• Fisheries and Aquatic Sciences
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• v.8 no.2
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• pp.76-82
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• 2005

We analyzed the paralytic shellfish poisoning (PSP) toxins of the toxic marine dinoflagellate Alexandrium tamarense collected from Dadaepo and Gaduck-do in Busan and from Sujeong-ri in Jinhae Bay, Korea, in April 2003. We also analyzed the PSP toxin of mussels (Mytilus galloprovincialis) and oysters (Crassostrea gigas) collected around Busan and Jinhae Bay. PSP toxin analyses were conducted by high performance liquid chromatography (HPLC). Fifteen cultured A. tamarense isolates contained 2.78 to 57.47 fmol/cell, with nearly identical toxin profiles: major components C2, GTX4; minor components C1, GTX1, NEO; and trace components GTX2, GTX3, STX. PSP toxin contents were 0 to $492\;\mu{g}$ STXeq/100 g in mussels and 0 to $48\;\mu{g}$ STXeq/100 g in oysters. Mussels at Gijang and Sujeong-ri contained the most PSP toxin contents ($492\;\mu{g}\;STXeq/100\;g\;and\;252\;\mu{g}\;STXeq/100\;g,\;respectively$), exceeding the quarantine level ($80\;\mu{g}$ STXeq/100 g). Their dominant toxin components were C2, C1, GTX2, and GTX3; the minor components GTX1, GTX4, GTX5, and NEO were sporadically detected. Phytoplankton contained 0.774 fmol/L seawater and 1.228 fmol/L seawater at Gijang and Sujeong-ri in April. At that time, Alexandrium cells were present in the water column at Gijang at 2,577 cells/mL and at Sujeong-ri at 6,750 cells/mL. Overall, we found the high and similar PSP toxin contents in AZexandrium isolates and mussels, and a correlation between occurrence of toxic Alexandrium cells in the water column and mussel intoxification. High densities of toxic Alexandrium cells in the water column immediately preceded shellfish intoxification at Gijang and Sujeong-ri in April.

• Journal of Korean Society on Water Environment
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• v.23 no.5
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• pp.659-664
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• 2007

The objective of this study is to evaluate the detoxification method for the endocrine disrupting chemicals by manganese oxide. Manganese coated sand and bisphenol-A (BPA) was used as the reactive medium and the contaminant. Results showed that manganese oxide effectively degrades BPA by oxidative coupling reaction. The nonlinear oxidative coupling reaction orders were obtained for BPA and oxide, respectively. The reaction rate of BPA decreased as initial BPA concentration increased, as oxide loading decreased and as pH increased. The higher ionic strength, the higher reaction rate was observed. Divalent cations were adsorbed on the oxide surfaces, resulting in the decreased degradation rate of BPA.

• YAKHAK HOEJI
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• v.36 no.3
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• pp.285-290
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• 1992

After rats were exposed to 5,000 ppm carbon monoxide for 30 minutes, the amounts of catecholamine neurotransmitters in stratum were measured using high performance liquid chromatograph equipped with electrochemical detector. The concentration of dopamine in stratum was significantly decreased after carbon monoxide intoxification, but those of dihydroxyphenylacetic acid, norepinephrine, and epinephrine was not changed. However the pretreatments of Ginseng total saponin and panaxatriol saponin increased the concentrations of dopamine and its acidic metabolites (DOPAC and HVA). Ginseng total saponin also increased the concentrations of norepinephrine and epinephrine. Similar results were obtained from aged rats.

• Journal of Microbiology and Biotechnology
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• v.16 no.11
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• pp.1784-1790
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• 2006

Bacillus anthracis is a causative agent of anthrax. Anthrax toxins are composed of a protective antigen (PA), lethal factor (LF), and edema factor (EF), in which the PA is a central mediator for the delivery of the two enzymatic moieties LF and EF. Therefore, the PA has been an attractive target in the prevention and vaccinization for anthrax toxin. Recently, it has been reported that the molecule consisting of multiple copies of PA-binding peptide, covalently linked to a flexible polymer backbone, blocked intoxification of anthrax toxin in an animal model. In the present study, we have screened novel diverse peptides that bind to PA with a high affinity (picomolar range) from an M13 peptide display library and characterized the binding regions of the peptides. Our works provide a basis to develop novel potent inhibitors or diagnostic probes with a diverse polyvalence.

• Journal of the Korean Society of Food Science and Nutrition
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• v.36 no.5
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• pp.521-526
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• 2007

The effects of red ginseng powder on hepatotoxicity in $benzo(\alpha)pyrene\;[B(\alpha)P]$-treated mice were investigated. Male ICR mice were pretreated with red ginseng powder (50 or 100 mg/kg/day, for 5 days, intraperitoneally) before treatment with $B(\alpha)P$ (0.5 mg/kg, i.p, single dose). The ability of red ginseng powder to protect against oxidative damage to the mouse liver was examined by determining the level of lipid peroxide, glutathione, and the antioxidant enzyme activities. The glutathione content depleted by $B(\alpha)P$ were significantly increased by red ginseng powder, but elevation of lipid peroxide content induced by $B(\alpha)P$ was decreased by red ginseng powder. The increased activities of superoxide dismutase, catalase and glutathione peroxidase after $B(\alpha)P$-treatment were decreased by the treatment of red ginseng Powder; however, glutathione S-transferase activity depleted by $B(\alpha)P$ were significantly increased. These results suggest that red ginseng powder can protect against $B(\alpha)P$ intoxification through its antioxidant properties.

• Journal of Ginseng Research
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• v.30 no.3
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• pp.112-116
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• 2006

To investigate the protective effect of saponin from red ginseng extract, 2,3,7,8-tetrachlorodibenzo--dioxin (TCDD) was exposed to female guinea pigs and then femur weights was measured. Forty eight female guinea pigs ($820{\pm}25\;g$) were divided into 6 groups. Normal control group (NC) received vehicle and saline; only TCDD-treated group (TT) received TCDD ($5.0\;{\mu}g/kg$, single dose) intraperitoneally; pretreated group of saponin 10 (PE 10) received 10 mg/kg of saponin i.p. for 4 weeks from 1 week before TCDD-exposure; pretreated group of saponin 20 (PE 20) also received 20 mg/kg of saponin i.p. for 4 weeks from 1 week before TCDD-exposure. While, post-treated group of saponin 10 (CE 10) received 10 mg/kg of saponin i.p for 3 weeks after TCDD-exposure. Post-treated group of saponin 20 (CE 20) received 20 mg/kg saponin i.p for 3 weeks after TCDD-exposure. Body weight of TT group was significantly decreased after TCDD-exposure. However, body weight in all saponin-treated groups increased throughout the experimental period, although the increasing rate was slower than that of NC group. Body weights of PE 10 and 20 groups showed more higher increase than those of CE groups during the experimental period. Decrease of femur weights in female guinea pigs by TCDD intoxification was significantly recovered by the saponin treatment. Decrease of $Ca^{2+}$ level of femurs in female guinea pigs exposed TCDD also recovered by the treatment of saponin from red ginseng extract. Especially, PE20 group showed the highest increase of the $Ca^{2+}$ level in femur among the saponin treated groups. These results suggest that ginseng saponin might be a useful protective agent against femur damage caused to decrease of $Ca^{2+}$ by TCDD.