• Environmental Analysis Health and Toxicology
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• v.24 no.1
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• pp.33-41
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• 2009

Among the toxicants in the environment dioxin-like compounds, including TCDD(2,3,7,8-Tetrachlorodibenzo-p-Dioxin), are well known as carcinogen and teratogen. TCDD the most toxic of these compounds, may result in a wide variety of adverse health effects in humans and environment, including carconogenesis, hepatotoxicity, teratogenesis, and immunotoxicity. Also TCDD increases superoxide, peroxide radicals and induces oxidative stress that leads to breakage of DNA single-strand and mitochondrial dysfunction. Recently, there have been reports that persistent organic pollutants(POPs) may be causing metabolic disease through mitochondrial toxicity. In order to examine if dioxin brings about toxicity on mitochondria directly, we measured the change of the mitochondrial membrane potential after exposure to TCDD using JC-1 dye. After short time exposure of dioxin, mitochondrial depolarization was observed but it recovered to the control level immediately. This TCDD effect on mitochondrial membrane potential was not correlated either to the production of reactive oxygen species(ROS) or extracellular $Ca^{2+}$ by TCDD. Less than 2 hours exposure of TCDD did not show any change in ROS production but 0.25 nM TCDD for 48 hours or 0.5 nM TCDD for 12 hours exposure did increase in ROS production. Under these conditions of ROS production by TCDD, no changes in the mitochondrial membrane potential by TCDD was observed.

• Environmental Analysis Health and Toxicology
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• v.17 no.4
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• pp.357-362
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• 2002

Tests for the toxicity of tributyltin (TBT) were conducted on mysid collected from Dadepo beach, Pusan, Korea. The toxic effects of tributyltin on the survival, growth and oxygen consumption of the mysid, Neomysis awatschensis have been evaluated. Mysids were exposed to several concentrations of TBT (0, 0.56, 1.15, 3.07 and 6.12 $\mu\textrm{g}$/L) for 6 weeks. Survival rate was decreased with increases in concentration and exposure time and the reduction of more than 40％ occurred at TBT concentration greater than 1.15 $\mu\textrm{g}$/L after 6 weeks. Growth rate was significantly decreased at concentrations greater than 1.15 $\mu\textrm{g}$/L. Oxygen consumption rate was also decreased in a concentration-dependent way and significantly decreased to 39,47 and 69％ of the control at 1.15, 3.07 and 6.12 $\mu\textrm{g}$/L, respectively. These results indicate that the contamination of aquatic environment by TBT has the potential to significantly reduce coastal and estuaries recruitment of mysids.

• Ocean Science Journal
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• v.43 no.2
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• pp.107-113
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• 2008

Laboratory bioassays were conducted to test the acute toxicity effects of sudden exposure to sodium cyanide (NaCN) on the endogenous rhythm of the oxygen consumption rate (OCR) in the black rockfish Sebastes schlegeli. The OCR of the black rockfish(n = 14, total length = $20.4{\pm}1.16\;cm$, wet weight = $158{\pm}25\;g$) was measured with an automatic intermittent-flow-respirometer. OCR decreased significantly when experimental fish were exposed to NaCN. When exposed to 10 ppb NaCN, fish were able to recover their OCR rhythmic activities. When fish were exposed to 20 ppb, however, the metabolic activity rhythms were not recovered. These results suggest that exposure to NaCN concentrations over 20 ppb cause severe physiological damage to the endogenous rhythms of black rockfish.

• Journal of the Korea Safety Management & Science
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• v.18 no.3
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• pp.47-54
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• 2016

A confined space means places where the risk of damage to health caused by lack of oxygen or hazardous gases in inadequate ventilation conditions and the risk of fire and explosion caused by flammable substances. Asphyxiation accidents in a confined space occured every year and also occurred more than two people at the same time. In this study, we surveyed the domestic statistical data occurred the lack of oxygen in confined space for the last 10 years(2006-2015) and, analyzed the accident by industries sector, workplace size etc. 17 fatal work accidents that occurred in confined spaces in Korea between 2013 and 2015 were investigated and analyzed using the database of the KOSHA and suggested interventions to minimize asphyxiation accidents in confined spaces. This paper is expected to be used to establish interventions planning and training as a preventive measures in workplace having confined spaces.

• Proceedings of the Korea Institute of Fire Science and Engineering Conference
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• 1997.11a
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• pp.178-184
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• 1997

The cone calorimeter as defined by ISO 5660, ASTM 1354, and NFPA 264A is used to assess the reaction to fire of almost any material that must be evaluated in the fire science field. Typical combustion gas analyses include oxygen, CO and CO2. Oxygen consumption is used to determine rate of heat release. Analysis of combustion gases other than oxygen, CO and CO2 has been attempted using filters to remove the solid smoke particles before analysis. This method has generated unreliable results due to the adsorption of many gas components on the active carbon . particles deposited on the filters. A technique using fourier Transform Infrared (FTIB) analysis without filtration will be disclosed and a discussion will be presented of the analytical results of toxic gases produced from various flame retarded polymeric materials. Use of such data in lethal toxic potency determinations is also reviewed.

• BMB Reports
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• v.37 no.4
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• pp.454-459
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• 2004

Experimental hyperoxia represents a suitable in vitro model to study some pathogenic mechanisms related to oxidative stress. Moreover, it allows the investigation of the molecular pathophysiology underlying oxygen therapy and toxicity. In this study, a modified experimental set up was adopted to accomplish a model of moderate hyperoxia (50% $O_2$, 96 h culture) to induce oxidative stress in the human leukemia cell line, U-937. Spectrophotometric measurements of mitochondrial respiratory enzyme activities, NMR spectroscopy of culture media, determination of antioxidant enzyme activities, and cell proliferation and differentiation assays were performed. The data showed that moderate hyperoxia in this myeloid cell line causes: i) intriguing alterations in the mitochondrial activities at the levels of succinate dehydrogenase and succinate-cytochrome c reductase; ii) induction of metabolic compensatory adaptations, with significant shift to glycolysis; iii) induction of different antioxidant enzyme activities; iv) significant cell growth inhibition and v) no significant apoptosis. This work will permit better characterization the mitochondrial damage induced by hyperoxia. In particular, the data showed a large increase in the succinate cytochrome c reductase activity, which could be a fundamental pathogenic mechanism at the basis of oxygen toxicity.

• Biomolecules & Therapeutics
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• v.26 no.6
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• pp.599-607
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• 2018

Fasiglifam (TAK-875) a G-protein coupled receptor 40 (GPR40) agonist, significantly improves hyperglycemia without hypoglycemia and weight gain, the major side effects of conventional anti-diabetics. Unfortunately, during multi-center Phase 3 clinical trials, unexpected liver toxicity resulted in premature termination of its development. Here, we investigated whether TAK-875 directly inflicts toxicity on hepatocytes and explored its underlying mechanism of toxicity. TAK-875 decreased viability of 2D and 3D cultures of HepG2, a human hepatocarcinoma cell line, in concentration-(>$50{\mu}M$) and time-dependent manners, both of which corresponded with ROS generation. An antioxidant, N-acetylcysteine, attenuated TAK-875-mediated hepatotoxicity, which confirmed the role of ROS generation. Of note, knockdown of GPR40 using siRNA abolished the hepatotoxicity of TAK-875 and attenuated ROS generation. In contrast, TAK-875 induced no cytotoxicity in fibroblasts up to $500{\mu}M$. Supporting the hepatotoxic potential of TAK-875, exposure to TAK-875 resulted in increased mortality of zebrafish larvae at$25{\mu}M$. Histopathological examination of zebrafish exposed to TAK-875 revealed severe hepatotoxicity as manifested by degenerated hypertrophic hepatocytes with cytoplasmic vacuolation and acentric nuclei, confirming that TAK-875 may induce direct hepatotoxicity and that ROS generation may be involved in a GPR40-dependent manner.

• Environmental Mutagens and Carcinogens
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• v.20 no.1
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• pp.7-13
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• 2000

The mechanisms of benzene toxicity is not fully elucidated, although the metabolism of benzene is very well understood. In order to study the mechanism of benzene toxicity, we investigated DNA damage induced by benzene metabolite, 1,2,4-benzenetriol (BT) in HL-60 cells by alkaline comet assay. To investigate the mechanism of cellular DNA damage induced by BT, the cells were treated with antioxidant such as vitamin C, SOD, catalase, and chelating agent such as deferoxamine (DFO), bathocuproinedisulfonic acid (BCDS). BT induced DNA damage in dose-dependent manner at concentration between 10$\mu\textrm{m}$ and 100$\mu\textrm{m}$. The antioxidant vitamin C itself induced DNA damage at higher concentration. The DNA damage induced by BT in HL-60 cells was protected at low concentraiton of vitamin C whereas no protective effect was found at high concentration. In hibitory effect of SOD on DNA damage by BT was observed and this suggested that BT produce superoxide anion (O2-) causing DNA damage. Catalase protected BT-induced DNA damage suggesting that BT produce H2O2 during autooxidation of BT. Both Fe(II)-specific cheiating agent, deferoxamine (DFO) and Cu(I)-specific chelating agent, bathocuproinedisulfonic acid (BCDS) inhibited BT0induced DNA damage. This suggested that DNA damage was caused by active species which was produced DAN damage. This suggested that DNA damage was caused by active species which was produced by the autooxidation of BT in the presence of Cu(II) and Fe(III). These findings suggest that reactive oxygen species play an important role in the mechanism of toxicity induced by benzene metabolites.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.38 no.2
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• pp.100-105
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• 2005

Two species of fish and five species of marine invertebrate showed different tolerances to the toxicity of composite slag and bituminaus coal. Especially, Hemicentrotus pulcherrimus and young Haliotis discus hannai displayed marked differences in tolerance from. H. pulcherrimus and young H. discus hannai showed lethal effects at higher concentrations than those concentrations of the composite slag in the 1.0 and $0.4\%$ range, respectively. H. pulcherrimus showed no lethal effects at a lower concentration of $1.0\%$ composite slag and some differences in the rate of oxygen consumption with this concentration of composite slag. The lethal effects of bituminous coal on marine and fisheries organisms, even with higher concentrations, were not observed. At a higher concentration than that of 500 mg/L (ppm) of bituminous coal, decrease effects appeared in the rate of oxygen consumption of the experimental organisms. Taking into consideration that the experimental concentration of composite slag and bituminous coal were impracticable in the ocean, the results of this experiment suggest that composite slag and bituminous coal pose no real threat to marine or fisheries organisms.

• Toxicological Research
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• v.27 no.3
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• pp.161-166
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• 2011

Carbon black, a particulate form of pure elemental carbon, is an industrial chemical with the high potential of occupational exposure. Although the relationship between exposure to particulate matters (PM) and cardiovascular diseases is well established, the cardiovascular risk of carbon black has not been characterized clearly. In this study, the cytotoxicity of carbon black to vascular smooth muscle and endothelial cells were examined to investigate the potential vascular toxicity of carbon black. Carbon black with distinct particle size, N330 (primary size, 28~36 nm) and N990 (250~350 nm) were treated to A-10, rat aortic smooth muscle cells and human umbilical vein endothelial cell line, ECV304, and cell viability was assessed by lactate dehydrogenase (LDH) leakage assay. Treatment of carbon black N990 resulted in the significant reduction of viability in A-10 cells at 100 ${\mu}g$/ml, the highest concentration tested, while N330 failed to cause cell death. Cytotoxicity to ECV304 cells was induced only by N330 at higher concentration, 200 ${\mu}g$/ml, suggesting that ECV304 cells were relatively resistant to carbon black. Treatment of 100 ${\mu}g$/ml N990 led to the elevation of reactive oxygen species (ROS) detected by dichlorodihydrofluorescein (DCF) in A-10 cells. Pretreatment of antioxidants, N-acetylcysteine (NAC) and sulforaphane restored decreased viability of N990-treated A-10 cells, and N-acetylcysteine, but not sulforaphane, attenuated N990-induced ROS generation in A-10 cells. Taken together, present study shows that carbon black is cytotoxic to vascular cells, and the generation of reactive oxygen contributes to the development of cytotoxicity. ROS scavenging antioxidant could be a potential strategy to attenuate the toxicity induced by carbon black exposure.