• Tuberculosis and Respiratory Diseases
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• v.58 no.4
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• pp.375-384
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• 2005

Background and Aims : Pre-induction of heat shock protein 70 (HSP70) is known to effectively attenuate the lipopolysaccharide (LPS)-induced inflammatory response in lung tissue. However, it is unclear if HSP70 induction after LPS exposure attenuates the subsequent LPS-induced inflammatory response in alveolar epithelial cells. This study examined the effects of HSP70 induction after LPS exposure on the IL-6 production and the cell viability after a subsequent LPS challenge in murine alveolar epithelial cells, and investigated whether or not HSP70 itself may be involved in those effects. Methods : Murine alveolar epithelial cells were cultured and divided into two groups; the Non-Pre-LPS group without a LPS pre-treatment and the Pre-LPS group with a LPS pre-treatment. Each group was subdivided into the following four subgroups: subgroup C (control), subgroup Q (quercetin), subgroup HSP70 (HSP70 induction), and subgroup HSP70-Inh (HSP70 inhibition). HSP70 expression, which was induced by sodium arsenite and inhibited by quercetin, was analyzed by western blot analysis. The IL-6 levels in the culture supernatant were measured by ELISA, and the cell viability was measured using a simplified MTT assay. Results : The IL-6 levels were lower in subgroup HSP70 than in subgroup C (P<0.01), and were higher in subgroup HSP70-Inh than in subgroup HSP70 in both the Non-Pre-LPS and Pre-LPS groups (P<0.05, P<0.01). The cell viability tended to decrease in the Pre-LPS group compared with the Non-Pre-LPS group. While the cell viability was higher in subgroups Q, HSP70, and HSP70-Inh than in subgroup C in the Non-Pre-LPS group (P<0.05, P<0.05, P<0.01), there was no difference in cell viability among the subgroups in the Pre-LPS group. Conclusion : HSP70 induction after a LPS pre-treatment in murine alveolar epithelial cells inhibits the subsequent LPS-induced IL-6 production without affecting the cell viability, and HSP70 by itself may play an important role in this proccess.

• Toxicological Research
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• v.19 no.3
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• pp.197-203
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• 2003

Apicidin, a histone-deacetylase inhibitor, has been successfully used to inhibit the growth of cancer cells. In this study, the apoptotic potential and mechanistic insights of apicidin were investigated in human myeloid leukemia U937 cells. Treatment of U937 cells with apicidin resulted in a decrease of cell viability with apoptotic characteristics, including chromatin condensation and ladder-pattern fragmentation of genomic DNA. Apicidin converted the procaspase-3 protease to catalytically active effector protease, resulting in subsequent cleavage of poly (ADP-ribose) polymerase (PARP) and inhibitor of caspase-activated deoxyribonuclease (ICAD). In addition, apicidin induced the activation of caspase-9 protease and the cytosolic release of mitochondrial cytochrome c with mitochon-drial membrane potential transition. Moreover, apicidin transiently increased the expression of Fas and Fas ligand proteins. Taken together, the results suggest that apicidin induces apoptosis of U937 cells through activation of intrinsic caspase cascades and Fas/FasL system with mitochondrial dysfunction.

• Biomolecules & Therapeutics
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• v.11 no.2
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• pp.112-118
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• 2003

1-Methylated $\beta$-carbolines (harmaline and harmalol) and antioxidants (N-acetylcysteine and ascorbate) reduced the loss of cell viability in differentiated PC 12 cells treated with 5 mM glutamate. $\beta$-Carbolines prevented the glutamate-induced decrease in mitochondrial membrane potential, cytochrome c release and caspase-3 activation in PC 12 cells. $\beta$-Carbolines reduced the formation of reactive oxygen species and depletion of glutathione due to glutamate in PC12 cells. $\beta$-Carbolines revealed a scavenging action on hydrogen peroxide and reduced the iron and EDTA-mediated degradation of 2-deoxy-D-ribose. The results suggest that I-methylated $\beta$-carbolines attenuate the cytotoxic effect of glutamate on PC12 cells by reducing the alteration of mitochondrial membrane permeability that seems to be mediated by oxidative stress.

• Journal of Microbiology and Biotechnology
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• v.17 no.3
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• pp.524-529
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• 2007

Pressure inactivation behavior of Bacillus amyloliquefaciens spores was investigated in deionized water. The spores of B. amyloliquefaciens were subjected to $105^{\circ}C$ and 700 MPa. The magnitude of the decrease in viability after pressure treatment was similar to that after pressure treatment followed by heat shock. The increase of dipicolinic acid (DPA) release was correlated with the spore inactivation, and the hydrophobicity did not significantly change during the pressure-assisted thermal processing (PATP). Lag phase duration increased with increasing pressure process time. The mechanisms of spore germination and inactivation during the PATP were related to a complex physiological process.

• Toxicological Research
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• v.18 no.3
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• pp.259-265
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• 2002

Resveratrol, a phytoalexin found in grapes, berries, and peanuts, is one of the most promising agents for cancer prevention. Recent studies show that the antitumor activity of resveratrol occurs through p53-mediated apoptosis. This study demonstrated the mechanism that resveratrol induced apoptosis in human osteosarcoma Saos-2 cells lacking p53. Treatment of osteosarcoma Saos-2 cells with resveratrol resulted in decrease of cell viability, which was revealed as apoptosis characterized by activation of caspase-3 protease as well as cleavage of poly(ADP-ribose) polymerase (PARP) with change of mitochondrial membrane potential transition. These results suggest that resveratrol may be potentially useful to treat osteosarcoma via activation of caspase protease and mitochondrial dysfunction.

• Toxicological Research
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• v.13 no.3
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• pp.187-191
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• 1997

Cell death induced by polychlorinated biphenyls (PCBs), environmental toxicant, was investigated in mouse splenocytes. The fragmentation of intact DNA, a parameter of apoptotic cell death, was evaluated qualitatively by agarose gel electrophoresis analysis and quantitatively by diphenylamine reaction method. PCBs induced apoptotic cell death of splenocytes in a dose- and time- dependent manner. The effect of serum on the apoptotic cell death induced by PCBs was also investigated. The DNA fragmentation induced by PCB treatment in serum-free medium was clearly inhibited by an addition of serum to the culture medium. The decrease of DNA fragmentation due to serum addition was accompanied with the increase of cell viability.

• The Journal of the Korean Society for Microbiology
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• v.21 no.2
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• pp.271-276
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• 1986

Amphotericin B and rifampin or 5-fluorocytosine were tested for synergism against Candida albicans in a synthetic mdium. The test was based on viability studies in which fungicidal activity was determined during the incubation hours of drug exposure. Concentration of amphotericin B(0.2ug per ml and 0.4ug per ml) in combination with inactive concentration of rifampin(12.5ug per ml) or 5-fluorocytosine(25ug per ml) resulted in rapid decrease of colony froming unit(CFU). On the basis of these and earlier studies, it is concluded that amphotericin Band rifampin or 5-fluorocytosine are synergistic against various yeasts and yeast-like fungi under widely differing experimental conditions.

• The Journal of Korean Medicine
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• v.20 no.4
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• pp.3-10
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• 2000

In order to elucidate the toxic mechanism of neurotoxical damage and neuroprotective effect of Jangwon-hwan(Zhuangyuan-wan) water extract, this experiment was performed. Neurotoxic effects of xanthine oxidase/hypoxanthine(XO/HX) were examined by MTT and NR assay, neuroprotective effects of Jangwon-hwan(Zhuangyuan-wan) water extract were examined by neurofilament enzymeimmuno assay(EIA). XO/HX induced an increase in cell viability, and a decrease in the amount of neurofilament on cultured mouse cerebral cortical neurons in dose-dependent manner. In neuroprotective effect of herb medicine, Jangwon-hwan(Zhuangyuan-wan) water extract increased the amount of neurofilament on cultured mouse cerebral cortical neurons damaged by XO/HX. From the results, it is suggested that XO/HX showed toxic effect in cultured mouse cerebral cortical Neurons and Jangwon-hwan(Zhuangyuan-wan) water extract is very effective in the prevention of neurotoxicity induced by XO/HX.

• The Journal of Fisheries Business Administration
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• v.39 no.2
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• pp.109-123
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• 2008

This study is aimed to establish an investment decision model for offshore aquaculture project of rock bream in Korea using a certainty equivalent method (CEM) based on the expected utility theory and to investigate its economic viability under risk and uncertainty. In the analysis with CEM, the effects of risk attitude and risk level on investment and risk premium were examined and the impacts of various risk and uncertainty factors on the investment decision were also assessed. In addition, the outcomes were compared to those evaluated by the traditional net present value (NPV) method. Results show that risk premium grew as the investors became more risk averse and uncertainty level (the variance of NPV) increased. Consequently, the certainty equivalent value was predicted to decrease from the value assessed by the traditional NPV method.

• Archives of Pharmacal Research
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• v.29 no.7
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• pp.577-581
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• 2006

Oxidative mechanisms are thought to have a major role in cataract formation and diabetic complications. Antioxidant enzymes play an essential role in the antioxidant system of the cells that work to maintain low steady-state concentrations of the reactive oxygen species. When HLE-B3 cells, a human lens cell line were exposed to 50-100 mM glucose for 3 days, decrease of viability, inactivation of antioxidant enzymes, and modulation of cellular redox status were observed. Significant increase of cellular oxidative damage reflected by lipid peroxidation and DNA damage were also found. The glycation-mediated inactivation of antioxidant enzymes may result in the perturbation of cellular antioxidant defense mechanisms and subsequently lead to a pro-oxidant condition and may contribute to various pathologies associated with the long term complications of diabetes.