• Proceedings of the Korean Environmental Health Society Conference
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• 2002.04a
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• pp.47-48
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• 2002

The purpose of this study was to investigate the metallothionein of acute cadmium poisoning mice as a Cadmium index. Forty male ICR mice were injected with cadmium chloride solution from 1/8LD$\sub$50/ to 1/2 LD$\sub$50/ dose. At 24 hours after exposed Cd, I examined Cd and metallothionein (MT) in tissues (liver and kidney) and fluids (whole blood and urine) and also measured low molecular proteins, N-acety1-${\beta}$-D-glucosaminidase (NAG) and ${\beta}$$\sub$2/- microglobuline (${\beta}$$\sub$2 /-MG) in urine. The concentration of Cd and MT of liver, kidney whole blood and urine were increased with dose dependent manner. Urinary Cd and urinary MT had very good significance (p＜0.01) and urinary MT had good significance with kidney Cd and NAG but not ${\beta}$$\sub$2/-MG. Conclusionally MT in urine was very correlated with kidney Cd and urine Cd. So MT maybe useful as a Cd poisoning index.

• Toxicological Research
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• v.13 no.3
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• pp.183-186
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• 1997

Acute toxicity of pectenotoxin 2 (PTX2) was examined in mice. Treatment of mice with a toxic dose of PTX2 resulted in clinical signs such as ataxia, cyanosis and an abrupt decrease in body temperature. Histopathological studies revealed that the liver is the major target organ for PTX2. Activities of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and sorbitol dehydrogenase (SDH) were significantly elevated by PTX2 administration. Glucose-6-phosphatase activities were not changed by the treatment. The PTX2 treatment decreased relative liver weight without changing the body weight. The effect of PTX2 on hepatic drug metabolizing enzyme system was determined. An ip dose of PTX2 (200 $\mu$g/kg) induced a significant decrease in the hepatic microsomal protein content. Cytochrome P-450 content, cytochrome b$_5$ content, NADPH cytochrome c reductase, aminopyrine N-demethylase activities, or hepatic glutathione content were not altered by PTX2 treatment.

• Journal of Food Hygiene and Safety
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• v.27 no.3
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• pp.306-311
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• 2012

Stevioside, a natural sweeteners presently used in various kinds of food and food products in Korea, was evaluated for its toxicity potential in the 14 day feeding study using B6C3F1 mice. Stevioside was added to the diet at different concentrations of 0.31, 0.62, 1.25, 2.5 and 5%, and was administered for 14 consecutive days. An increase of liver organ weight in male mice was observed. No diet-related differences were noted in clinical signs, food consumption, and gross and histopatholgical evaluation. Based on these results, we concluded that the concentration of 5% in the diet was a suitable maximum tolerable dose of stevioside for a 90 day study in mice.

• Korean Journal of Poultry Science
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• v.19 no.4
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• pp.217-225
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• 1992

This research was carried out to determine the 25-Hydroxyvitamin $D_3$[25(OH)$D_3$] content in liver of broiler Hubbard chicks fed vitamin VD-deficient diet for 31 days in a subdued light room and exposed to UVB light (maximum intensity at 297nm) with dose of 0.204 or 0.408 mJ/$\textrm{cm}^2$(30 or 60 min irradiation) . The lipid in liver collected at 0~138 hr after irradiation was extracted by chloroform-methanol(2：1, v /v) and 25(OH)$D_3$ fraction was separated by Sep-Pak silica cartridge. The 25(OH)$D_3$ concentration was measured by normal phase HPLC. The negative control chicks Presented 25(OH)D$_3$17.5 ng/g liver. When 0.204mJ/$\textrm{cm}^2$ was treated to whole body of chicks, the 25(OH)$D_3$ level was increased to 37.8 ng/g at 12 hr after irradiation, the peak concentration, 40.5 ng /g was appeared at the time of 86 hr, and decreasing trend was shown thereafter until 138 hr, the final time in this study. When 0.408 mJ/$\textrm{cm}^2$ was applied, the 25(OH)$D_3$ content was 36.7 ng /g liver at 12 hr, 61.4 ng/g(maximum value ) was appeared at 42 hr, and 39.5 ng /g at 138 hr. The increased absolute amounts in liver 25(OH)$D_3$ were 23 and 43.9 ng/g as chicks were exposed to UVB light with dose of 0.204 and 0.408mJ/$\textrm{cm}^2$, respectively. Consequently, it was found that when double dose of UVB light was irradiated to the chicks, their liver samples produced nearly double 25(OH)$D_3$ at 42 hr after exposure, and the peak value was presented earlier by 24 hr than that in the low dose treatment.

• 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.

• Toxicological Research
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• v.13 no.4
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• pp.385-391
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• 1997

Inductive effects of cytochrome P450 2B1 by $\alpha$- and $\beta$-ionone were characterized in individual liver lobes of male Sprague Dawley rats. When rats were administered ionones orally at 100, 300, and 600 mg/kg for 24 hr, cytochrome P450 2B1 was induced dose-dependently in liver S-9 fractions as measured by P450 2B-specific monooxygenases and Western immunoblotting. The activity of P450 1A- and P450 2B-specific monooxygenases was differentially expressed in each lobe of normal liver. In addition, the monooxygenase activity was induced by $\alpha$- and $\beta$-ionone with different potency in each lobe of the liver. Our present results indicate that the different induction of P450s by $\alpha$- and $\beta$-ionone in each lobe may explain different susceptibilities of rat liver lobes to certain hepatotoxicants which require metabolic activation for their toxicity and that $\alpha$- and $\beta$-ionone may be useful model inducers of P450 2B1 in studying the toxic mechanism of certain toxicants which may require the metabolic activation by P450.

• Journal of the Korean Society of Food Science and Nutrition
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• v.27 no.4
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• pp.739-744
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• 1998

To evaluate an effect of ethanol pretreatment on the liver xanthine oxidase(XO) activity, 0.25ml of xylene(50% in olive oil) per 100g body weight was daily given four days to the rats at 2hrs after aministration of ethanol each day, while each control group(ethanol, xylene, olive oli) was treated as the same dose described as above. The animals were sacrificed at 24hrs after last injection. Xylene-treated rats showed the more decreased activity of liver XO compared to the control. But the pretreatment of ethanol to the xylene-treated rats enhanced the liver XO activity. Furthermore, the xylene-treated rats led to more increased Vmax value in liver XO compared to the only xylene-treated rats. On the other hadn, hepatic aldehyde dehydrogenase activity was more decreased in xylene-treated rats pretreated with ethanol than in xylene-treated rats. And the intermediated xylene metabolites, methyl benzylalcohol or aldehyde inhibited the XO activity "in vitro". In conclusion, the phenomenon that pretreatment of ethanol to the xylene-treated rats led to the enhancement of liver XO activity, may be due to an influence of acetaldehyde.taldehyde.

• Journal of Yeungnam Medical Science
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• v.39 no.3
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• pp.256-261
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• 2022

Sarcoidosis often involves the liver. However, primary hepatic sarcoidosis confined to the liver without evidence of systemic involvement is rare. We report the case of a 37-year-old man with hepatic sarcoidosis who initially presented with elevated liver enzymes and suspicious cirrhotic nodules on computed tomography. The patient had cirrhosis but did not have portal hypertension. Based on the initial histopathologic finding of chronic granulomatous inflammation and the common clinical characteristics of sarcoidosis, he was initially diagnosed with primary biliary cholangitis, and his daily dosage of ursodeoxycholic acid was increased to 900 mg. After 14 months of treatment, his total serum bilirubin concentration was 10.9 mg/dL (upper normal limit, 1.2 mg/dL). Additionally, a transjugular liver biopsy revealed multiple noncaseating granulomas. He was diagnosed with primary hepatic sarcoidosis involving the lungs, heart, spleen, kidneys, and skin. Treatment with methylprednisolone was initiated. Two weeks later, he was started on azathioprine, and the dose of steroid was simultaneously reduced. These findings indicate the importance of including hepatic sarcoidosis as a possible diagnosis in patients with elevated liver enzymes or cryptogenic cirrhosis.

• Toxicological Research
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• v.15 no.1
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• pp.47-53
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• 1999

The effects of methidathion on humoral immune response were studied in BALB/c mice. 0.5 or 5.0 mg/kg/day methidathion were administered orally for 14 days. The parameters examined to assess apparent toxicity of methidathion included changes of body weight, relative weight of spleen, thymus, sidney and liver, and viable spllenic cell numbers. To evaluate the humoral immune response, thymus, kidney and liver, and viable splenic cell numbers. To evaluate the humoral immune resopnse, the plaque forming cell(PFC) responses sheep the red blood cells (SRBC) and the lovels of serum IgG to hen egg lysozyme (HEL) were determined. No alterations were observed in changes of body weights, relative organ weights and the numbers of viable splenocytes by exposure to any dose of methidathion. At the dose of 0.5mg/kg only PFC response was decreased, whereas both PFC response and the level of serum IgG were decreased significantly at the dose of 5.0 mg/kg. These results indicate that exposure to methidathion may cause sup[pression of humoral immune reponse in mice without overt changed in lymphoid organ weight or viability of splenocytes.

• Asian-Australasian Journal of Animal Sciences
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• v.12 no.6
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• pp.944-950
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• 1999

Hexavalent chromium (CrVI) was fed to one day old chicks of Gallus domesticus in the form of different concentrations (250 and 500 mg/kg feed) of potassium dichromate mixed with the feed, ad libitum, for 32 weeks. After 20 weeks of feeding, the total body weight was higher in the low dose (260 mg/kg (feed) group and lower in the high dose (500 mg/kg feed) group, as compared with the control chicks. After 32 weeks of feeding, however, the total body weight was significantly decreased in both the treated groups. Egg laying was enhanced. Fertility remained unaffected, whereas hatchability was considerably decreased after CrVI-treatment. The egg shell thickness increased significantly (13%). Cr was deposited in a dose dependent manner in the liver and lungs. Some structural derangements in liver were also noted in treated chicks. The results of this study i.e., rapid ageing, excessive Cr deposition, decreased hatchability and hepatotoxicity indicate toxic effects of CrVI.