• Korean Journal of Clinical Laboratory Science
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• 제45권3호
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• pp.114-119
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• 2013

Potassium is essential for the proper functioning of the ears. The inner ear's endolymph differs from all other extracellular fluids (in its positive potential) and in the ionic compositions in the various parts of the endolymphatic space. Ion concentration of the endolymph is 150 mM of potassium, which is comparable to the concentrations in other organs. Cisplatin (cis-diamminedichloroplatinum II: CDDP) is one of the most effective anticancer drugs, widely used against various tumors. However, its clinical use is limited by the onset of severe side effects, including ototoxicity and nephrotoxicity. For ototoxicity, a number of evidences in cytotoxic mechanism of cisplatin, including perturbation of redox status, increase in lipid peroxydation, and formation of DNA adduct, have been suggested. Therefore, in this study, the author investigated the relationship between the potassium ions on cisplatin-induced cytotoxicity in HEI-OC1 cells associated with reactive oxygen species (ROS). KCNE1 gene expression by the concentration of intracellular potassium appeared in the plasma membrane and increased the concentration of intracellular potassium. Cisplatin decreased the viability of HEI-OC1 cells, but the KCNE1 gene increased. Also, the KCNE1 gene significantly suppressed generation of intracellular ROS by cisplatin. Western blot analysis showed that the KCNE1 gene increased phase II detoxification enzymes markers such as superoxide dismutase 1 (SOD1), superoxide dismutase (SOD2), NAD(P)H:quinine oxidoreductases (NQO1), which were associated with the scavenger of ROS. These results suggest that the KCNE1 gene for intracellular potassium concentration ultimately prevents ROS generation from cisplatin and further contributes to protect auditory sensory hair cells from ROS produced by cisplatin.

• Journal of Radiation Protection and Research
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• 제21권2호
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• pp.99-105
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• 1996

After high-dose irradiation(8 Gy). the viability of lymphocyte with a prior low-dose irradiation was 3.7-fold higher than that without a prior low-dose irradiation The viability could be increased by the reduction of oxygen radicals or the removal of damaged molecules-DNA, protein. lipid membrane. or the removal of damaged cells. In this paper. we studied the radioresistance mechanism in lymphocytes and lymphoma cells by examining the activities of radical scavengers(catalase. peroxidase, superoxide dismutase, and glucose-6-phosphate dehydrogenase), and a radical protector(glutathione). Different enzymes were induced in lymphocyte and lymphoma with low-dose irradiation. The activity of peroxidase increased most(133.3%) in lymphoma while the enzymes increased most in lymphocyte were superoxide dismutase (138.5%), glucose-6-phosphate dehydrogenase (122.4%) and glutathione(120.8%). The activities of these enzymes were highest when the interval was 7 hours between low-dose and high-dose irradiation.

• Journal of Korean Society on Water Environment
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• 제23권3호
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• pp.319-323
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• 2007

The Advanced Oxidation Process (AOP) is being increasingly used to oxidize complex organic constituents in treated effluents from domestic wastewater treatment plants. Generally, ${NO_3}^--N$ concentrations ranges between 5 and 8 mg/L for biologically well-treated effluents. However, nitrate ions, ${NO_3}^-$, affects on oxidation as not only a well-known strong absorber of UV light below 250 nm of wavelength but also as an OH radical scavenger. The objective of this study was to evaluate the AOP systems for degradation of 2,4-DCP, and to delineate the effect of nitrate ions on UV oxidation of 2,4-DCP by conducting a bench-scale operation at various reaction times and initial concentrations of $H_2O_2$. The experimental results indicated that 2,4-DCP could be completely oxidized by $UV/H_2O_2$ process with an initial $H_2O_2$ concentration of 20 mg/L at a retention time of 1.0 min or longer. Nitrate ions did not show any adverse effect on 2,4-DCP oxidation at this high $H_2O_2$ concentration, and the practical initial $H_2O_2$ concentration and reaction time for the 80% oxidation turned out to be 5 mg/L and 1.0 min, respectively.

• Asian-Australasian Journal of Animal Sciences
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• 제24권9호
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• pp.1204-1210
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• 2011

Objective of this study was to examine the effect of sodium nitroprusside (SNP), a nitric oxide (NO) donor on steroid synthesis, growth and apoptosis of buffalo granulosa cells (GCs) in vitro. Follicular fluid of antral follicles (3-5 mm diameter) was aspirated and GCs were cultured in 0 (control), $10^{-3}$, $10^{-5}$, $10^{-7}$, $10^{-9}\;M$ of SNP for 48 h. To evaluate whether this effect was reversible, GCs were cultured in presence of $10^{-5}\;M$ SNP+1.0 mM $N^{\omega}$-nitro-L-arginine methyl ester (L-NAME) a NO synthase (NOS) inhibitor or hemoglobin (Hb, $1.0{\mu}g$) as NO scavenger. Nitrate/nitrite concentration was evaluated by Griess method, progesterone and estradiol concentrations by RIA and apoptosis by TUNEL assay. SNP ($10^{-3}$, $10^{-5}$, $10^{-7}\;M$) significantly (p<0.05) inhibited estradiol and progesterone synthesis, growth, disorganized GCs aggregates and induced apoptosis in a dose dependent manner. However, $10^{-9}\;M$ SNP induced the progesterone synthesis and stimulated GCs to develop into a uniform monolayer. Combination of SNP $10^{-5}$ M+L-NAME strengthened the inhibitory effect while, SNP+Hb together reversed these inhibitory effects. In conclusion, SNP at greater concentrations ($10^{-3}$, $10^{-5}$ and $10^{-7}\;M$) has a cytotoxic effect and it may lead to cell death whereas, at a lower concentration ($10^{-9}\;M$) induced progesterone synthesis and growth of GCs. These findings have important implications that NOS derived NO are involved at physiological level during growth and development of buffalo GCs which regulates the steroidogenesis, growth and apoptosis.

• Proceedings of the Korean Society of Applied Pharmacology
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• 한국응용약물학회 1996년도 춘계학술대회
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• pp.207-207
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• 1996

Through molecular cloning, five muscarinic receptors have been identified. The muscarinic receptors can be generally grouped according to their coupling to either stimulation of phospholipase C (m1, m3, and m5) or the inhibition of adenylate cyclase (m2 and m4). Each m1, m3, and m5 receptors has the additional potential to couple to the activation of phospholipase A$_2$, C, and D, tyrosine kinase, and the mobilization of Ca$\^$2+/. However, the differences in coupling efficiencies to different second messenger systems between these receptors have not been studied well. Ectopic expression of each of these receptors in mammalian cells has provided the opportunity to evaluate the signal transduction of each in some detail. In this work we compared the coupling efficiencies of the m1, m3 and m5 muscarinic receptors expressed in chinese hamster ovary (CHO) cells to the Ca$\^$2+/ mobilization and the stimulation of neuronal nitric oxide synthase (nNOS). Because G protein/PLC/PI turnover/[(Ca$\^$2+/])i/NOS pathway was supposed as a main pathway for the production of nitric oxide via muscarinic receptors, we studied on ml, m3 and m5 receptors. Stimulation of guanylate cyclase activity in detector neuroblastoma cells was used as an index of generation nitric oxide (NO) in CHO cells. The agonist carbachol increased the cGMP formation and the intracellular [Ca$\^$2+/] in concentration dependent manner in three types of receptors and the increased cGMP formation was significantly attenuated by scavenger of NO or inhibitor of NOS. m5 receptors was most efficiently coupled to stimulation of nNOS, And, the coupling efficiencies to the stimulation of neuronal nitric oxide synthase in three types of receptors were parallel with them to the Ca$\^$2+/ mobilization.

• Journal of Environmental Science International
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• 제23권5호
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• pp.963-972
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• 2014

In this study, ibuprofen(IBP) degradation by the photochemical ($UV/S_2O{_8}^{2-}$) and sonochemical ($US/S_2O{_8}^{2-}$) processes was examined under various parameters, such as UV ($10{\sim}40{\pm}5W/L$) and US ($50{\sim}90{\pm}5W/L$) power density, optimum dosage of persulfate ion ($S_2O{_8}^{2-}$), temperature ($20{\sim}60^{\circ}C$) and anions effect ($Cl^-$, $HCO_3{^-}$, $CO{_3}^{2-}$). The pseudo-first-order degradation rate constants were in the order of $10^{-1}$ to $10^{-5}min^{-1}$ depending on each processes. The synergistic effect of IBP degradation in $UV/S_2O{_8}^{2-}$ and $US/S_2O{_8}^{2-}$ processes could investigated, due to the generation of $SO_4{^-}$ radical. This result can confirm from the produced $H_2O_2$ and $SO{_4}^{2-}$ concentration in each processes. IBP degradation rate affected by the $S_2O{_8}^{2-}$ dosage, temperature, power and anion existence parameters. In particular, IBP degradation rate increased with the increase of the temperature ($60^{\circ}C$) and applied power density (UV:$40{\pm}5W/L$, US:$90{\pm}5W/L$). On the other hand, anions effect on the IBP degradation was negative, due to the anion play as a the scavenger of radical.

• Journal of Korean Neurosurgical Society
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• 제49권4호
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• pp.205-211
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• 2011

Objective : We investigated the neuroprotective effect of anthocyanin, oxygen radical scavenger extracted from raspberries, after traumatic spinal cord injury (SCI) in rats. Methods : The animals were divided into two groups : the vehicle-treated group (control group, n=20) received an oral administration of normal saline via stomach intubation immediately after SCI, and the anthocyanin-treated group (AT group, n=20) received 400 mg/kg of cyanidin 3-O-${\beta}$-glucoside (C3G) in the same way. We compared the neurological functions, superoxide expressions and lesion volumes in two groups. Results : At 14 days after SCI, the AT group showed significant improvement of the BBB score by $16.7{\pm}3.4%$, platform hang by $40.0{\pm}9.1%$ and hind foot bar grab by $30.8{\pm}8.4%$ (p<0.05 in all outcomes). The degree of superoxide expression, represented by the ratio of red fluorescence intensity, was significantly lower in the AT group ($0.98{\pm}0.38$) than the control group ($1.34{\pm}0.24$) (p<0.05). The lesion volume in lesion periphery was $32.1{\pm}2.4\;{\mu}L$ in the control and $24.5{\pm}2.3\;{\mu}L$ in the AT group, respectively (p<0.05), and the motor neuron cell number of the anterior horn in lesion periphery was $8.3{\pm}5.1$ cells/HPF in the control and $13.4{\pm}6.3$ cells/HPF in the AT group, respectively (p<0.05). Conclusion : Anthocyanin seemed to reduce lesion volume and neuronal loss by its antioxidant effect and these resulted in improved functional recovery.

• The Journal of Korean Medicine
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• 제29권1호
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• pp.106-116
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• 2008

Objectives : Peroxynitrite $(ONOO^-)$, superoxide anion radical $({\cdot}O_2^-)$ and nitric oxide (NO) are cytotoxic because they can oxidize several cellular components such as proteins, lipids and DNA. They have been implicated in the aging processes, and age-related diseases such as Alzheimer's disease, rheumatoid arthritis, cancer and atherosclerosis. The aim of this study was to investigate the $ONOO^-$, NO, and $({\cdot}O_2^-)$ scavenging and anti-inflammatory activities of Mori Fructus in ob/ob mice. Methods : Mice were grouped and treated for 5 weeks as follows. Both the normal lean (C57/BL6J black mice) and control obese (ob/ob mice) groups received the standard chow. The experimental groups were fed a diet of chow supplemented with 7.5, 15 and 30 mg Mori Fructus per 1 kg of body weight for 14 days. For this study, the fluorescent probes, namely 2',7'-dichlorodihydrofluorescein diacetate (DCFDA), 4,5-diaminofluorescein (DAF-2) and dihydrorhodamine 123 (DHR 123) were used. Western blotting was performed using anti-phospho $I{\kappa}B-\alpha$, anti-IKK-$\alpha$, anti-NF-${\kappa}B$ (p50, p65), anti-COX-2 and anti-iNOS respectively. Results : Mori Fructus inhibited the generation of $ONOO^-$, NO and $({\cdot}O_2^-)$ in the lipopolysaccharide (LPS)-treated mouse kidney postmitochondria in vitro. The generation of $ONOO^-$, NO and $({\cdot}O2^-)$ were inhibited in the Mori Fructus-administered ob/ob mice groups. The GSH/GSSG ratio decreased in the ob/ob mice, whereas they improved in the Mori Fructus-administered groups. Mori Fructus inhibited the expression of phospho $I{\kappa}B-\alpha$, IKK-$\alpha$, COX-2, iNOS genes, and thereby the activation of NF-$I{\kappa}B$. Conclusions : These results suggest that Mori Fructus is an effective $ONOO^-$, $({\cdot}O_2^-)$ and NO scavenger, and therefore it might be a potential therapeutic drug against the inflammation process and inflammation-related diseases.

• The Journal of Internal Korean Medicine
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• 제25권2호
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• pp.268-276
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• 2004

Objective : Peroxynitrite $(ONOO^-)$, formed from the reaction of $O_2^-$ and NO, is a cytotoxic species that can oxidize several cellular components such as proteins, lipids and DNA. It has been implicated in the aging process and age-related disease such as Alzheimer's disease, rheumatoid arthritis, cancer and atherosclerosis. The aim of this study was to investigate scavenging activities of $ONOO^-$ and its precursors. NO and $O_2^-$ and its scavenging mechanism using fluorescent probes, DCFDA, DAF-2 and DHR 123.. Methods : Psoralea corylifolia was crushed. The crushed Psoralea corylifolia was extracted 3 times, each time with 3 volumes of methyl alcohol at $60^{\circ}C$ for 24 h. The extract was filtered and evaporated under reduced pressured using a rotary evaporator to yield 16g. This was done to investigate scavenging activities of $ONOO^-$, NO, $O_2^-$ and its scavenging mechanism using fluorescent probes, DCFDA, DAF-2 and DHR 123. Results : After Psoralea corylifolia was added authentic $ONOO^-,\;{\cdot}\;O_2^-$ and NO was markedly scavenged. Also, $ONOO^-$ induced by $O_2^-$ and NO (these derived from SIN-1) was inhibited. The data showed a decrease in $ONOO^-$ mediated nitration of tyrosine through electron donation after Psoralea corylifolia was added. Data showed a dose-dependent correlation with inhibition of nitration of bovine serum albumin induced by $ONOO^-$, Furtheremore, LPS-induced ROS and RNS generation was blocked. Conclusions: These results suggest potential for use of Psoralea corylifolia as an effective $ONOO^-$ scavenger to counter the aging process and age-related diseases.

• Journal of Oriental Neuropsychiatry
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• 제24권3호
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• pp.309-320
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• 2013

Objectives : There is a possibility LRE as remedy in Alzheimer disease (AD), but it's nerve protection effect and mechanism have to be elucidate. In this research, we applied LRE on $A{\beta}_{25-35}$ pre-treated SH-SY5Y cells, to find out the nerve protection effect and mechanism in AD cell model. Methods : We tried to confirm that effect by experimenting with 20, 50, and $100{\mu}g/ml$ concentration of LRE as a medicine. Next experiment, we assessed damage effect which induced $A{\beta}_{25-35}$, known to cause AD, on SH-SY5Y cell. In addition, cellular viability test is executed under $H_2O_2$ treatment condition in a SH-SY5Y cell. Results : 1. In $A{\beta}_{25-35}$ treated SH-SY5Y cell, LRE exhibited an anti-phosphorylation effect about tau protein, JNK, and IKB. 2. LRE prevent nerve cell apoptosis, which indued $A{\beta}_{25-35}$ and oxidative stress, modify JNK engaged synaptic structure and $NF{\kappa}B$ induced p75-neurotrophin receptor polymorphism. Conclusions : We found that LRE prevented oxidative stress-induced cellular destruction, for example, increased SOD activity of $A{\beta}_{25-35}$ treated SH-SY5Y cell and reduced toxicity of oxygen free radical. Consequently, the ingredients of LRE have a role as a catalyzer for $A{\beta}_{25-35}$ clearance and as scavenger for active oxygen free radical.