver function tests which were done simultaneously remained within normal limit except SGOT and SGPT which were somewhat increased. 3. In each case, there has been good correlation between the extent of liver cell damage and degree of increased iron absorption rate or serum iron level. 4. The method of liver damage appeared to make no obvious difference in the pattern of iron deposit in liver. This may be partly due to the fact that tissue specimens were obtained too late, for by this time the elevated serum iron level had returned within normal range and the pathological changes were almost healed. 5. The possible factors and relationship between intestinal iron absorption and hepatic parenchymal cell damage has been discussed.

• Journal of the Korean Society of Food Science and Nutrition
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• v.31 no.1
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• pp.81-86
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• 2002

The present study was conducted to investigate the effect of dietary supplementation of vitamin A or $\beta$-carotene on oxidative damage induced by acute ethanol administration. Sprague-Dawley rats were fed on the experimental diets supplemented with retinyl acetate (2.86 mg/kg diet) or $\beta$-carotene (15.2 mg/kg diet) for 5 weeks. After fed the diet, rats were administered 20% ethanol solution (3g/kg B.W.) acutely. Lipid peroxide values in hepatic tissue, hepatic antioxidative enzyme activities and contents of antioxidative nutrient such as vitamins A and E in serum and hepatic tissue were measured. Hepatic level of malondialdehyde decreased in $\beta$-carotene group compared to the control group. However, there was no significant difference between retinal acetate and $\beta$-carotene groups. Superoxide dismutase activity was higher in retinal acetate group than in the control group. Hepatic glutathione-S-transferase activity of retinal acetate and $\beta$-carotene groups significantly decreased as compared with that of control group. The hepatic content of retinol increased in retinal acetate and $\beta$-carotene groups, especially, in retinyl acetate group. But there was no significant difference in serum content of retinol among the groups. Hepatic content of $\alpha$-tocopherol was significantly increased in retinyl acetate and $\beta$-carotene groups. In conclusion, acute ethanol administration might induce lipid peroxidation, and the dietary supplementation of retinyl acetate or $\beta$-carotene improve partly the antioxidative system through activation of superoxide dismutase and retention of hepatic $\alpha$-tocopherol in ethanol-treated rats.

• Biomedical Science Letters
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• v.7 no.2
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• pp.79-83
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• 2001

To evaluate an effect of toluene application to skin on the enhancement of liver damage in $CCl_4$-pretreated rats, toluene (35 mg/$cm^2$) was sequentially applied for 5 days to the skin of liver damaged rats with $CCl_4$ (6 times every other day: 0.1 ml/100 g body weight-50% $CCl_4$ in olive oil) On the basis of the functional and morphological findings in rat liver, appling toluene to the skin in liver damaged animals led to the more enhanced liver damage. In addition, by applying toluene to skin of liver damaged rats, the hepatic cytochrome P450 content was somewhat more increased, but the hepatic benzylalcohol dehydrogenase activity was significantly decreased (P<0.001), whereas benzaldehyde dehydrogenase activity was not statistically changed. In conclusion, the toluene application to skin in liver-damaged rat led to enhancement of liver injury that may be due to the accumulation of toluene metabolite in liver.

• Proceedings of the Korean Society of Veterinary Clinics Conference
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• 2009.10a
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• pp.253-253
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• 2009

• Journal of the East Asian Society of Dietary Life
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• v.5 no.3
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• pp.385-394
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• 1995

Our previous reports on the effect of dietary protein on methanethiol, ethacrynic acid, bromobenzene and carbon tetrachloride metabolism were overall reviewed. The methanethiol, ethacrynicacid and bromobenzene treated rats showed the more severe liver damage in those fed a low protein diet than those fed a standard protein diet. These xenobiotics treated rats showed the lower content of hepatic glutathione and its conjugated enzyme, glutathione S-transferase activities in those fed a low protein diet than those fed a standard protein diet. In case of carbon tetrachloride treated rats, the liver damage was more reduced in rats fed a low protein diet than those fed a standard protein diet. Concomitantly the hepatic cytochrome P-450 content, and its decreasing rate to the control were lower in rats fed a low protein diet than those fed a standard protein diet.

• Biomolecules & Therapeutics
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• v.16 no.1
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• pp.34-39
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• 2008

Oxidative stress may represent a common link between chronic liver damage and hepatic fibrosis. In the present study, we investigated activity changes of sphingomyelin catabolic enzymes, such as sphingomyelinases and ceramidases by using dimethylnitrosamine (DMN)-treated Sprague-Dawley (SD) male rats hepatic fibrosis model as a hepatic fibrosis model. Twenty rats divided into five groups received: (1) saline; (2) DMN for 1 week, (3) DMN for 2 weeks, (4) DMN for 3 weeks, and (5) DMN for 4 weeks by intraperitoneally 10 mg/kg of body weight for three consecutive days a week. Activities of acidic and neutral sphingomyelinases and acidic, neutral and alkaline ceramidases were measured in the liver and kidney from DMN-treated rats. We found increased ceramidase activities from 2-week and/or 3-week DMN treated rat livers compared to control rat liver. Acidic sphingomyelinase and alkaline ceramidase activities were significantly increased in 3-week DMN-treated rat kidneys compared to control rat kidney. Therefore, sphingolipid metabolizing enzymes and sphingolipid metabolites are supposed to be involved in liver fibrosis, although further investigation is necessary to elucidate meanings of sphingolipids during the liver fibrosis

• YAKHAK HOEJI
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• v.56 no.4
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• pp.260-267
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• 2012

This study examined the effects of baicalin, a bioactive flavonoid isolated from Scutellaria baicalensis, on hepatic injury caused by ischemia/reperfusion (I/R) in alcoholic fatty liver. Rats were fed an ethanol liquid diet or a control isocaloric diet for 5 weeks, and then subjected to 60 min of hepatic ischemia and 5 h of reperfusion. Baicalin (200 mg/kg) was administered intraperitoneally 24 and 1 h before ischemia. After reperfusion, baicalin attenuated the increase in serum alanine aminotransferase activity. The levels of cytosolic cytochrome c protein expression, caspase-3 activity, the number of apoptotic cells increased after reperfusion, which were higher in ethanol-fed animals, were attenuated by baicalin. Following I/R, the hepatic lipid peroxidation was elevated, whereas hepatic glutathione content was decreased. These changes attenuated by baicalin. In ethanol-fed animals, baicalin augmented the increases in heme oxygenase-1 protein and mRNA expressions, and nuclear Nrf2 expression. In conclusion, our findings suggest that baicalin ameliorates I/R-induced hepatocellular damage by suppressing apoptosis and oxidative stress in alcoholic fatty liver.