• Korean Journal of Fisheries and Aquatic Sciences
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• v.31 no.4
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• pp.581-586
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• 1998

The present study was conducted to prepare seaweed extracts suppressing mutagenic activity of 2-amino-1-methyl-6-phenylimidazo[4,5-b] pyridine ( PhIP ) ana 2-amino-3,8-dimethylmidazo[4,5-f]quinoxaline (MeIQx) derived from cooked meat produce. The tumor initiation activity of PhIP and MeIQx was assayed with Ames method using Salmonella typhimurium TA98 in the presence of S-9 mixtures before and after addition of methanol-solubles of seaweed, such as, Phaeophyta; Undaria pinnatifida, Ecklonia stolonifera Ecklonia cava, Laminaia japonica Sargassum fulvellum, Sargassum hornezi, Sargassum miyabei, Sargassum thunbergii, Agarum cribrosum and Hizikia fusifomis, Rhodophpei Porphyra yezoensis, Grateloupia eiliptiut Lomentraria catenata, Ploemium telfairiae and Glarilaria verrucosa, Chlorophyta; Codium fragile, Enteromorpha compresa and Ulva pertusa. Among seaweed tested, Phaeophyta was shown the higher desmutagenic activity than Rhodophyta and Chlorophyta. E. stolonifera, E. cava and S. miyabei, among Phaeophyta exerted the stronger desmutagenic activity (above $90\%$/2 mg). The ethyl acetate, diethyl ether and chlomform extracts except water extracts from E. stolonifera exhibited a high desmutagenic activity. The ethyl acetate extract of E. stolonifera which showed highest activity was fractionated with Sephadex LH20 column chromatography to give active fraction A-7, which showed desmutagenicity of $90\%$/mg against PhIP and $80\%$/mg against MeIQx. The active fraction had the absorbance at 207.7 and 232nm.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.31 no.4
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• pp.587-593
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• 1998

To elucidate anti-tumor promoter from seaweed, the anti-tumor promoting activity of Ecklonia stolonifera, Undaria pinnatifida and Laminaria japonica extracts were determined by Epstein-Barr virus (EBV)-early antigen (EA) induction caused by a tumor promoter, teleocidin B-4. The methanol extracts of seaweed were subsequently fractionated with diethyl ether, distilled water, chloroform and ethyl acetate. Among the solvent fractions tested, chloroform and ethyl acetate fraction of E. stolonifera showed a high anti-tumor promoting activity at the levels of 88.0 and $85.9\%$ by the addition of 20 ${\mu}g/m{\ell}$, respectively. To characterize anti-tumor promoters from solvent fractions of E. stolonifera, the effects of phenols, chlorophyll derivatives and carotenoids on the anti-tumor promoting activity were investigated. Phenols, such as bromophenol and phloroglucinol showed anti-tumor promoting activity of $57\~66\%$ at 20 ${\mu}g/m{\ell}$. Pigments, such as chlorophylls and carotenoids exerted high anti-tumor promoting activities. Chlorophyll a and pheophorbide a exhibited the activity of $77.4\%$ and $66.6\%$ at 5${\mu}M/m{\ell}$, respectively. The active compounds of carotenoids were tentatively identified as lutein and $\alpha-cryptoxanthin$ from the profiles of visible spectra and R_f value of their authentic compounds, and showed anti-tumor promoting activities of $76.9\%$ and $84.4\%$ at dose of 20 ${\mu}g/m{\ell}$, respectively.

• Proceedings of the Korean Aquaculture Society Conference
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• 2006.05a
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• pp.228-229
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• 2006

• Proceedings of the Korean Society of Fisheries Technology Conference
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• 2002.05a
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• pp.469-470
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• 2002

• Landscaping Tree
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• s.98
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• pp.26-28
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• 2007

• Korean Journal of Pharmacognosy
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• v.27 no.2
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• pp.117-122
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• 1996

The methanolic extracts of some marine natural products were tested for investigating the effects on the formation of lipid peroxide and the activities of free radical generating enzymes. The methanolic extracts of Styela clava, Ecklonia stolonifera, Pachymeniopsis elliptica and Hypnea charoides which decreased the formation of lipid peroxide inhibited the activity of xanthine oxidase about 41, 20, 20 and 21% by adding $100\;{\mu}g/ml$ of each methanolic extracts, respectively. However, the four extracts didn't inhibit the activity of aldehyde oxidase.

• Journal of the Korean Society of Food Science and Nutrition
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• v.29 no.3
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• pp.448-452
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• 2000

실험동물에서 곰피로부터 분리한 phlorglucinol은 acetaminophen의 투여로 현저히 증가된 간조직에 있어서 지질과선화의 함량을 억제하였다. Acetaminophen 투여에 따른 간 cytochrome P-450, aminopyrine N-deme-thylase 및 aniline hydroxylase 활성변동은 관찰할 수 없었다. 곰피 성분 투여군은 glutathione S-transferase의 활성에서는 대조군의 수준에는 미치지 않으나 효소의 활성이 acetaminophen 단독 투여군보다 현저히 증가되었다. 그리고 간조직중 glutathione의 함량은 phlorglucionl을 전처리군에서 acetaminophen 단독 투여군보다 증가되었다. Glutathione reductase 활성에서는 acetaminophen 투여군은 대조군보다 활성이 감소되었으며, 성분으로 전처리한 군은 acetaminophen 단독 투여군보다 증가 되었다. 따라서 곰피에서 분리한 페놀성화합물인 phloroglucinol은 acetaminophen 투여로 증가되던 지질과 산화함량을 감소시키며, acetaminophen 대사효소활성에서는 glutathione S-transferase의 활성이 증가되어 acetaminophen 의 대사를 촉진시키는 것으로 추정된다.

• Proceedings of the Korean Nutrition Society Conference
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• 2003.05a
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• pp.271.2-271.2
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• 2003

• Journal of Ecology and Environment
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• v.38 no.4
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• pp.437-442
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• 2015

Studies to estimate seed longevity and dormancy of creeping bentgrass (Agrostis stolonifera L.) were conducted from 2000 to 2005 at Corvallis and Hermiston, Oregon. Seeds from three transgenic glyphosate resistant creeping bentgrass lines, 48-10, 48-13, and ASR368, and one non-transgenic glyphosate susceptible line, SR1020, were used. Creeping bentgrass seeds were buried at 3, 18 and 31 cm in 2000 and removed 6, 12, 18, 24, and 51 months later. Soil type and climatic conditions were different at the two locations. At Corvallis, the soil was a Malabon silty clay loam, and the winters wet and mild. The soil at Hermiston was an Adkins fine sandy loam, and winters drier and colder. Seeds of all creeping bentgrass lines deteriorated faster at Corvallis than at Hermiston. The estimated half-lives of creeping bentgrass lines buried at Corvallis were 8.4 to 20.2 months, while those buried at Hermiston were 8.4 to 37.7 months. At both sites, seeds of the glyphosate resistant lines, 48-10 and 48-13, deteriorated faster than the susceptible line, SR1020. However, seed deterioration in the resistant line, ASR368, was slower than all other creeping bentgrass lines. Based on the germination test, exhumed intact seeds at Corvallis were more dormant than those at Hermiston. If buried, it could be expected that viable creeping bentgrass seeds will persist more than 4 years after the seeds are introduced to a site, but environmental conditions can influence both seed longevity and dormancy.

• Biomolecules & Therapeutics
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• v.24 no.6
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• pp.650-658
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• 2016

Chronic alcohol consumption causes alcoholic liver disease, which is associated with the initiation of dysregulated lipid metabolism. Recent evidences suggest that dysregulated cholesterol metabolism plays an important role in the pathogenesis of alcoholic fatty liver disease. Ecklonia stolonifera (ES), a perennial brown marine alga that belongs to the family Laminariaceae, is rich in phlorotannins. Many studies have indicated that ES has extensive pharmacological effects, such as antioxidative, hepatoprotective, and antiinflammatory effects. However, only a few studies have investigated the protective effect of ES in alcoholic fatty liver. Male Sprague-Dawley rats were randomly divided into normal diet (ND) (fed a normal diet for 10 weeks) and ethanol diet (ED) groups. Rats in the ED group were fed a Lieber-DeCarli liquid diet (containing 5% ethanol) for 10 weeks and administered ES extract (50, 100, or 200 mg/kg/day), silymarin (100 mg/kg/day), or no treatment for 4 weeks. Each treatment group comprised of eight rats. The supplementation with ES resulted in decreased serum levels of triglycerides (TGs), total cholesterol, alanine aminotransferase, and aspartate aminotransferase. In addition, there were decreases in hepatic lipid and malondialdehyde levels. Changes in liver histology, as analyzed by Oil Red O staining, showed that the ES treatment suppressed adipogenesis. In addition, the ES treatment increased the expression of fatty acid oxidation-related genes (e.g., PPAR-${\alpha}$ and CPT-1) but decreased the expression of SREBP 1, which is a TG synthesis-related gene. These results suggest that ES extract may be useful in preventing fatty acid oxidation and reducing lipogenesis in ethanol-induced fatty liver.