• Asian Pacific Journal of Cancer Prevention
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• v.15 no.13
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• pp.5253-5257
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• 2014

Formaldehyde (FA) is an economically important chemical, and has been found to cause various types of toxic damage to the body. Formaldehyde-induced toxic damage involves reactive oxygen species (ROS) that trigger subsequent toxic effects and inflammatory responses, which may increase risk of cancer. Therefore, in the present study, we aimed to investigate the possible toxic mechanism in bone marrow caused by formaldehyde. In accordance with the principle of randomization, the mice were divided into four groups of 6 mice per group. One group was exposed to ambient air and the other three groups were exposed to different concentrations of formaldehyde (20, 40, $80mg/m^3$) for 15 days in the respective inhalation chambers, 2h a day. At the end of the 15-day experimental period, all mice were killed. Bone marrow cells were obtained. Some of those were used for the determination of blood cell numbers, bone marrow karyote numbers, CFU-F, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content; others were used for the determination of mitochondrial membrane potential (MMP), cell cycle and Bcl-2, Bax, CytC protein expression. WBC and PLT numbers in median and high dose groups were obvious reduced, but there was no change on RBC numbers. There was also reduced numbers of bone marrow karyotes and CFU-F in the high dose group. SOD activity was decreased, but MDA content was increased. MMP and Bcl-2 expression were decreased with increasing formaldehyde concentration, while expression of Bax and Cyt C was increased. We also observed change in cell cycling, and found that there was S phase arrest in the high dose group. Our study suggested that a certain concentration of formaldehyde could have toxic effects on the hematopoietic system, with oxidative stress as a critical effect.

• Korean journal of applied entomology
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• v.23 no.3 s.60
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• pp.166-171
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• 1984

The present studies were conducted to investigate the relative toxicity of several insecticides to the rice insect pests and the predatious spider, Pirate subpiraticus. In laboratory test by topical application, BPMC and MIPC for the plant and leafhoppers were toxic to Nilaparvata lugens, but less toxic to Pirata subpiraticus. Other carbamate insecticides such as carbaryl, carbofuran, and MTMC showed highly toxic effect on P. subpiraticus as well as N. lugens. No organophosphates showed selective toxicity to P. subpiraticus. Thiocyclam, effective to Chilo suppressalis and Sesamia inferens, had highly good selective toxicity to P. subpiraticus. In case of insecticides for Nephotettix cincticeps, BPMC only had a little selective toxicity between N. cincticeps and P. subpiraticus. Organophosphate insecticides which had been reported to induce chemical resistance to N. cincticeps showed high $LD_{50}$ value to N. cincticeps. In pot trials, dust formulation was more toxic to P. subpiraticus than emulsifiable concentrate. It was more toxic to P. subpiraticus to increase number. of insecticide application.

• Journal of the Korean Institute of Gas
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• v.23 no.1
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• pp.54-61
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• 2019

As the market for portable electronic devices expands, the demand for Lithium Ion Battery (LIB) is also increasing. LIB has higher efficiency than other secondary batteries, but there is a risk of explosion / fire due to thermal runaway reaction. Especially, Electric Vehicles (EV) equipped with a large capacity LIB cell also has a danger due to a large amount of toxic gas generated by a fire. Therefore, it is necessary to analyze the risk of toxic gas generated by EV fire to minimize accident damage. In this study, the flow of toxic gas generated by EV fire was numerically analyzed using Computational Fluid Dynamic. Scenarios were established based on literature data and EV data to confirm the effect distance according to time and exposure standard. The purpose of this study is to analyze the risk of toxic gas caused by EV fire and to help minimize the loss of life and property caused by accidents.

• Biomolecules & Therapeutics
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• v.10 no.3
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• pp.152-158
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• 2002

The present study elucidated the effect of $\beta$-carbolines (harmaline and harmalol) on brain mitochondlial dysfunction caused by the tyrosinase-induced oxidation of dopamine. Harmaline, harmalol and antioxidant enzymes (SOD and catalase) attenuated the dopamine-induced alteration of membrane potential, cytochrome c release and thiol oxidation in mitochondria. In contrast, antioxidant enzymes failed to reverse mitochondrial dysfunction induced by dopmnine plus tyrosinase. $\beta$-Carbolines decreased the damaging effect of dopamine plus tyrosinase against mitochondria, except no effect of harmalol on thiol oxidation. Antioxidant enzymes decreased the melanin formation from dopamine in the reaction mixture containing mitochondria but did not reduce the formation of dopamine quinone caused by tyrosinase. Both harmalol and harmaline inhibited the formation of reactive quinone and melanin. Harmalol being more effective for quinone formation and vise versa. The results indicate that compared to MAO-induced dopamine oxidation, the toxic effect of dopamine in the presence of tyrosinase against mitochondria may be accomplished by the dopamine quinone and toxic substances other than reactive oxygen species. $\beta$-Carbolines may decrease the dopamine plus tyrosinase-induced brain mitochondrial dysfunction by inhibition of the formation of reactive quinone and the change in membrane permeability.

• Korean Journal of Pharmacognosy
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• v.14 no.4
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• pp.149-160
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• 1983

It has been known that Gentianae macrophyllae Radix is reputed to be effective in removal of 'Pungseub' and 'Heoyeol', and to be analgesic. Since ancient times, however, there have been many examples of substituting Lycoctoni Radix for Gentianae macrophyllae Radix. For that reason, this experiment was conducted to compare the diuretic, analgesic, anti-inflammatory, anti-pyretic, anti-bacterial effect, and toxicity of Lycoctoni Radix with those of Gentianae macrophyllae Radix. The results obtained in this work were summarized as follows; In the test of acute toxicity, Lycoctoni Radix was found to be toxic in comparison to Gentianae macrophyllae Radix which was found to be non-toxic. Both herbs were found to be diuretic and Gentianae macrophyllae Radix was more effective than the other and to be ineffective for the blood pressure and respiration. Lycoctoni Radix was found to be more analgesic than the other. Gentianae macrophyllae Radix was found to be more anti-inflammatory of the two and both demonstrated anti-pyretic effect. Anti-bacterial effect was detected only in Lycoctoni Radix. It is concluded that Gentianae macrophyllae Radix has mild diuretic, analgesic, anti-inflammatory and anti-pyretic effect, but Lycoctoni Radix, due to its toxicity, can not be substituted for Gentianae macrophyllae Radix.

• The Korea Journal of Herbology
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• v.29 no.1
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• pp.1-6
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• 2014

Objectives : Many of currently used anti-cancer drugs were developed to target cell death mechanisms and had serious side effects by causing damage to normal cells. Hangambujeongsan or Kangai Fuzheng Powder was a mixture based on the traditional Chinese medicine. It had been used in the local Chinese hospitals to treat cancer patients for decades and had shown a certain level of beneficial effects without major toxic effects. But its mechanism of action had not been elucidated yet. Thus this study aimed to investigate the effects of Kangai Fuzheng Powder in an in vitro experiment. Methods : Cancer lines or RAW264.7 mouse macrophage cells were treated with Kangai Fuzheng Powder. Cell viability was measured by MTT assay, and morphological observation was also performed. Gene expression of cytokines in macrophages was determined by real-time polymerase chain reaction. Phagocytic function assay was also performed in macrophage cells. Results : Kangai Fuzheng Powder had no direct detrimental effect on cancer cells. When macrophages were co-cultured with cancer cells, Kangai Fuzheng Powder had toxic effect on cancer cells. After exposing macrophages to Kangai Fuzheng Powder, macrophages transformed into activated form and the mRNA level of tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, interleukin-10 and monocyte chemotactic protein-1 was significantly enhanced. Phagocytic activity of macrophages was dramatically potentiated. Conclusions : We demonstrated that anti-cancer effect of Kangai Fuzheng Powder was related to activation of macrophages including enhanced cytokine production and phagocytic function.

• Biomolecules & Therapeutics
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• v.12 no.1
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• pp.49-54
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• 2004

The present study was conducted to investigate the potential subacute toxicity of CKD-602 by a 5-day repeated intravenous administration in Sprague-Dawley rats. CKD-602 was administered intravenously to male rats at dose levels of 0, 0.08, 0.2, and 0.5 mg/kg for 5 days. Studies included general observation, body weight changes, ophthalmoscopic examination, hematology, se겨m biochemistry, gross findings at necropsy and organ weight measurement. There were no deaths in any treatment group and treatment related clinical sign was depilation in the 0.5 mg/kg groups. The decrease or suppression of body weight was also observed dose-dependently in all treatment groups. Decreased leukocyte in all treatment groups, decreased platelet in the above 0.2 mg/kg groups and increase in the serum levels of total cholesterol in the 0.5 mg/kg group were considered as a treatment related toxic effects. Decreased weight of thymus in all treatment groups anti decreased weight of spleen in the above 0.2 mg/kg group were observed. The intravenous administration of CKD-602 caused depilation and decreased weight and had toxic effect on the leukocyte, platelet, spleen and thymus. In the condition of this study, the target organs were spleen and thymus and the toxic effect level was determined to be 0.2 mg/kg, but no-observed-adverse-effect level (NOAEL) was considered to be lower than 0.08 mg/kg.

• Journal of Microbiology and Biotechnology
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• v.31 no.6
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• pp.867-874
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• 2021

Epalrestat (EPS) is a brain penetrant aldose reductase inhibitor, an approved drug currently used for the treatment of diabetic neuropathy. At near-plasma concentration, EPS induces glutathione biosynthesis, which in turn reduces oxidative stress in the neuronal cells. In this study, we found that EPS reduces neurodegeneration by inhibiting reactive oxygen species (ROS)-induced oxidative injury, mitochondrial membrane damage, apoptosis and tauopathy. EPS treatment up to 50 µM did not show any toxic effect on SH-SY5Y cell line (neuroblastoma cells). However, we observed toxic effect at a concentration of 100 µM and above. At 50 µM concentration, EPS showed better antioxidant activity against H₂O₂ (100 µM)-induced cytotoxicity, ROS formation and mitochondrial membrane damage in retinoic acid-differentiated SH-SY5Y cell line. Furthermore, our study revealed that 50 µM of EPS concentration reduced the glycogen synthase kinase-3 β (GSK3-β) expression and total tau protein level in H₂O₂ (100 µM)-treated cells. Findings from this study confirms the therapeutic efficacy of EPS on regulating Alzheimer's disease (AD) by regulating GSK3-β and total tau proteins phosphorylation, which helped to restore the cellular viability. This process could also reduce toxic fibrillary tangle formation and disease progression of AD. Therefore, it is our view that an optimal concentration of EPS therapy could decrease AD pathology by reducing tau phosphorylation through regulating the expression level of GSK3-β.

• The Korean Journal of Pain
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• v.29 no.4
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• pp.229-238
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• 2016

Background: The goal of this in vitro study was to investigate the effect of lipid emulsion on vasodilation caused by toxic doses of bupivacaine and mepivacaine during contraction induced by a protein kinase C (PKC) activator, phorbol 12,13-dibutyrate (PDBu), in an isolated endothelium-denuded rat aorta. Methods: The effects of lipid emulsion on the dose-response curves induced by bupivacaine or mepivacaine in an isolated aorta precontracted with PDBu were assessed. In addition, the effects of bupivacaine on the increased intracellular calcium concentration ($[Ca^{2+}]_i$) and contraction induced by PDBu were investigated using fura-2 loaded aortic strips. Further, the effects of bupivacaine, the PKC inhibitor GF109203X and lipid emulsion, alone or in combination, on PDBu-induced PKC and phosphorylation-dependent inhibitory protein of myosin phosphatase (CPI-17) phosphorylation in rat aortic vascular smooth muscle cells (VSMCs) was examined by western blotting. Results: Lipid emulsion attenuated the vasodilation induced by bupivacaine, whereas it had no effect on that induced by mepivacaine. Lipid emulsion had no effect on PDBu-induced contraction. The magnitude of bupivacaine-induced vasodilation was higher than that of the bupivacaine-induced decrease in $[Ca^{2+}]_i$. PDBu promoted PKC and CPI-17 phosphorylation in aortic VSMCs. Bupivacaine and GF109203X attenuated PDBu-induced PKC and CPI-17 phosphorylation, whereas lipid emulsion attenuated bupivacaine-mediated inhibition of PDBu-induced PKC and CPI-17 phosphorylation. Conclusions: These results suggest that lipid emulsion attenuates the vasodilation induced by a toxic dose of bupivacaine via inhibition of bupivacaine-induced PKC and CPI-17 dephosphorylation. This lipid emulsion-mediated inhibition of vasodilation may be partly associated with the lipid solubility of local anesthetics.

• Korean Journal of Pharmacognosy
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• v.13 no.3
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• pp.116-121
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• 1982

In order to investigate the side-effects of crude drugs, twenty drugs have been tested for the teratogenic effect in rats. Among seven drugs contained alkaloid as their ingredients, no one showed teratogenic effect, but Veratri rhizoma showed embryo-toxic as revealed by severe retardation in growth of the fetuses. The other thirteen drugs which have been used freguently in oriental medicines exhibited no teratogenic effect. Cyclophosphamide used as a reference compound showed severe malformation and retardation in the growth of rat fetuses. These findings suggest that the drug extracts adopted for the study might have no teratogenic effect in the rats.