• Tuberculosis and Respiratory Diseases
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• v.59 no.1
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• pp.30-38
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• 2005

Background : Arsenic trioxide ($As_2O_3$) has been used to treat acute promyelocytic leukemia, and it induces apoptosis in a variety of solid tumor cell lines including non-small cell lung cancer cells. However, nonsteroidal antiinflammatory drugs (NSAID) can enhance tumor response to chemotherapeutic drugs or radiation. It was previously demonstrated that a combination treatment with $As_2O_3$ and sulindac induces the apoptosis of NCI-H157 human lung carcinoma cells by activating the caspase cascade. This study aimed to determine if a combination treatment augmented its apoptotic potential through other pathways except for the activation of the caspase cascade. Material and Methods : The NCI-H157 cells were treated with $As_2O_3$, sulindac and antioxidants such as glutathione (GSH) and N-acetylcysteine (NAC). The cell viability was measured by a MTT assay, and the level of intracellular hydrogen peroxide ($H_2O_2$) generation was monitored fluorimetrically using a scopoletin-horse radish peroxidase (HRP) assay. Western blotting and mitochondrial membrane potential transition analysis were performed in order to define the mechanical basis of apoptosis. Results : The viability of the cells was decreased by a combination treatment of $As_2O_3$ and sulindac, and the cells were protected using antioxidants in a dose-dependent manner. The increased $H_2O_2$ generation by the combination treatment was inhibited by antioxidants. The combination treatment induced changes in the mitochondrial transmembrane potential as well as the expression of the Bcl-2 family proteins, and increased cytochrome c release into the cytosol. However, the antioxidants inhibited the effects of the combination treatment. Conclusion : Combination treatment with $As_2O_3$ and sulindac induces apoptosis in NCI-H157 human lung carcinoma cells via ROS generation with a mitochondrial dysfunction.

• 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.

• 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.