• Journal of the Korean Society of Food Science and Nutrition
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• v.32 no.2
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• pp.278-286
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• 2003

Alcohol is well known agent which can damage the human tissues such as liver via stimulating lipid peroxidation. On the other hand, carotenoids in addition to vitamins A, C and I play important roles in protecting these oxidative damages as well as preventing the production of free radicals. This study was carried out to investigate the effect of dietary vitamin A on lipid peroxidation and antioxidants status in ethanol-treated rats. In the experiment, male Sprague-Dawley rats weighing 160~180 g were given a liquid diet containing 36% of total calories as ethanol for 7 weeks. The pair-fed control rats received an isocaloric amount of diet containing sucrose instead of ethanol on the following day Additionally, the liquid diet contained adequate amount of $\beta$-carotene, retinyl acetate or 13-sis-reinoic acid except vitamin A-deficient diet. The results obtained are as follows. The levels of plasma and hepatic lipid peroxide were increased after chronic ethanol feeding in rats. Retinyl acetate supplementation significantly reduced lipid peroxidation induced by ethanol feeding Glucose 6-phosphatase activity was significantly reduced in rats fed vitamin A-deficient diet with ethanol and alkaline phosphatase activity was significantly induced in rats fed 13-cis-reinoic acid diet with ethanol. Catalase and alcohol dehydrogenase activities did not show a consistent tendency in experiment groups. The hepatic antioxidant enzyme activities did not significantly changed by chronic ethanol feeding groups. The striking decrease in conversion of $\beta$-carotene to retinol was observed in rats fed a $\beta$-carotene diet with ethanol feeding The level of retinol and retinoic acid in plasma and liver was decreased after chronic ethanol administration Based on this result, these data suggest that ethanol feeding enhances oxidative stress especially in those fed a vitamin A-deficient diet, and vitamin A supplementation, especially, retinyl acetate intake can prevent enhanced lipid peroxidation and related damage to some extent.

• Korean Journal of Poultry Science
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• v.36 no.1
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• pp.39-45
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• 2009

This study was carried out to investigate the effect of dietary supplementation of Acanthopanax (A) senticosus and Eucommiaceae on the expression of lipogenic, myogenic and oxidative stress genes in broiler chickens. Birds were subjected (assigned) to one of the following 5 dietary treatments: control (CON), A. senticosus 0.5% (T1), 1.0% (T2), Eucommiaceae 0.5% (T3) and 1% (T4). Each treatment was replicated 8 times with 4 birds per replication, housed in 4 birds per cage. Birds were arranged according to randomized block design. Feeding trial was conducted from day 4 to 35th day of age. Liver and muscle tissues were collected for analysis. Broilers subjected to 1% A. senticosus had higher feed conversion ratio than the other treated birds whereas no significant differences were found in body weight, weight gain and feed intake. The gene expression levels of fatty acid synthase were not different among the treatments while the transcription factor $PPAR{\gamma}$ was highly expressed in Eucommiaceae but not in control and A. senticosus. The gene expression levels of myogenin were high in both A. senticosus and Eucommiaceae compared to control group. MyoD also showed high expression in treated groups furthermore, Eucommiaceae stimulated the expression of MyoD more than that of A. senticosus. The antioxidant gene expressions (SOD, CAT, SOD, GPX) generally were not much different among the treatments, however, SOD and GPX were stimulated in broilers consumed 1% Eucommiaceae diet. The result of this experiment showed that dietary supplementation of A. senticosus and Eucommiaceae in broiler may improve the antioxidant defence system through SOD and GPX without affect of growth performance in broilers.

• Journal of Nutrition and Health
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• v.36 no.1
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• pp.9-17
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• 2003

The preparation method of a soluble dietary fiber from oak wood (Quercus mongolica) and the effect of the soluble dietary fiber on physiological function in rat fed high cholesterol diets was investigated. The best condition for steam explosion method was 25 kgf/㎤ pressure for 6 min. The exploded samples were delignified by the filtration treatment with 1% NaOH for several times, which is the best condition. The enzymatic hydrolysis of Cellusoft cellulase was more effective than Onozuka R-10 cellulase. The manufactured soluble dietary fiber was assayed using gel permeation chromatography (GPC) and it was dissolved in water. Average molecular weight distribution of manufactured soluble dietary fiber was about 348-1,200 and it was assumed the oligomer form fraction. In order to compare the manufactured soluble dietary fiber with commercial soluble dietary fiber (pectin) on the physiological function, Sprague-Dawley male rats weighing 100$\pm$10 g were randomly assigned to one normal diet and five high cholesterol diet containing 1% cholesterol. The high cholesterol diet groups were classified to fiber free diet (FF group), 5% pectin (5P group), 10% pectin (l0P group), 5% manufactured soluble dietary fiber (5M group) and 10% manufactured soluble dietary fiber (10M group). Body weight gains in all soluble dietary fiber groups were lower than FF group. Food intakes were increased in all soluble dietary fiber groups than that of FF group. Food efficiency ratio (FER) was significantly decreased in all soluble dietary fiber groups than that of the FF group, and it was especially was highest in 10% supplemented soluble dietary fiber group. The weight of liver of the soluble dietary fiber supplemented groups were lower than those of the FF group, but weights of cecum and small intestine of all supplemented soluble dietary fiber groups were significantly increased, compared with that of FF group. The weights and water contents in feces were significantly increased by the soluble dietary fiber. The activity of the glutamic oxaloacetic transaminase in soluble dietary fiber groups were significantly decreased than those of FF group. The hepatic glutathione S-transferase activity in all soluble dietary fiber supplemented groups were higher than that of FF group. The physiological effects of the manufactured soluble dietary fiber are the same as the commercial soluble dietary fiber (pectin). The preparation method of the soluble dietary fiber from the oak chips suited to its purpose. (Korean J Nutrition 36(1) : 9~17, 2003)

• Korean Journal of Poultry Science
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• v.39 no.3
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• pp.223-232
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• 2012

The effects of dietary supplementation of dried coffee meal (CM) on growth performance, blood biochemical profiles, the weights of immune-related organs, and the antioxidant defense system in broiler chicks were examined. A total of 162, 3-day-old male broiler chickens were assigned to three dietary groups: control group (CON), control diet added with 0.5% CM (CM0.5), and control diet added with 1.0% CM (CM1.0). In vitro antioxidant activity test, coffee extracts showed concentration-dependent increase in radical scavenging activity. Dietary addition of 0.5 and 1.0% of CM did not have negative effects on growth performance and feed conversion during the experimental periods, whereas dietary CM significantly (P<0.05) increased the relative weight of thymus without changes in the other organ weights. In addition, birds fed the diet supplemented with CM (0.5 and 1.0%) significantly increased blood albumin without affecting other components including glucose, triglyceride and cholesterol compared with those fed control diet. In antioxidant defense system, the specific activities of superoxide dismutase, glutathione peroxidase and glutathione S-transferase and the level of glutathione in the small intestine and liver were not affected by dietary supplementation of CM. However, hepatic lipid peroxidation in birds fed the diet supplemented with 0.5% CM was significantly (P<0.05) decreased compared with that in control birds. In conclusion, dietary supplementation of CM(0.5~1.0%) has potential for use as a natural antioxidant source without negative effect on growth performance in broiler chickens.

• Tuberculosis and Respiratory Diseases
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• v.50 no.4
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• pp.450-461
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• 2001

Background : The underlying pathogenesis of radiation-induced lung fibrosis (RTLF) has not been very well defined. However, the role of TGF-$\beta$ in the generation of RTLF has been a major focus because there is an increase in the expression of both the TGF-${\beta}m$-RNA and its protein preceding RTLF lesions. The down stream signal after a TGF-$\beta$ stimulated lung fibrosis includes the activation of many mediators such as Smad and c-Jun N-terminal kinase (JNK) through TAK1. It is we hypothesized that JNK activation may play a pivotal role in RTLF pathogenesis through increased transcription of the fibrogenic cytokines. The present study evaluates JNK activity in alveolar macrophages after irradiation and the relationship between JNK activity and the amount of collagen in the lung tissues. Methods : C57BL/6 mice(20-25 gr, males) received chlorotetracycline(2g/L) in their drinking water 1 week prior to irradiation and continuously there after. The mice were irradiated once with 1400 cGy of $60CO{\gamma}$-ray over the whole chest. The cellular composition of the whole lung bronchoalveoalr lavage fluids(BALF), elastin expression in the lung tissues, the level of hydroxyproline in lung tissues, and an in vitro JNK assay was measured before irradiation and one, four, and eight weeks after irradiation (RT). Results : The volumes of BALF retrieved from instilled 4 mL of saline with 2% heparin were 3.7-3.8 mL for each group. The cell numbers were similar before($4.1{\times}10^4{\pm}0.5{\times}10^4/mL$) and 1 week($3.1{\times}10^4{\pm}0.5{\times}10^4/mL$) after RT. At four and eight weeks after RT, the cell number reached to $14.0{\times}10^4{\pm}1.5{\times}10^4mL$ and $10.0{\times}10^4{\pm}1.3{\times}10^4/mL$, respectively. There we no changes in the lymphocytes and neutrophils population observed in the BALF after RT. The H-E stain of the lung tissues did not show any structural and fibrotic change in the lung tissues at 4 and 8 weeks after RT. In addition, the amount of elastin and collagen were not different on Verhoeff staining of the lung tissues before RT to eight weeks after RT. The hydroxyproine content was measured with the left lung dissected from the left main bronchus. The lung were homogenized and hydrolyzed with 6 N Hel for 12 hours at $110^{\circ}C$ then measured as previously described. The content of hydroxyproline, standardized with a lung protein concentration, reached a peak 4 weeks after RT, and thereafter showed a plateau. AnIn vitro JNK assay using c-$Jun_{1-79}$-GST sepharose beads were performed with the alveolar macrophages obtained from the BAL. JNK activity was not detected prior to RT, However, the JNK activity increased from one week after RT and reached a peak four weeks after RT. Conclusion : JNK may be involved in the pathogenesis because the JNK activity showed similar pattern observed with the hydroxyproine content. However, it is necessary to clarify that the JNK increases the transcription of fibrogenic cyiokines through the transcription factor.