• Journal of Microbiology and Biotechnology
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• v.28 no.1
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• pp.40-49
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• 2018

We evaluated the antioxidant activity and neuronal cell-protective effect of fucoidan extract from Ecklonia cava (FEC) on hydrogen peroxide ($H_2O_2$)-induced cytotoxicity in PC-12 and MC-IXC cells to assess its protective effect against oxidative stress. Antioxidant activities were examined using the ABTS radical scavenging activity and malondialdehyde-inhibitory effect, and the results showed that FEC had significant antioxidant activity. Intracellular ROS contents and neuronal cell viability were investigated using the DCF-DA assay and MTT reduction assay. FEC also showed remarkable neuronal cell-protective effect compared with vitamin C as a positive control for both $H_2O_2$-treated PC-12 and MC-IXC cells. Based on the neuronal cell-protective effects, mitochondrial function was analyzed in PC-12 cells, and FEC significantly restored mitochondrial damage by increasing the mitochondrial membrane potential (${\Delta}{\Psi}m$) and ATP levels and regulating mitochondrial-mediated proteins (p-AMPK and BAX). Finally, the inhibitory effects against acetylcholinesterase (AChE), which is a critical hydrolyzing enzyme of the neurotransmitter acetylcholine in the cholinergic system, were investigated ($IC_{50}$ value = 1.3 mg/ml) and showed a mixed (competitive and noncompetitive) pattern of inhibition. Our findings suggest that FEC may be used as a potential material for alleviating oxidative stress-induced neuronal damage by regulating mitochondrial function and AChE inhibition.

• 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.

• 한국신재생에너지학회:학술대회논문집
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• 2009.11a
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• pp.132-132
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• 2009

To achieve the commercialization of PEM fuel cell, the durability problem must be solved. Recently, many researchers have focused on this durability problem and degradation studies about membrane and electrode have been reported. But durability characteristics of gas diffusion layer is not much reported yet. Durability of GDL is very important to maintain the performance of PEM fuel cell because the main function of GDL is a path of fuel and water and the GDL degradation causes the loss of the GDL function. In this study, the degradation of GDL, especially, the mechanical degradation process was investigated with the leaching test. The effect of water dissolution was observed through the test and the amount of GDL degradation was measured with various measurement methods such as weight measurement, static contact angle measurement, scanning electron microscope. After 2,000 hours test, the GDL showed structural damage and loss of hydrophobicity.

• Nutrition Research and Practice
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• v.15 no.1
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• pp.12-25
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• 2021

BACKGROUND/OBJECTIVES: The study was conducted to investigate the efficacy of the combination treatment of phytochemical resveratrol and the anticancer drug docetaxel (DTX) on prostate carcinoma LNCaP cells, including factors related to detailed cell death mechanisms. MATERIALS/METHODS: Using 2-dimensional monolayer and 3-dimensional spheroid culture systems, we examined the effects of resveratrol and DTX on cell viability, reactive oxygen species (ROS) levels, mitochondrial membrane potential, apoptosis, and necroptosis by MTT, flow cytometry, and Western blotting. RESULTS: At concentrations not toxic to normal human prostate epithelial cells, resveratrol effectively decreased the viability of LNCaP cells depending on concentration and time. The combination treatment of resveratrol and DTX exhibited synergistic inhibitory effects on cell growth, demonstrated by an increase in the sub-G0/G1 peak, Annexin V-phycoerythrin positive cell fraction, ROS, mitochondrial dysfunction, and DNA damage response as well as concurrent activation of apoptosis and necroptosis. Apoptosis and necroptosis were rescued by pretreatment with ROS scavenger N-acetylcysteine. CONCLUSIONS: We report resveratrol as an adjuvant drug candidate for improving the outcome of treatment in DTX therapy. Although the underlying mechanisms of necroptosis should be investigated comprehensively, targeting apoptosis and necroptosis simultaneously in the treatment of cancer can be a useful strategy for the development of promising drug candidates.

• Korean Journal of Microbiology
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• v.6 no.2
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• pp.54-62
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• 1968

The effect of gamma-ray on yeast cells Sacch. cerevisiae, and the leakage of cellular constituents such as carbohydrates, ribose, amino acids, inorganic phosphates and organic phosphates have been studied. The samples of yeast cells washed throughly and starved intensively, radiation effects were compared with those of control (un-starved), the irradiation dose rates are in the range from 24 Kr. up. to 480, Kr. The loss of 260m$\mu$. absorbing material, are also observed. Mechanisms of membrane damage by gamma-irradiation are discussed corelating to permeability changes and loss of substances, then active and passive transport process are also under considerations in discussion. The experimental results are as follows, 1. Carbohydrates of yeast cell leak out by gamma-irradiation, and amounts of loss increase proportionally as the increasing of radiation dose, curve of carbohydrates loss in starved cells is parallel with those of non-starved cells. 2. Ribose leak out less than that of carbohydrate from irradiated cell, the dose response curve of loss is straight and proportional to the increasing of radiation doses, slope of the curve is much lower than of carbohydrates. 3. Amino acids also leak out and the curve of losses to radiation is not proportional, it is revealed that there are little losses from yeast at lower doses of irradiation. 4. The losses of inorganic phosphates increase unproportionally to the increasing of irradiation doses, there are little leakage at the lower doses of irradiation. The losses of organic phosphates increase proportionally to the increasing of irradiation doses, and the amount of losses are much more than that of inorganic phosphate at lower doses of irradiation. 5. Leakage from irradiated yeast cells was shown to be due to passive transport process not an energy requiring process of ion transport. 6. Loss of 260 m$\mu$. absorbing material is little more than that of control yeast by the gamma-irradiation dose of 120K.r. and 240K.r.

• Biomolecules & Therapeutics
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• v.22 no.2
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• pp.136-142
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• 2014

We investigated the protective effects of chlorogenic acid (CGA), a polyphenol compound, on oxidative damage induced by UVB exposure on human HaCaT cells. In a cell-free system, CGA scavenged 1,1-diphenyl-2-picrylhydrazyl radicals, superoxide anions, hydroxyl radicals, and intracellular reactive oxygen species (ROS) generated by hydrogen peroxide and ultraviolet B (UVB). Furthermore, CGA absorbed electromagnetic radiation in the UVB range (280-320 nm). UVB exposure resulted in damage to cellular DNA, as demonstrated in a comet assay; pre-treatment of cells with CGA prior to UVB irradiation prevented DNA damage and increased cell viability. Furthermore, CGA pre-treatment prevented or ameliorated apoptosis-related changes in UVB-exposed cells, including the formation of apoptotic bodies, disruption of mitochondrial membrane potential, and alterations in the levels of the apoptosis-related proteins Bcl-2, Bax, and caspase-3. Our findings suggest that CGA protects cells from oxidative stress induced by UVB radiation.

• Environmental Analysis Health and Toxicology
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• v.23 no.4
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• pp.315-323
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• 2008

In this study, the backs with a hair cut of 6-week-old healthy ICR male mice were once exposed to a dose of $400\;mJ/cm^2$ UVB. An acute dermal inflammation was observed, and the certified 100% pure and natural lavender essential oil were applied to the UVB-exposed mice skin twice a day. It was observed that the mice exposed to UVB resulted in an acute inflammation, and when treated with lavender oil the degree of inflammation was much alleviated, and the inflamed skins of both the control and lavender oil-treatment groups were cured almost completely after 6 days of the UVB exposure. At 24 hours after UVB exposure, the epidermal keratinocytes in the control group showed a cell-membrane damage with the destruction of intercellular junctions, agglutination of tonofilaments within the cytoplasm and nucleus damage, while the lavender oil-treatment group had much less cell damage than the control group. While the control group showed a significant increase (p<0.05) in the activity of XO up to 144 hours, the lavender oil-treatment group did not show any significant increase except for 48 hours after the UVB exposure. Both the control and lavender essential oil-treatment groups had a significant decrease in the activities of CAT and SOD up to 96 hours. Particularly, the CAT activity was significantly lower(p<0.05) in the lavender oil-treatment group than the control group up to 48 hours, and higher than the control group at and after 96 hours. The GST activity was significantly decreased in both the control and lavender oil-treatment groups up to 96 hours after the UVB exposure except for the control group at 24 hours, and that of the lavender oil-treatment group was higher than the control group at and after 96 hours. Therefore, it is assumed that the application of the lavender oil to the ultraviolet-damaged mice skin can be effective in treatment for the damaged skin.

• Restorative Dentistry and Endodontics
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• v.20 no.2
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• pp.549-576
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• 1995

Bacteria are one of the most important causative agents of the pulpal and periapical diseases. Streptococci are one of the most frequently isolated facultative anarerobic bacteria in the infected root canals. Bacterial cell wall components have a direct effect in the pathogenesis of the pulpal and periapical infections. Hyaluronidase produced by bacteria has been implicated in dissemination of the diseases. The purpose of this study was to evaluate the effect of cell wall extract of streptococci on the L929 cells using inverted microscope and the transmission electron microscopy (TEM). Hyaluronidase production of streptococcal strains were investigated to determine the correlation between the severity of cell damage and the activity of enzymes. Bacterial cell wall extracts of S. sanguis, S. mitis and S. uberis isolated from infected root canals and ATCC type strains of S. mutans (ATCC 10449) and E. faecalis (ATCC 19433) were prepared by sonication and confirmed with SDS-PAGE. Silver stain of SDS-PAGE of sonic extract was efficient at $100{\mu}g$/ml concentration of cell wall protein, while Coomasie blue stain was efficient at $100{\mu}g$/ml concentration. Inverted microscope showed that sonic extract-treated L929 cells were round and detached from the substratum while others lost their fibroblastic shapes. Transmission electron microscopic examination revealed that streptococcal extracts induced death of L929 cells. Sonic extracts of streptococci had variable effect on microstructure of L929 cells. significant chromatin condensation was observed in the nucleus of the cells. Disappearance of cell surface microvilli and nuclear fragments with dense chromatin were observed. The cell nucleus had an irregular shape and numerous large vacuoles were seen in the cytoplasm and some breaks of the cell membrane could be seen. Cell organelles were in various stages of destruction and cristae of mitochondria were disoriented or disappeared. Eighteen strains of streptococci did not produce hyaluronidase.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.6
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• pp.565-570
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• 1999

Intracellular accumulation of bile acids in the hepatocytes during cholestasis is thought to be pathogenic in cholestatic liver injury. Due to the detergent-like effect of the hydrophobic bile acids, hepatocellular injury has been attributed to direct membrane damage. However histological findings of cholestatic liver diseases suggest apoptosis can be a mechanism of cell death during cholestatic liver diseases instead of necrosis. To determine the pattern of hepatocellular toxicity induced by bile acid, we incubated primary cultured rat hepatocytes with a hydrophobic bile acid, Glycochenodeoxycholate (GCDC), up to 5 hours. After 5 hours incubation with $400\;{\mu}M$ GCDC, lactate dehydrogenase released significantly. Cell viability, quantitated in propidium iodide stained cells concomitant with fluoresceindiacetate was decreased time- and dose-dependently. Most nuclei with condensed chromatin and shrunk cytoplasm were heavily labelled time- and dose-dependently by a positive TUNEL reaction. These findings suggest that both apoptosis and necrosis are involved in hepatocytes injury caused by GCDC.

• Proceedings of the Korean Society of Toxicology Conference
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• 2005.05a
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• pp.51-82
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• 2005

To compare the pulmonary toxicity between ultrafine colloidal silica particles (UFCSs) and fine colloidal silica particles (FCSs), mice were intratracheally instilled with 3 mg of 14-nm UFCSs and 230-nm FCSs and pathologically examined from 30 mill to 24 hr post-exposure. Histopathologically, lungs exposed to both sizes of particles showed bronchiolar degeneration and necrosis, neutrophilic inflammation in alveoli with alveolar type II cell proliferation and particle-laden alveolar macrophage accumulation. UFCSs, however, induced extensive alveolar hemorrhage compared to FCSs from 30 min onwards. UFCSs also caused more severe bronchiolar epithelial cell necrosis and neutrophil influx in alveoli than FCSs at 12 and 24 hr post-exposure. Laminin positive immunolabellings in basement membranes of bronchioles and alveoli of UFCSs treated animals was weaker than those of FCSs treated animals in all observation times. Electron microscopy demonstrated UFCSs and FCSs on bronchiolar and alveolar wall surface as well as in the cytoplasm of alveolar epithelial cells, alveolar macrophages and neutrophils. Type I alveolar epithelial cell erosion with basement membrane damage in UFCSs treated animals was more severe than those in FCSs treated animals. At 12 and 24 hr post-exposure, bronchiolar epithelia cells in UFCSs treated animals showed more intense vacuolation and necrosis compared to FCSs treated animals. These findings suggest that UFCSs has greater ability to induce lung inflammation and tissue damages than FCSs.