• Asian Pacific Journal of Cancer Prevention
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• v.15 no.21
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• pp.9153-9157
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• 2014

Background: Capparis spinosa L., a Uygur medicine, had been shown to have anti-tumor activity in our early experiments with an N-butanol extract (CSBE) as its active fraction. However, the mechanisms responsible for its effects are not clearly understood. Here, we report that treatment of SGC-7901 cells with CSBE resulted in dose-dependent reduction of cell viability and induction of apoptosis. Materials and Methods: To observe the inhibitory and killing effects of CSBE on SGC-7901, the SRB method was adopted, apoptosis being observed by electron microscopy. To clarify the mechanisms of apoptosis, Western blot and enzyme-labeled methods were used to examine the release of cytochrome c (Cyt c) and the activation of the caspase cascade. Results: By electron microscopy, apoptotic morphologic changes were detectable after CSBE administration. In this study, it was also demonstrated that CSBE induced apoptosis in SGC-7901 cells by inhibiting mPTP open, mitochondrial cytochrome c release, caspase-9 and caspase-3 activation. Conclusions: The findings indicated that CSBE induces aap optosis through mitochondrial pathway.

• Proceeding of Spring/Autumn Annual Conference of KHA
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• 2009.04a
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• pp.332-337
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• 2009

The stronghold diffusion style method is resident participation style residential environment improvement plan that first of all, the general public constructs base facilities which the temporary occupancy public housings, commonness use facilities, roads, etc. And then with using the public housing of the stronghold sector, the resident oneself improves the house with independence or commonness. As a result induction of the voluntary participation of economic situation and the resident where the improvement will is reflected and introduction of versatile maintenance method through stronghold development with participation of the general public, this study tries to present the residential improvement method of diffusion style. San-Jun was selected in the subject of investigation area in stronghold diffusion style residential environmental improvement plan area. Investigation contents population register quality and quality of present house, the degree which is a house environmental improvement plan, about residential improvement the fact etc. Because unsatisfactorily in compliance with the deterioration and spatial narrow of the house, The above of half is an improvement intention. Hereafter residential improvement, According to the condition which is economic, residential improvement will change. The plan will be able to augment the economic enemy capability of the resident should grope and the residents oneself creates the environment will be able to improve the house. Also with creating, activating a resident organization, through autonomous decision-making process, the residential improvement could be advanced continuously.

• Journal of Environmental Health Sciences
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• v.29 no.2
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• pp.23-28
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• 2003

To evaluate the effect of cyclohexane(CH) treatment on the liver cytochrome P-450 dependent aniline hydroxylase(CYPdAH) activity in alcohol-pretreated animals, CH(1.56 g/kg body weight) was intraperitoneally administered to Sprague-Dawley male rats, which had been drunk 15％ alcohol in distilled water for 1,3 and 6 weeks. CH was injected to rats 4 times every other day and the animals were sacrificed at 24 hours after injection of CH. In the alcohol-pretreated rats, liver injuries were not demonstrated on the basis of the liver weight per body weight, the levels of serum alanine aminotransferase and hepatic microsomal glucose-6-phosphatase activities. By the CH treatment, alcohol-pretreated animals showed the significantly increased activity of hepatic microsomal CYPdAH. Concomitantly $V_{max}$ value in CYPdAH was more increased, whereas $K_{M}$ value more decreased in alcohol-pretreated animals by the treatment of CH. In conclusion, the increasing cause of microsomal CYPdAH in CH-treated rats pretreated with alcohol may be due to induction of enzyme protein in rat liver.r.r.

• Environmental Mutagens and Carcinogens
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• v.16 no.1
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• pp.35-42
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• 1996

Aragonite is one of polymorphs of calcium carbonate of which main form is calcite. We found that white precipitate is formed in much amount by boiling underwater of Inchon, Korea and confirmed that it is aragonite. This study is to evaluate the dimensional characteristics, solubility, acid resistance of aragonite and the cytotoxicity, cell division disturbance and cell transforming ability of it on BALB/3T3 cells. The results are as follows: Lengths of the aragonite were reduced to the 72.7% and 22.7% respectively after 5 months and 7 months of intrapleurai injection to the Sprague-Dawley rat. Strong acid such as 1M HCl dissolved the aragonite instantly but weaker acid pH 2.0 or more could not dissolved aragonite easily. The result of cell growth inhibition showed that cell numbers were decreased as log-doses of treatment of the aragonite were increased 24 hours, 48 hours, and 72 hours later. Cell plating efficiency after the aragonite treatment also showed dose-dependent decrease. Multinuclear giant cell formation was increased in the aragonite treated cells until ID$_{50}$ and after the dose the multinucleate cells were decreased, but remained much higher than negative control cells. Morphological transformation assay showed that the aragonite did not induce transformation in all treated doses.

• Environmental Mutagens and Carcinogens
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• v.22 no.2
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• pp.90-96
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• 2002

Benzene is a widespread human carcinogen, inducing leukemia and hematotoxicity. Exposure to benzene metabolites has been shown to cause genetic damage, including aneusomy and chromosome aberrations. Fluorescence in situ hybridization(FISH) procedure was used to determine if the benzene metabolite, 1, 2, 4-benzenetriol(BT), hydroquinone(HQ) and trans, trans-muconic acid(t,t-MA) induced specific chromosomal change in HL-60 cells. Treatment with BT, HQ and t,t-MA resulted in the induction of monosomy 8 and 21 in HL-60 cells in a dose-dependent manner. All of these metabolites also induced trisomy 8 and 21, but no correlation between frequencies of trisomy and concentration was found. Translocations between chromosome 8 and another unidentified chromosome ［t(8:\ulcorner)］, and between chromosome 21 and another unidentified chromosome ［t(8:21)］ were found. However, translocation between chromosome 8 and 21 ［t(8:21)］ was not found. Results indicate that the benzene metabolites, BT, HQ and t,t-MA, induce chromosome specific numerical and structural aberrations, and the fluorescence in situ hybridization (FISH) approach may be a useful and powerful technique for detection of aneuploidy.

• Environmental Mutagens and Carcinogens
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• v.25 no.3
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• pp.97-103
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• 2005

The genotoxic effect of antimalarial drugs amodiaquine (AQ), mefloquine (MQ) and halofantrine (HF) was investigated in.at liver cells using the alkaline comet assay. AQ, MQ and HF at concentrations between $0-1000{\mu}mol/L$ significantly increased DNA strand breaks of rat liver cells dose-dependently. The order of induction of strand breaks was AQ>MQ>HF. The rat liver cells exposed to AQ and HF (200 and 400 ${\mu}mol/L$) and treated with (Fpg) the bacterial DNA repair enzyme that recognizes oxidized purine showed greater DNA damage than those not treated with the enzyme, providing evidence that AQ and HF induced oxidation of purines. Such an effect was not observed when MQ was treated with the enzyme. Treatment of cells with catalase, an enzyme inactivating hydrogen peroxide, decreased significantly the extent of DNA damage induced by AQ, and HF but not the one induced by MQ. Similarly quercetin, an antioxidant flavonoid at $50{\mu}mol/L$ attenuated the extent of the formation of DNA strand breaks by both AQ and HE. Quercetin, however, did not modify the effects of MQ. These results indicate the genotoxicity of AQ, MQ and HF in rat liver cells. In addition, the results suggest that reactive oxygen species may be involved in the formation of DNA lesions induced by AQ and HF and that, free radical scavengers may elicit protective effects against genotoxicity of these antimalarial drugs.

• Journal of Microbiology and Biotechnology
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• v.17 no.9
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• pp.1477-1482
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• 2007

Gluconacetobacter diazotrophicus strain PA15 exhibited a minimum inhibitory concentration value of 11 mM in an LGI medium amended with $ZnCl_2$. When an LGI medium was amended with Zn metal, solubilization halos were observed in a plate assay, and further solubilization was confirmed in a broth assay. The maximum solubilization was recorded after 120 h with a 0.1% Zn metal amendment. During solubilization, the culture growth and pH of the broth were indirectly correlated. Using a Fourier Transform Infrared Spectroscopy analysis, one of the agents solubilizing the Zn metal was identified as gluconic acid. When the Zn-amended broth was observed under a bright field microscope, long involution cells were observed, and further analysis with Atomic Force Microscopy revealed highly deformed, pleomorphic, aggregate-like cells.

• Environmental Analysis Health and Toxicology
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• v.19 no.3
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• pp.287-294
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• 2004

Diabetic complication is one of major risk factors leading to vascular disease such as atherosclerosis, stroke, coronary heart disease and etc. Several factors affecting the acceleration of diabetic vascular complication have been known such as hypertension, hyperlipidemia, immune complex and genetic factors. To screen and develop new therapeutics agents for diabetic vascular complication, it is strongly needed to develop animal models for diabetic complications. However in rodents models, diabetic complications is not well developed. Furthermore to assess the possibility of new therapeutics for diabetic vascular complications, diabetic animal models which have the risk factors of diabetic complications is needed. We aim to develop and establish an diabetic animal model which have diabetic complications with hyperlipidemia which is one of risk factors for diabetic complications. We induced insulin -dependent diabetes by intra. venous injection of streptozotocin (35 mg/kg/day) in RICO rats which is a spontaneous animal model for hyperlipidemia. Our models (STZ RICO) showed hyperglycemia, persistent high level of plasma cholesterol and triglyceridemia with severe diabetic renal changes until 28 weeks after induction of diabetes. STZ-RICO rats could be used for the evaluations of newly developed diabetic drugs.

• Environmental Analysis Health and Toxicology
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• v.19 no.3
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• pp.261-269
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• 2004

Although the biological functions of metallothioneins (MTs) are still being investigated, they have been suggested to be involved in detoxification of heavy metals, scavenging of free radicals, and protection against alkylating agents. MTs have been reported to be induced in most of animal tissues by heavy metals such as zinc, copper, mercury and cadmium, and the proteins have binding affinities to the metals. However, the presence or induction of MTs was reported not to be clear in leydig cells, which produce testosterone for the maturation of spermatozoa in male testes. In this study, we investigated the inducibility of metallothionein isomers by cadmium in cultured mouse leydig cells. Total RNA was extracted from the near confluent grown leydig cells and RT-PCR was Performed using the Primers which were synthesized on the basis of MT-1, 2, 3 and 4 cDNA from GenBank database. As results, MT-1 and MT-2 mRNA were found to be expressed in cadmium non-treated control cells and MT 1 mRNA expression was dose-dependent when leydig cells were treated with cadmium chloride. But MT-3 which is known to be brain specific and MT-4 which is another isoform of metallothionein, were not expressed. Other genes induced or depressed in cadmium treated leydig cells were also identified by microarray techniques.

• 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.