• BMB Reports
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• v.29 no.5
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• pp.393-397
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• 1996

Sprague-Dawley male rats (150 g) were chronically treated with 5 v/v % ethanol admixed with nutritionally complete liquid diet and fed ad libitum for 3 weeks. Controls were pair fed with the isocaloric sucrose liquid diet. One half of each group was exposed to cold stress at $4^{\circ}C$ either for 24 h (for determination of mRNA by in situ hybridization) or for 48 h (for determination of enzyme activity). Chronic ethanol treatment (ethanol) did not affect tyrosine hydroxylase (TH) mRNA level in locus coeruleus (LC) of brain and adrenal medulla (AM) compared to controls. Cold stress showed strong increase of TH mRNA level in LC and AM compared to controls. Pretreated ethanol reduced the increased TH mRNA level by cold stress in LC and AM. Ethanol did not affect TH activity in LC and adrenal glands (adrenals). Cold stress increased TH activity in LC but not in adrenals. Pretreated ethanol did not reduce the increased TH activity by cold stress in LC but this result was not shown in adrenals. It is suggested that ethanol does not affect the message level and enzyme protein level for TH in LC and AM in normal rat. It is also hypothesized that pretreated ethanol reduces the magnitude of acute cold stress response, that is induction of TH mRNA in LC and AM, and does not reduce the increased TH enzyme protein that is also acute cold stress response in LC.

• Journal of the Korean Society of Food Science and Nutrition
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• v.19 no.1
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• pp.80-86
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• 1990

This experiment was conducted to study the effects of dietary zinc and ethanol on the zinc content of serum and tissues. Eight male rats of Sprague-Dawley strain with average weight of 80$\pm$5g were divided into five groups such as C group: ad libitum control diet(100 ppm Zn) plus isocaloric sucrose solution CE group ; ad libitum control diet plus 25% ethanol solution PF group ; pair fed control to zinc deficient diet(5ppm Zn) plus isocaloric sucrose solution ZD grop ; ad libitum zinc deficient diet plus isocaloric sucrose solution and ZDE group ; ad libitum zinc deficient diet plus 25% ethanol solution. The rats were sacrificed after 4 and 7 weeks of feeding periods. The liver weights of ZD and ZDF groups were increased however the weight of testis was decreased in the same groups The content of serum zinc was infiuenced by the dietary zinc level and the amount was significantly decreased in the ZD group. The content of liver zinc was influnced by the dietary zinc level and the amount was decreased by ethanol feeding. The content of testis zinc was significantly low in the ZDE group. The zinc level of feces to be increased by the ethanol feeding.

• Journal of Life Science
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• v.11 no.5
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• pp.447-456
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• 2001

We have recently demonstrated that the fluoroquinolone antibacterial DW-116 caused a significant developmental toxicity in rats. The present study was conducted to determine whether the development toxicity induced by DW-116 treatment was the result of malnutrition fro reduced food intake or the direct effects of test chemical on conceptuses. The test chemical was administered by gavage to pregnant rats from gestational days 6 through 16 at dose levels of 0 and 500 mg/kg/day. A pair-feeding study was also performed in which the pregnant rats received the same amount of diet consumed by the DW-116-treated pregnant rats. All dams were subjected to caesarean section on day 20 of gestation and their fetuses were examined for examined for external, visceral, and skeletal abnormalities. In this treatment group, the maternal toxicities included increased abnormal clinical signs, decreased maternal body weight, suppressed body weight gain during treatment and posttreatment periods, and reduced food intake. The significant developmental toxicities included increased fetal deaths, decreased live fetuses, reduced fetal body weight and placental weight, increased incidence of fetal abnormalities, and increased fetal ossification delay. In this pair-fed group, however, slight maternal toxicities including decreased body weight and suppressed body weight gain during treatment period were observed in comparison with the control group, and minimal development toxicities including reduced fetal and placental weights and increased fetal ossification delay were found. The number of fetal deaths and live fetuses, and the incidences of malformed fetuses and litters with affected fetuses were comparable to the control values. Based on the results, it could be concluded that the development toxicity observed in the treatment group is attributable to the direct effects of Dw-116 treatment, but not to the maternal malnutrition from reduced food consumption during pregnancy.

• Journal of Life Science
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• v.20 no.1
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• pp.133-141
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• 2010

The protective effect of a mixed powder from solid-cultured and liquid-cultured Lentinus edodes mycelia (2:1, w/w) (designate LED) on the carbon tetrachloride ($CCl_4$)- and ethanol-induced hepatotoxicity of male Sprague-Dawley (SD) rat was investigated. In the $CCl_4$-induced rat hepatotoxicity experiment, rats of 4 groups (6 rats/group) were administere with Normal (0.2 ml distilled water), Control (0.2 ml distilled water), LED (LED 200 mg/kg BW + 0.2 ml distilled water), and Silymarin (200 mg/kg BW + 0.2 ml distilled water), p.o., daily for 2 weeks. Afterwards, all groups except for the Normal group were subjected to abdominal injection with $CCl_4$ ($CCl_4$ : corn oil, 1:1 v/v; 0.5 ml/kg BW). For the ethanol- induced rat hepatotoxicity experiment, rats were divided into 5 groups (5 rats/group): Normal; Pair-fed control (PFC); Control (ethanol); LED (ethanol + LED 200 mg/kg BW); and Silymarin (ethanol + silymarin 200 mg/kg BW). Rats of the Normal and PFC groups were fed a basal liquid diet, and rats of the Control, LED, and Silymarin groups were fed a liquid ethanol diet containing LED or Silymarin. Eight weeks later, blood and liver samples were collected to analyze biomarkers. In $CCl_4$-induced SD rats, LED elevated hepatic superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH peroxidase) activities and thiobarbituric reactive substances (TBARS) were reduced, resulting in the reduction of glutamate-oxalate transaminase (GOT), glutamate-pyruvate transaminase (GPT) and lactic dehydrogenase (LDH) activities in plasma. Similar results of these enzymes and biochemical markers in both liver tissues and plasma were seen in ethanol-induced hepatotoxicity of SD rats. In addition, elevated alcohol dehydrogenase (ADH) activity and reduced expression of cytochrome p450 mixed monooxygenase enzyme (CYP2E1) were seen in liver tissues from ethanol-treated rats by LED treatment. These effects of LED were similar to those of Silymarin. In in vitro experiments, LED showed antioxidant activity in a 2,2-diphenyl-1-picrylhydrazyl (DPPH) system and mouse liver mitochondria system induced by NADPH/$Fe^{2+}$ and cumine hydroperoxide (CuOOH). These results indicate that LED protected SD rat hepatotoxicity, induced by $CCl_4$ and ethanol, through its antioxidative activity and might be useful as a material for protection from hepatoxicity in humans.

• Journal of the Korean Society of Food Science and Nutrition
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• v.33 no.2
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• pp.305-310
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• 2004

The present study was aimed at investigating effects of chicory inulin and three kinds of oligosaccharides on lipid metabolism in rats fed a high-cholesterol diet. Nine Sprague-Dawley male rats weighing, about 190g were given one of five experimental diets, which were basal cholesterol diet (Control) isomaltooligosaccharide diet (IMO), Iructooligosaccharide diet (FO), chicory inulooligosaccharide diet (CIO) and chicory inulin diet (CI) for 5 weeks. In the oligosaccharide and inulin diets, 6% was added at the expense of sucrose. Rats were pair-fed to the intake of FO group which consumed the least amount, and their feces were collected during the last 4 days. Body weight gain was lower in Fo and CI groups compared with the Control group. Plasma glucose levels of FO and CIO groups were lower and plasma triglyceride concentrations of FO, CIO, and CI groups were lower than those of IMO group. Plasma cholesterol concentration did not differ among groups. Relative liver weight was lower in CIO group. Hepatic triglyceride and cholesterol did not differ among. groups. Fecal excretion of neutral steroid and bile acid were not different among groups, but fecal triglyceride excretion was significantly increased in FO and CI groups compared with the Control group. In conclusion, supplementation of oligosaccharides and chicory inulin at 6% of diets showed no significant hypolipidemic effect in rats fed a high cholesterol diet.

• Journal of the Korean Society of Food Science and Nutrition
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• v.24 no.6
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• pp.859-866
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• 1995

This study was done to investigate the effects of chronic ethanol feeding on hepatic microsomal cytochrome system, lipid peroxidation and peroxide metabolizing enzyme activities in 2-acetylaminofluorene(2-AAF) treated rats. Male Sprague-Dawley rats, weighing 120~125g, were pair-fed liquid diets containing 35% of total calories either as ethanol or isocaloric carbohydrates for 6 weeks. After 4 weeks of experimental diet feeding, 2-AAF(100mg/kg body weight) was injected twice a week intraperitoneally. Both weight and percent liver weight per body weight were significantly changed by ethanol feeding. Hepatic microsomal lipid peroxide value and the activities of glutathione(GSH) peroxidase and GSH reductase were not changed by either ethanol or 2-AAF treatment. However the analysis of cytochrome systems showed that both ethanol and 2-AAF increased cytochrome P-450 and bs contents although cytochrome P-450 content was moe affected by 2-AAF while cytochrome b5 content by ethanol. Cytosolic GSH S-transferase activity, which is often elevated during chemical carcinogenesis, also significantly increased by either ethanol feeding or 2-AAF treatment. Overall values for the cytochrome contents and GSH S-transferase activities were highest in 2-AAF treated rats fed ethanol. These results might support the hypothesis that the increase in liver cancer risk associated with chronic ethanol consumption might be due to, at least in part, enhancement of carcinogen bioactivation by ethanol.

• Journal of the Korean Society of Food Science and Nutrition
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• v.20 no.5
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• pp.409-417
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• 1991

To investigate effects of chronic alcohol consumption and tocopherol on lipid peroxidation and mitochondrial respiration 48 male rats of Sprague-Dawley strain were divided into 4 groups. Each group received for 3 weeks one of 4 experimental diets: tocopherol deficient control (TDC), tocopherol deficient-ethanol (TDE), tocopherol-supplemented control (TSC) and tocopherol-supplemented-ethanol (TSE). Composition of the diets was based on the Lieber and Decarli liquid diet and $\alpha$-tocopherol was supplemented at the level of 30mg/liter of diet, and ethanol supplied 36kcal%. TDC and TSC were pair-fed to TDE and TSE, respectively. Increase of body weight of tocopherol deficient-ethanol group was the lowest and the effect was diminished with tocopherol supplementation. Respiration of liver mitochondria was depressed in ethanol-administered groups and the effect became larger with tocopherol deficiency. Hepatic lipid peroxide level was not influenced by ethanol, but hepatic tocopherol content decreased with ethanol treatment. The result indicated that, although lipid perroxide level was unchanged with chronic ethanol consumption, oxidative stress exists in tissues of rate administered ethanol and may be relieved by tocopherol supplementation.

• Journal of Periodontal and Implant Science
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• v.30 no.2
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• pp.359-374
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• 2000

Cyclosporine A(CsA) is a widely used immunosuppressant for transplant patients and is also used for the treatment of a wide variety of systemic diseases with immunologic disorders. However, its use is frequently limited because of complications such as nephrotoxicity or gingival hyperplasia. Although several hypotheses have been postulated for CsA-induced gingival hyperplasia, i.e. various cytokine effects of inflammatory cells, existence of plaque or CsA itself, but its pathogenesis is still unclear. For experimental chronic CsA toxicity, salt depletion has been shown to increased susceptibility of rodents to the effects of CsA, and this maneuver facilitates production of arteriolopathy and interstitial fibrosis in kidney that mimic the changes found in human. The purpose of this study was to evaluate pathogenesis of CsA-induced gingival hyperplasia by comparing changes between CsA administration groups of normal standard diet and those of low salt diet group. Specific pathogen-free, 20 to 25 days old(120 to 150 g), male Fisher-344 rats(KIST, Korea), 120 to 150g of body weight, were assigned to four groups of six animals each after one week of adaptation period for powder food. Group 1 received olive oil($300{\mu}l/g\;of\;diet$) with normal standard diet(0.4% of sodium)(NSD). Group 2 received CsA(Cypol-N, Jonggundang, Korea; $300{\mu}g/g\;of\;diet$) with normal standard diet(NSD+CsA). Group 3 received same amount of olive oil with low salt diet(0.05 % of sodium, Teklad Premier, U.S.A.)(LSD). Group 4 received same dose of CsA with low salt diet(LSD+CsA). Rats were pair fed and were sacrificed after six weeks. Renal histologic lesions associated with CsA, consisted of cortical interstitial fibrosis, tubular atrophy and hyalinization of arterioles and the impairment of renal function including increase of serum creatinine and decrease of glomerular filtration rate was more severe in low salt diet group. These were proved as the results of activated of renin-angiotensin system in the kidney by low salt condition. Meanwhile the degree of gingival hyperplasia at incisor and molar tooth was less severe in low salt diet group compared with normal sodium diet group. Hyperplastic gingiva showed mild epithelial hyperplasia and expanded underlyng stroma which consisted of matrix increasement, capillary proliferation and dilatation. While the number and the activation of fibroblasts were increased, inflammatory cells were rare in the stroma. The immunohistochemistry for TGF-${\beta}_1$ in the kidney and gingiva revealed stronger positive in LSD+CsA in kidney but in gingiva of NSD+CsA. These results suggested followings; Gingival hyperplasia can be developed without inflammatory cells infiltration and seemed not induced by CsA by itself. The major role for gingival hyperplasia by CsA would be the secondary effect of TGF-${\beta}$, which maybe upregulated by CsA administration. Low salt diet can attenuate this hyperplasia perhaps by decreasing the activation of $TGF-{\beta}$.