• Applied Biological Chemistry
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• v.47 no.1
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• pp.1-16
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• 2004

The purpose of this paper is to review the occurrence, analytical methods and reduction methods of aflatoxins in foods. Aflatoxins are produced by the secondary metabolism of various fungal species and have the highest toxicity among mycotoxins. Due to their toxicity including carcinogenic activity, aflatoxins affect not only the health of humans ana animals but also the economics of agriculture and food. As a food-importing country, because aflatoxins could contaminate raw commodities and foodstuffs, there should be inspection on the exposure and the regulation of risk assessment as a food safety measure. In addition, studies on rapid analytical methods and reduction of toxicity by various processes for aflatoxins should be carried out in conjunction with those of the risk assessment of aflatoxins.

• Journal of the Korean Magnetic Resonance Society
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• v.15 no.1
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• pp.54-68
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• 2011

$^1H$ nuclear magnetic resonance (NMR) spectroscopy of biological samples has been proven to be an effective and nondestructive approach to probe drug toxicity within an organism. In this study, ketoprofen toxicity was investigated using $^1H$-NMR spectroscopy coupled with multivariate statistical analysis. Histopathologic test of ketoprofen-induced acute gastrointestinal damage in rats demonstrated a significant dose-dependent effect. Furthermore, principal component analysis (PCA) derived from $^1H$-NMR spectra of urinary samples showed clear separation between the vehicle-treated control and ketoprofen-treated groups. Moreover, PCA derived from endogenous metabolite concentrations through targeted profiling revealed a dose-dependent metabolic shift between the vehicle-treated control, low-dose ketoprofen-treated (10 mg/kg body weight), and high-dose ketoprofen-treated (50 mg/kg) groups coinciding with their gastric damage scores after ketoprofen administration. The resultant metabolic profiles demonstrated that the ketoprofen-induced gastric damage exhibited energy metabolism perturbations that increased urinary levels of citrate, cis-aconitate, succinate, and phosphocreatine. In addition, ketoprofen administration induced an enhancement of xenobiotic activity in fatty oxidation, which caused increase levels of N-isovalerylglycine, adipate, phenylacetylglycine, dimethylamine, betaine, hippurate, 3-indoxylsulfate, N,N-dimethylglycine, trimethyl-N-oxide, and glycine. These findings demonstrate that $^1H$-NMR-based urinary metabolic profiling can be used for noninvasive and rapid way to diagnose adverse drug effects and is suitable for explaining the possible biological pathways perturbed by nonsteroidal anti-inflammatory drug toxicity.

• Journal of Environmental Health Sciences
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• v.40 no.2
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• pp.105-113
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• 2014

Objectives: It is necessary to apply quantitative structure activity relationship (QSAR) for the various chemicals with insufficient toxicity data that are used in the workplace, based on the precautionary principle. This study aims to find application plan of QSAR software tool for predicting health hazards such as genetic toxicity, and carcinogenicity for some chemicals used in the electronics industries. Methods: Toxicity prediction of 21 chemicals such as 5-aminotetrazole, ethyl lactate, digallium trioxide, etc. used in electronics industries was assessed by Toxicity Prediction by Komputer Assisted Technology (TOPKAT). In order to identify the suitability and reliability of carcinogenicity prediction, 25 chemicals such as 4-aminobiphenyl, ethylene oxide, etc. which are classified as Group 1 carcinogens by the International Agency for Research on Cancer (IARC) were selected. Results: Among 21 chemicals, we obtained prediction results for 5 carcinogens, 8 non-carcinogens and 8 unpredictability chemicals. On the other hand, the carcinogenic potential of 5 carcinogens was found to be low by relevant research testing data and Oncologic TM tool. Seven of the 25 carcinogens (IARC Group 1) were wrongly predicted as non-carcinogens (false negative rate: 36.8%). We confirmed that the prediction error could be improved by combining genetic toxicity information such as mutagenicity. Conclusions: Some compounds, including inorganic chemicals and polymers, were still limited for applying toxicity prediction program. Carcinogenicity prediction may be further improved by conducting cross-validation of various toxicity prediction programs, or application of the theoretical molecular descriptors.

• Journal of Integrative Natural Science
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• v.5 no.2
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• pp.107-119
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• 2012

Polymerization of monomeric amyloid-${\beta}$ peptides ($A{\beta}$) into soluble oligomers and insoluble fibrils is one of the major pathways triggering the pathogenesis of Alzheimer's disease (AD). Using small molecules to prevent the polymerization of $A{\beta}$ peptides can, therefore, be an effective therapeutic strategy for AD. In this study, we investigated the effects of mono- and bi-flavonoids on $A{\beta}42$ toxicity and fibrillogenesis and found that the bi-flavonoid, taiwaniaflavone (TF) effectively and specifically inhibits $A{\beta}$ toxicity and fibrillogenesis. Compared to TF, the mono-flavonoid apigenin (AP) is less effective and less specific. Our data showed that differential effects of the mono- and bi-flavonoids on $A{\beta}$ fibrillogenesis correlate with their varying cytoprotective efficacies. We also found that other bi-flavonoids, namely 2',8"-biapigenin, amentoflavone, and sumaflavone, can also effectively inhibit $A{\beta}$ toxicity and fibrillogenesis, implying that the participation of two mono-flavonoids in a single bi-flavonoid molecule enhanced their activity. Bi-flavonoids, while strongly inhibited $A{\beta}$ fibrillogenesis, accumulated nontoxic $A{\beta}$ oligomeric structures, suggesting that these are off-pathway-oligomers. Moreover, TF abrogated the toxicity of preformed $A{\beta}$ oligomers and fibrils, indicating that TF and other bi-flavonoids may also reduce the toxicity of toxic $A{\beta}$ species. Altogether, our data clearly show that bi-flavonoids, possibly due to the possession of two $A{\beta}$ binders separated by an appropriate size linker, are likely to be promising therapeutics to suppress $A{\beta}$ toxicity.

• Archives of Pharmacal Research
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• v.7 no.1
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• pp.61-62
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• 1984

The toxicity of water extracts from intestine parts (digestive tract respiratory tree) of Korean Stichopus japonicus was determined using mouse units and more purified substance decreases the amplitude of contraction of guinia pig atria in vitro; showes negative chronotropic and ionotropic effects in the spontaneously beating guinea pig atria.

• Proceedings of the Korean Environmental Sciences Society Conference
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• 2002.05b
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• pp.452-454
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• 2002

A biosurfactant-producing microorganism, .Pseudomouos sp. EL-G527 was isolated from activated sludge by enrichment culture when grown on mineral salt medium containing n-hexadecane as a carbon source. The biosurfactant from .Pseudomonar sp. EL-G527 exhibited lesser toxicity to bacterial population than synthetic surfactants and in the biodegradation test, biosurfactant was rapidly degraded and lost its activity as surface active material after 1 day incubation. In this study, the biosurfactant from Pseudomonas sp. EL-G527 was effective surface-active compound, more biodegradable and less toxic to microbial ecosystem than various synthetic surfactants.

• Toxicological Research
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• v.2 no.1
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• pp.31-36
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• 1986

The present work was undertaken to investigate the effect of glycyrrhetinic acid on pyridine toxicity. When glycyrrhetinic acid was pretreated, pyridine-induced CNS depression and mortality were decreased. A striking enhancement of serum transaminase activities after pyridine administration was markedly decreased by glycyrrhetinic acid pretreatment. It was also observed that the hepatic microsomal aniline hydroxylase activity, which is concerned with pyridine metabolism, was significantly increased in glycyrrhetinic acid pretreated mice.

• Journal of Plant Biology
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• v.30 no.3
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• pp.181-187
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• 1987

Copper inhibited PSII-mediated O2 evolution (H2OlongrightarrowDCIP, H2OlongrightarrowSiMo) but not PSImediated O2 uptake(DCIP. Asc.longrightarrowMV) in isolated Chinese cabbage chloroplasts. Copper toxicity on PSII-mediated O2 evolution was higher at alkaline condition than at acidic condition and was inhanced by light illumination after copper treatment. The increased toxicity by light illumination was not recovered by subsequent dark treatment. The inhibitory effect of copper on H2OlongrightarrowDCIP reaction was higher than that on H2OlongrightarrowSiMo reaction. This result suggests that there may be another inhibitory site of copper on PSII other than water oxidizing side of PSII.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.358.2-358.2
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• 2002

Platinum(II) coordination complex(cisplatin) has been currently used as one of the most effective compounds in the treatment of various solid tumors. However. its use has been limited by severe side effects such as renal toxicity. Our platinum-based drug discovery program has been aimed at developing drugs capable of diminishing toxicity and improving selective cytotoxicity. (omitted)

• Journal of Nutrition and Health
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• v.17 no.3
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• pp.193-198
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• 1984

Rice, the staple food in Korea, is deficient to some extent in protein, lipid and vitamins. This study was carried out in order to investigate the effects of dietary supplementation to the rice diet of cellulose, ginseng, and ${\alpha}$-tocopherol on lead toxicity in rats. Using male rats fed the rice diet with the distilled drinking water containing 750mg of lead as nitrate per liter, for 11 weeks, organ weights, hemoglobin levels, serum glutamic pyruvic transaminase activity and accumulation of lead in liver, blood and kidney were observed. Supplementation of cellulose, ginseng and ${\alpha}$-tocopherol to the lead groups showed the protective effect significantly in the weight of liver but no influence in hemoglobin levels. Ginseng especially decreased the serum glutamic pyruvic transaminase activity to normal level. The three supplemented diets reduced the lead accumulation in kidney and blood, but not in liver.