• Toxicological Research
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• v.12 no.2
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• pp.203-211
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• 1996

Methanol has been widely used as an industrial solvent and environmental exposure to methanol would be expected to be increasing. In humans, methanol causes metabolic acidosis and damage to ocular system, and can lead to death in severe and untreated case. Clinical symptoms are attributed to accumulation of forrnic acid which is a metabolic product of methanol. In humans and primates, formic acid is accumulated after methanol intake but not in rodents due to the rapid metabolism of methanol. Neverthless, the developmental and reproductive toxicity were reported in rodents. Previous reports showed that perinatal exposure to ethanol produces a variety of damage in human central nervous system by direct neurotoxicity. This suggests that the mechanism of toxic symptoms by methanol in rodents might mimic that of ethanol in human. In the present study I hypothesized that methanol can also induce toxicity in neuronal cells. For the study, primary culture of rat hippocampal neurons and glias were empolyed. Hippocampal cells were prepared from the embryonic day-17 fetuses and maintained up to 7 days. Effect of methanol (10, 100, 500 and 1000 mM) on neurite outgrowth and cell viability was investigated at 0, 18 and 24 hours following methanol treatment. To study the changes in proliferation of glial cells, protein content was measured at 7 days. Neuronal cell viability in culture was not altered during 0-24 hours after methanol treatment. 10 and 100 mM methanol treatment significantly enhanced neurite outgrowth between 18-24 hours. 7-day exposure to 10 or 100 mM methanol significantly increased protein contents but that to 1000 mM methanol decreased in culture. In conclusion, methanol may have a variety of effects on growing and differentiation of neurons and glial cells in hippocampus. Treatment with low concentration of methanol caused that neurite outgrowth was enhanced during 18-24 hours and the numbers of glial cell were increased for 7 days. High concentration of methanol brought about decreased protein contents. At present, the mechanism responsible for the methanol- induced enhancement of neurite outgrowth is not clear. Further studies are required to delineate the mechanism possibly by employing molecular biological techniques.

• The Korean Journal of Nuclear Medicine
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• v.34 no.4
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• pp.360-365
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• 2000

We experienced a case of cerebral hypoperfusion due to cyclosporine neurotoxocity confirmed only by Tc-99m ECD brain SPECT. A 53-year-old female had received allogenic peripheral blood stem cell transplantation due to refractory plasmacytoid lymphoma. Cyclosporine and steroid had been administrated to prevent graft versus host disease. Twenty days after transplantation, she became delirious and suffered from generalized tonic-clonic seizure. Immediately, brain MRI and MR angiography were performed and these studies did not show any abnormal findings. However, Tc-99m ECD brain SPECT showed diffuse hypoperfusion in the left cerebral hemisphere and blood cyclosporine level was 962.6 ng/ml. Cyclosporine administration was stopped and discontinuation of cyclosporine resulted in disappearance of all neurological symptoms. The same neurological symptoms recurred with cyclosporine re-administration for management of exacerbated graft versus host disease. In this case, Tc-99m ECD brain SPECT proved very helpful in the diagnosis of cycloporine neurotoxicity.

• Journal of the Korean Society of Urban Environment
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• v.18 no.4
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• pp.391-399
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• 2018

In this study, Diazinon which is the most widely used organophosphorus pesticides (OPPs) among pesticides was removed by ozone/hydrogen peroxide advanced oxidation process (Peroxone AOP). Diazinon is mainly found in groundwater, drinking water, rivers and ponds that are near agricultural areas using the pesticide. Accumulation of Diazinon on the body in the form of metabolites causes neurotoxicity, confusion, dizziness and vomiting. Diazinon is not easily removed by conventional water treatment processes. This study investigated the Diazinon removal characteristics with OH radicals with strong oxidizing power generated by using ozone and hydrogen peroxide. We determined optimal hydrogen peroxide/ozone injection molar ratio and confirmed the elimination reaction to initial Diazinon concentration, pH and DOC concentration, which are factors influencing the removal efficiency. Domestic researches on pesticide removal in the environment are much less than the cases of overseas. This study is expected to provide a basis for the process design for pesticide removal.

• Journal of Life Science
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• v.22 no.8
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• pp.1099-1106
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• 2012

The cytotoxicity of the colorant in conjugated linoleic acid (CLA) was investigated in human cancer cell lines and a normal human cell line. Commercially-available CLA with a brown color (designate crude CLA; c-CLA) was distilled in a vacuum (10 mmHg-$220^{\circ}C$, 10 mmHg-$235^{\circ}C$, 10 mmHg-$240^{\circ}C$, and 20 mmHg-$260^{\circ}C$) for 30 min to obtain pure CLA (distilled CLA; d-CLA) and dark brown-colored CLA (residual CLA; r-CLA) samples. No color intensity was shown in the d-CLA sample obtained under 10 mmHg-$220^{\circ}C$ conditions of distillation when the L (brightness), a (red/blue), and b (yellow/green) parameters were analyzed, whereas the r-CLA sample showed a dark brown color. The composition of CLA isomers in both the d- and r-CLA samples, as compared to that of the c-CLA sample, was not significantly different when analyzed by gas chromatography. When the cytotoxicity of the r-CLA and d-CLA samples obtained under 10 mmHg-$220^{\circ}C$ conditions were compared against human breast cancer cells (MCF-7), human lung cancer cells (A-549), human colon cancer cells (HT-29), human prostate cancer cells (PC-3), and human neuroblastoma cells (SK-N-SH), no significant cytotoxicity was seen in the cell lines. These results suggest that the color or colorant in the CLA samples did not have any effects on the proliferation of human cancer and normal cells and imply that the colorant in commercially available CLA samples is safe for human consumption.

• Journal of the Korean Society of Food Science and Nutrition
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• v.33 no.2
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• pp.262-270
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• 2004

It is well known that long-term heavy ethanol intake causes alcoholic dementia, cerebellar degeneracy or Wernicke-Korsakoff syndrome and aggravates the conditions of many other neuro-psychotic disorders. Recently it is indicated that protein kinase C (PKC) plays an important role in the action of ethanol and in the neuro-adaptational mechanisms under chronic ethanol exposure. In order to investigate the effect of ethanol on PKC isoforms levels within the range of not showing any cytotoxicity, B103 neuroblastoma cell line trans-formed from murine central nervous system was employed and western blot analysis was carried out by using PKC isoform-specific antibodies. The changes of PKC-$\alpha$, ${\gamma}$, $\varepsilon$ and ζ level in the range of ethanol concentration 50∼200 mM were examined at the exposure time 1, 2, 8, 18 and 24 hrs in both cytosolic and membrane fraction. A typical ethanol concentration inducing the PKC isozymes was 100 mM, and the transforming time ranges of PKC isozymes could be considered as two different parts to each PKC isoform such as initial (0∼2 hrs) and prolonged (8∼24 hrs) stages. PKC-${\gamma}$ and PKC-$\varepsilon$ were clearly induced during the prolonged stages in cytosol at 18 hrs, and membrane fraction at 8 hrs and 18 hrs, respectively. On the other hand the PKC-$\alpha$ and PKC-ζ isozymes were largely induced in the prolonged stages at 18 hrs and 24 hrs, where the PKC-$\alpha$ isozyme was induced in both cytosol and membrane fractions at 200 mM ethanol concentration while the PKC-ζ isozyme was induced only in the membrane fractions at 100,200 mM. At 200 mM ethanol concentration of 24 hrs incubation in the prolonged stage, the PKC-$\alpha$ was maximally induced by 150% of the control values whereas the PKC-${\gamma}$ was significantly decreased to 47% of the control values. These results suggest that 100∼200 mM ethanol may modulate the signal transduction and neurotransmitter release in the central nervous system through the regulation of PKC isozymes, and the action of these isoforms may act differently each other in the cell.

• Journal of the Korean Society of Food Science and Nutrition
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• v.44 no.3
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• pp.347-355
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• 2015

Oxidative stress is one of the key mechanisms involved in neuronal damage. Neuroprotective effects and underlying mechanisms of action of several wild vegetables, Cirsium setidens (CS), Pleurospermum kamtschaticumin (PK), and Allium victorials (AV), against oxidative stress induced by hydrogen peroxide in SK-N-SH cells were investigated. CS and AV up to $400{\mu}g/mL$ showed no detectable effects on cell viability of human SK-N-SH neuro-blastoma cells compared with control. Incubation of SK-N-SH cells with hydrogen peroxide resulted in significant induction of cell death and reaction oxygen species (ROS) production, whereas treatment of cells with CS and AV significantly reduced cell death and ROS production, respectively. Among the wild vegetables tested, CS and PK showed more effective DPPH radical scavenging activity than AV, whereas PK showed strong cytotoxicity in SK-N-SH cells compared with the control. CS showed much higher inhibitory effects on cell death and ROS generation against oxidative stress than AV. Thus, CS was selected for subsequent experiments. Ethyl acetate (EA), hexane, butanol, aqueous, and chloroform extracts from CS significantly inhibited cell death and ROS generation in SK-N-SH cells induced by oxidative stress. EA extract from CS (CS-EA) showed the highest DPPH radical-scavenging activity, intra-cellular ROS-scavenging activity, and neuroprotective effects. CS-EA attenuated apoptosis signal-regulating p38 activation by inhibiting phosphorylation. The findings suggest that CS-EA protects neuronal cells through antioxidant activity and inhibition of phosphorylation of p38 in brain neural cells.

• Journal of Food Hygiene and Safety
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• v.22 no.4
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• pp.395-400
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• 2007

Apricot Kernel, consumed as herbal medicine, contains amygdalin which generate HCN upon hydrolysis. Dyspnea was reported by ingesting large amount of apricot kernel, and neurological disorders such as tropic ataxic neuropathy or konzo were known as chronic toxicity of amygdalin. Other cyanogen containing plants, including flaxseed and almond, are consumed as food around the world. Moreover, some of them are promoted as functional food, leading to higher consumption, and posing health risk by cyanogenic components. The objective of this study was to find a method for the reduction of the cyanogenic compound, using apricot kernel as a model food. The most effective reduction was obtained by boiling the slices of the kernel for one hour in pH 1 HCl solution, showing 90% removal. However, the common process known to reduce the cyanogen contents, i.e., long incubation at the low temperature, did not show significant change in cyan concentration. Our data contribute to the safety of the plants containing cyanogenic compounds if they were to be developed as foodstuff.

• Korean Journal of Environmental Agriculture
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• v.10 no.2
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• pp.167-177
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• 1991

O-ethyl S-methyl ethylphosphonothioate [$LD_{50}$ (rat, oral) 4.6mg/kg ; $K_i$(bovine erythrocyte acetylcholinesterase) 303 $M^{-1\;min-1}$] was selected as a model compound to study the mode of action of O, S-dialkyl alkylphosphonothioates which have been hypothesized to be toxic via a bioactivation process. Two chemical oxidants, meta-chloroperoxybenzoic acid and monoperoxyphthalic acid, and rat liver microsomal oxidases were used to mimic the action of mixed function oxidases on the model compound. The formation of S-oxide, a very unstable active intermediate, was proposed based on the identification of metabolic products.Furthermore, a trapping experiment with ethanol showed that the unstable intermediate S-oxide had the ability to phosphorylate acetylcholinesterase which is an important enzyme in nerve systems. The S-oxide intermediates are presumed to be responsible for the toxicity of O,S-dialkyl alkylphosphonothioates.

• Journal of Life Science
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• v.23 no.1
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• pp.84-94
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• 2013

The cytotoxicity of coffee-like green tea (CLGT) was determined in a human breast cancer cell line, MCF-7; a human prostate cancer cell clone, PC-3; a human neuroblastoma cell line, SK-N-SH; and a rat cardiomyoblast cell line, H9c2, with reference to green tea leaves (GTL). The CLGT was prepared by roasting the GTL for 60 min at $240^{\circ}C$ in a temperature-controlled frying pan. The CLGT preparation imitated the flavor and taste characteristics of coffee fairly well according to sensory analysis. The CLGT preparation had no adverse cytotoxic effects on the cancer cells or the normal cells compared to GTL. No significant change in the antioxidant activity was seen in the CLGT preparation compared to that of GTL. The amount of total protein, sugar, and phenolic compounds was reduced in the preparation relative to those in GTL, a fact that might explain the coffee-like flavor and/or taste characteristics of the CLGT preparation. These results suggest that CLGT prepared by roasting GTL for 60 min at $240^{\circ}C$ does not show any adverse effects on cancer cells and normal cells compared to GTL. They imply that CLGT could be safe for human consumption.

• Proceedings of the Korean Society for Emotion and Sensibility Conference
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• 2009.11a
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• pp.190-192
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• 2009

Kainic acid (KA), an agonist for kainate and AMPA receptors, is an excitatory neurotoxic substance. Vitamin E such as alpha-tocopherol and alpha-tocotrienol is a chain-breaking antioxidant, preventing the chain propagation step during lipid peroxidation. In the present study, we have investigated the neuroprotective effects of alphatocopherol and alpha-tocotrienol on KA-induced neuronal death using organotypic hippocampal slice culture (OHSC). After 15h KA treatment, delayed neuronal death was detected in CA3 region. Alpha-tocopherol and alpha-tocotrienol increased cell survival and reduced the number of TUNEL-positive cells in CA3 region. These data suggest that alpha-tocopherol and alpha-tocotrienol treatment have protective effects on KA-induced cell death