• Korean Journal of Veterinary Research
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• v.35 no.4
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• pp.713-727
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• 1995

The present study was investigated fatty acid composition of the phospholipid in the RBC membrane, liver and microsomal fraction after vitamin E and/or insulin treatment to evaluate the effect of vitamin E on the oxidative stress in STZ-treated rat and BB rat. Results obtained through the experiments were summarized as follows; 1. Effect of vitamin E and/or insulin treatment in STZ-treated rat 1) In the insulin treated group and the combination treated groups of vitamin E with insulin, body weights were increased compared to STZ-treated rat(STZ control group). Especially it was more significantly increased in the combination treated group of high dose vitamin E with insulin. 2) The composition of fatty acids of the phospholipid in RBC membrane, liver and microsomal fractions was shown a decreased C16:1, C18:1, C20:4 and an increased C16:0, C18:0, C18:2 in STZ control group compared to normal control group. In RBC membrane, liver and microsomal fractions after vitamin E with insulin treatment in STZ-treated rat, effect on the composition of fatty acids of the phospholipid was shown the result of a decreased C16:0, C18:0, C18:2 and an increased C16:1, C18:1, C20:4. 3) Hemolysis rate of the RBC to $H_2O_2$ was increased in the STZ control group and it was decreased below the hemolysis level of normal control group by vitamin E treatment. 2. Effect of vitamin E and/or insulin treatment in BB rat 4) Only in microsomal fraction, fatty acid composition was different between insulin treatment group and vitamin E with insulin treatment group. It was increased C16:0 and C18:1, and decreased C18:0 and C18:2 in vitamin E with insulin treatment group: But C20:4 was not different in two groups. These results suggest that the combination treatment of vitamin E and insulin could prevent the oxidative change of fatty acids in P-lipid of the RBC membrane, liver and microsomal fraction in STZ-treated rats and BB rats.

• Journal of Life Science
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• v.20 no.2
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• pp.169-175
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• 2010

Intestinally absorptive and distributive aspects of the subtoxic level of selenite in rats were investigated using a double perfusion system. The double-perfusion technique is an in situ, in vitro preparation in which the intestinal lumen and its vasculature are perfused simultaneously. In the previous study, the subtoxic level of sodium selenite was determined to be 1.2 mM through inhibition of 3-0-methyl glucose (3MG) absorption. Thus, the selenite used to identify the intestinally absorptive mechanism of selenite was perfused at a luminal concentration of 1, 10, 50, 100 and $200\;{\mu}M$. Appearance of radiolabeled-Selenium (Se) was identified in three compartments: luminal perfusate, small intestine and vascular perfusate. Dose-response curves for Se in the three compartments indicate that selenite is absorbed by non-mediated passive diffusion. Regarding the distributive aspect, $21.02{\pm}3.92%$ of the total amount of selenite in the lumen was transported into the blood vessels across the small intestine. However, $4.75{\pm}1.75%$ of the total amount of selenite in the lumen is retained by the small intestine. Therefore, a total of $25.67{\pm}4.46%$ of the test dose was taken up from the luminal perfusate.

• Korean Journal of Food Science and Technology
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• v.32 no.4
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• pp.964-969
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• 2000

Di-(2-ethylhexyl) adipate(DEHA) has been used extensively as a plasticizer in the manufacture of plastic products such as PVC films. Though, phthalate esters plasticizers have been known to induce endocrine system-mediated responses, few studies have been conducted for the screening of estrogenic activity of DEHA, an adipate plasticizer. This study was initiated to evaluate the estrogenic activity of DEHA by in vitro E-screen assay and in vivo uterotrophic assay. MCF-7 human breast cancer cells were treated with $DEHA(5{\times}10^{-9}{\sim}5{\times}10^{-4}\;M)$, for 144 hr, and cell proliferation was determined by sulforhodamine B(SRB) assay. DEHA dissolved in corn oil was administered subcutaneously to ovariectomized(OVX) female Sprague-Dawley rats at dosage levels of 0, 2, 20 and 200 mg/kg/day for three consecutive days. Rats were sacrificed 24 hr after final treatment and vagina and uterus(wet and blotted) weights were obtained. E-screen assayed DEHA did not generate cell proliferation at treated concentrations$(5{\times}10^{-9}{\sim}5{\times}10^{-4}\;M)$, whereas 17 ${\beta}-estradiol$(E2), the positive control, induced cell proliferation at low concentrations$(5{\times}10^{-14}{\sim}5{\times}10^{-9}\;M)$. In the uterotrophic assay, DEHA did not change vagina and uterus(wet and blotted) weights at dosage levels up to 200 mg/kg/day treatment. These results demonstrated that DEHA did not exhibit the estrogenic activity as determined by in vitro E-screen assay and in vivo uterotrophic assay.

• Radiation Oncology Journal
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• v.7 no.1
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• pp.15-22
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• 1989

Investigations were carried out into the time-and dose-related changes in acute skin reaction following graded single dose (20,30 and 40 Gy) of x-ray irradiation in Wistar rats, in order to evaluate the radioprotective effect of Diethon on skin. For the duration of skin response over 1. 5 score in dose of 40 Gy, the Diethone group of 24.7 days was significantly different (p<0.02) from that of control (29.8 days) and vaseline (29.2 days) groups, it was $17.1\%$ diminution of skin response period compared with that of control group. By the averaging daily scores for 10 days during peak skin reaction the mean scores were obtained. Mean score of Diethone group $(2.43\pm0.22)$ was significantly different (p<0.01) from that of control $(2.91\pm0.23)$ and vaseline $(2.81\pm0.18)$ groups of 40Gy dose. By iso-effect dose obtained at level of 2.5 score the dose reduction factor (DRF) was 1.41 which reduced radiation dose of $41\%$ by radioprotective effect of Diethone. From this experimental data, it may be possible to give higer radiation dose to large and/or radioresistant tumor mass rather than conventional treatment doses for improving therapeutic ratio by using topical application of skin radioprotector.

• Journal of Food Hygiene and Safety
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• v.26 no.4
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• pp.377-382
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• 2011

This test was performed to evaluate the acute oral toxicity and skin irritation of Lamia-Kill$^{(R)}$, disinfectant, containing 20% benzalkonium chloride and 10% citric acid. In acute oral toxicity, Lamia-Kill$^{(R)}$ was orally administered at dose levels of 2,000, 1,000, 500, 250 and 0 mg/kg body weight. After single oral administration to both sexes of SD rats, the rats were observed for 14 days. In primary skin irritation test, New Zealand white rabbits were dermally treated with Lamia-Kill$^{(R)}$ for 24 hr and observed for 3 days. All rats treated with Lamia-Kill$^{(R)}$ were induced no toxic signs in mortalities, clinical findings, body weights and gross findings. Also, the disinfectant did not induce any adverse reactions such as erythema and edema on intact skin sites for the most part rabbits, but on abraded skin sites, some rabbits showed very slight erythema on 24 hr after topical application. With the results of this study, Lamia-Kill$^{(R)}$ have no effect on acute toxicity and side effect in SD rats and was classified as a practically non-irritating material based on the score 0.50 of primary irritation index.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.33 no.6
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• pp.520-523
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• 2000

Anti-ulcer effects of depolymerized alginate (HAG-10, average molecular weight 10,000; HAG-50, average molecular weight 50,000; HAG-100, average molecular weight 100,000) obtained by hydrolysis of alginate by heating at $121^{\circ}C$, against $HCl{\cdot}ethanol$ and water-immersion stress in rats were investigated. The acute gastritis, induced by $HCl{\cdot}ethanol$, and the gastric ulcer, induced by water-immersion stress, were inhibited dose-dependently by administration of HAG-50, HAG-100 and alginate. Histopathological lesions of the gastritis and gastric ulcer in rats treated with HAG-50, HAG-100 and alginate were significantly lower than those in rats fed with HAG-10. The inhibition rates (${\%}$) on acute gastritis induced by $HCl{\cdot}ethanol$ and gastritis ulcer induced by water-immersion stress in rats, were $13.00{\%}\;and\;15.74{\%}$of HAG-10, $41.15{\%}\;and\;35.72{\%}$ of HAG-50, $41.58{\%}\;and\;35.37{\%}$ of HAG-100, and $45.17{\%}\;and\;41.11{\%}$ of alginate, respectively. These results suggested that HAG-50, HAG-100 and slginate had a protective effect against the gastritis and gastric ulcer. The effect was not as visible when using HAG-10 in rats. From the present results, it was suggested that HAG-50 was an effective anti-ulcer agent against $HCl{\cdot}ethanol$and water-immersion stress in rats.

• The Korean Journal of Food And Nutrition
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• v.26 no.3
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• pp.383-390
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• 2013

Mistlero C was shown to be non-genotoxic in a series of genotoxicity tests, including a bacterial reverse mutation test and a combined in vivo mammalian erythrocyte micronucleus test. In a bacterial reverse mutation assay, no significant increases in the number of revertant colonies, compared to the negative control, was detected in $5,000{\mu}g/plate$ of Mistlero C. In addition, with Mistlero C, no changes were shown in the number of micronucleated polychromatic erythrocytes (MNPCE) among 2,000 polychromatic erythrocytes compared to the negative control. Mistlero C was administered orally in rats to investigate acute toxicity. The $LD_{50}$ values in rats were above 2,000 mg/kg. In a repeated dose, 13-week, oral toxicity study conducted in rats, no compound-related adverse effects were shown at doses of Mistlero C of up to 1,000 mg/kg body weight/day. The results of these studies support the safe use of Mistlero C in food for human consumption.

• Korean Journal of Veterinary Research
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• v.36 no.1
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• pp.57-63
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• 1996

The biliary excretion kinetics of the active folate derivatives were examined after an intravenous injection of methotrexate at doses of 0.3 and 10mg/kg to clarify the mechanism of the acute decrease in the plasma folate by the dihydrofolate reductase inhibitors. Even at a higher dose than used in the clinical therapy, methotrexate did not cause any acute depletion of folate denvatives in the excreted bile. Therefore, the decrease in the plasma folate appeared not to be related with the biliary excretion process of folates. A factor responsible for the plasma folate depletion by DHFR inhibitors may be due to the malabsorption of folate derivatives excreted into the small intestine.

• Korean Journal of Environmental Agriculture
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• v.22 no.2
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• pp.94-99
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• 2003

The objective of present study was to investigate the antioxidative and hepatoprotective effects of selenium on cadmium-induced toxicity and lipid peroxidation in rat hepatocyte primary culture. To do this, two separate experiments were conducted. In Experiment 1, primary cultures of rat hepatocytes were incubated for 6 hr in the presence of various concentrations (1, 10, 50, 100, and $500\;{\mu}M$) of cadmium chloride. Cytotoxicity and lipid peroxidation were evaluated using the MTT assay and TBARS assay, respectively. Antioxidative and hepatoprotective effects were determined by measuring the activity of GOT and GSH-Px, respectively. Cell viability was reduced and lipid peroxidation was increased by cadmium in dose-dependent manners. There was significantly negative correlation (r=-0.943, p<0.01) between cell viability and lipid peroxidation GOT activity was increased and GSH-Px activity was decreased by cadmium at the concentration of $50\;{\mu}M$. In Experiment 2, primary cultures of rat hepatocytes were incubated for 6hr in the presence of 100\;{\mu}M$ of cadmium chloride and various concentrations (0.01, 0.1 and 1 ppm) of sodium selenite to assess the effect of selenium on cadmium-induced toxicity and lipid peroxidation. Cell viability and GSH-Px activity were increased by sodium selenite at the concentration of 1 ppm Whereas, lipid peroxidation and GOT activity were reduced by 0.1 ppm of sodium selenite. These results demonstrate that selenium has an antioxidative and hepatoprotective potentials against cadmium.

• Journal of Food Hygiene and Safety
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• v.6 no.1
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• pp.27-40
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• 1991

;ABSTRACT-The effects of gastric ulcer induced by restraint and water-immersion stress on gastric carcinogenesis in Wistar male rats treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were examined. Rats of group 1 were 2iven stress for 8 hours before they were received MNNG (100 mg/l) in drinking water for 20 weeks. Rats of group 2 were received MNNG first for 2 weeks and then were given stress once a week from 3rd to 12th weeks, with simultaneous MNNG adminitration and followed by MNNG only until 20th weeks. Rats of group 3 were received MNNG only as a positive control and rats of group 4 were not treated with carcinogen. All groups were sacrificed in 20 weeks. Sections of the pyloric mucosa were stained by avidin-biotin peroxidase complex (ABC) immuno-histochemical method. PAPG (pepsinogen isozyme 1 altered pyloric gland), body weight change, gross lesions and histopathological changes were examined. The results obtained from these studies were summarized as follows: 1. The mean body weight gains of the rats fed with carcinogens (group 1, 2, 3) were significantly lower than that of group 4 (control group, without carcinogen. p<0.05). However, the differences of the mean body weight of rats treated with carcinogen were not significant. 2. Stress treatment (group 1 and 2) increased the appearance of the numbers of PAPG (Pepsinogen 1 Altered Pyloric Gland) induced by carcinogen significantly compared with that of group 3 (carcinogen only, p<0.01). 3. The incidence rate of mucosal hyperplasia in pylorus was significantly increased in group 2 compared with group 3 (p<0.05).0.05).