• Journal of Microbiology and Biotechnology
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• v.12 no.1
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• pp.31-38
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• 2002

Bacteria have evolved various types of resistance mechanism to toxic heavy metals, such as arsenic and antimony. An arsenical and antimonial resistant bacterium was isolated from a shallow creek draining a coal-mining area near Taebaek City, in Kangwon-Do, Korea. The isolated bacterium was identified and named as Pseudomonas sp. KM20 after biochemical and physiological studies were conducted. A plasmid was identified and its function was studied. Original cells harboring the plasmid were able to grow in the presence of 15 mM sodium arsenite, while the plasmid-cured (plasmidless) strain was sensitive to as little as 0.5 mM sodium arsenate. These results indicated that the plasmid of Pseudomonas sp. KM20 does indeed encode the arsenic resistance determinant. In growth experiments, prior exposure to 0.1 mM arsenate allowed immediate growth when they were challenged with 5 mM arsenate, 5 mM arsenite, or 0.1 mM antimonite. These results suggested that the arsenate, arsenite, and antimonite resistance determinants of Pseudomonas sp. KM20 plasmid were indeed inducible. When induced, plasmid-bearing resistance cells showed a decreased accumulation $of\;73^As$ and showed an enhanced efflux $of\;^73As$. These results suggested that plasmid encoded a transport system that extruded the toxic metalloids, resulting in the lowering of the intracellular concentration of toxic oxyanion. In a Southern blot study, hybridization with an E. coli R773 arsA-specific probe strongly suggested the absence of an arsA cistron in the plasmid-associated arsenical and antimonial resistance determinant of Pseudomonas sp. KM20.

• International Journal of Oral Biology
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• v.38 no.2
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• pp.61-65
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• 2013

Erythromycin is a macrolide antibiotic and inhibits bacterial protein synthesis by stimulating the dissociation of the peptidyl-tRNA molecule from the ribosomes during elongation. The use of macrolides has increased dramatically over the last few years and has led to an increase in bacterial resistance to these antibiotics. Bacterial resistance to erythromycin is generally conferred by the ribosome methylation and/or transport (efflux) protein genes. Among the identified erythromycin-resistant genes, erm(B) (erythromycin methylation) and mef(A) (macrolide efflux) are generally detectable in erythromycin-resistant streptococcal species. The distribution of these genes in oral streptococcal isolates has been reported in studies from other countries but has not been previously examined in a Korean study. We here examined by PCR the presence of erm(B) and mef(A) in oral streptococci isolated from Korean dental plaques. Among the 57 erythromycin-resistant strains tested, 64.9% harbored erm(B) whereas 40.4% were positive for mef(A). Eleven isolates had both the erm(B) and mef(A) genes. Twenty six isolates had only erm(B) and 12 isolates had only mef(A). Eight of the 57 strains examined were negative for both genes.

• Journal of Nutrition and Health
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• v.41 no.5
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• pp.381-390
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• 2008

Present study was conducted to investigate the effects of exercise and cholesterol diet on plasma and liver lipids, platelet aggregation, erythrocyte Na efflux and liver index such as GOT and GPT using Sprague Dawley rats. Forty rats were divided into four groups and fed control or 0.5% cholesterol diet with and without treadmill for six weeks. The final body weight of group fed cholesterol diet with exercise was somewhat decreased compared with group fed cholesterol diet without exercise. L.W/B.W ratio was significantly increased in groups fed cholesterol diet (p < 0.01), but exercise tended to decrease this ratio. Plasma total cholesterol was significantly increased and HDL-cholesterol was decreased in groups fed cholesterol diet (p < 0.01). Plasma triglyceride was significantly decreased in groups fed cholesterol diet compared with groups fed control diet (p < 0.01). Plasma triglyceride of groups with exercise was significantly decreased compared with their non exercising counterparts regardless diet (p < 0.05). Liver total cholesterol and triglyceride was significantly increased in groups fed cholesterol diet (p < 0.01), but exercise did not affect on these levels. Na-K ATPase was somewhat decreased in groups fed cholesterol diet, and exercise tended to recover the reduced Na-K ATPase. Na passive transport was significantly decreased in group fed control diet without exercise and significantly increased in group fed cholesterol diet with exercise, there were significant differences between groups (p < 0.05). There were no differences in total Na efflux and intracellular Na among groups, and total Na efflux was not correlated with intracellular Na. Hematocrit was significantly lower (p < 0.05) in group fed cholesterol diet without exercise compared with other groups. Platelet aggregation in the initial slope and the maximum was increased in groups fed cholesterol diet, but not statistically significant. Exercise especially increased the initial slope of aggregation. Plasma GOT and GPT was significantly increased in groups fed cholesterol diet (p < 0.01), and exercise in group fed cholesterol diet significantly decreased both GOT and GPT compared with the non exercising counterpart (p < 0.01). This study showed that cholesterol diet increases plasma and liver lipids and GOT and GPT, and exercise improves plasma and liver lipid profile and liver index of GOT and GPT preventing fatty liver.

• 대한핵의학회:학술대회논문집
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• 2001.05a
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• pp.66-75
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• 2001

Although diverse mechanisms are involved in multidrug resistance for chemotherapeutic drugs, the development of cellular P-glycoprotein(Pgp) and multidrug-resistance associated protein (MRP) are important factors in the chemotherapy failure to cancer. Various detection assays provide information about the presence of drug efflux pumps at the mRNA and protein levels. However these methods do not yield information about dynamic function of Pgp and MRP un vivo. Single photon emission tomography (SPECT) and positron emission tomography (PET) are available for the detection of Pgp and MRP-mediated transport. $^{99m}Tc$-sestaMIBl and other $^{99m}Tc$-radiopharmaceuticals are substrates for Pgp and MRP, and have been used in clinical studies for tumor imaging, and to visualize blockade of Pgp-mediated transport after modulation of Pgp pump. Colchicine, verapamil and daunorubicin labeled with $^{11}C$ have been evaluated for the quantification of Pgp-mediated transport with PET in vivo and reported to be feasible substrates with which to image Pgp function in tumors. Leukotrienes are specific substrates for MRP and N-$[^{11}C]$acetyl-leukotriene E4 provides an opportunity to study MRP function non-invasively in vivo. Results obtained from recent publications are reviewed to confirm the feasibility of using SPECT and PET to study the functionality of MDR transporters in vivo.

• The Korean Journal of Physiology
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• v.21 no.2
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• pp.283-289
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• 1987

Uric acid transport across the basolateral membrane of renal proximal tubules was studied in rabbit kidney cortical slices. Uric acid uptake was greater under $O_2$ atmosphere compared to under $N_2$ atmosphere, and was increased with $Na^{2+}$ concentration in incubation medium. Uric acid inhibited PAH uptake but not TEA uptake and did trans-stimulated PAH efflux. PAH also inhibited uric acid uptake. Uric acid uptake was inhibited by harmaline, ouabin, SITS, DIDS and pyrazinoic acid. The inhibition of PAH uptake by these inhibitors also was reasonably comparable to that of uric acid uptake. These results suggest that uric acid was transported across the basolateral membrane of renal tubule by a carrier-mediated process which was by a common transport system with PAH in rabbit.

• Biomedical Science Letters
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• v.20 no.2
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• pp.49-55
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• 2014

RalBP1 is an ATP-dependent non-ABC transporter, responsible for the major transport function in many cells including many cancer cell lines, causing efflux of glutathione-electrophile conjugates of both endogenous metabolites and environmental toxins. RalBP1 is expressed in most human tissues, and is over-expressed in non-small cell lung cancer cell lines and in many other tumor types. Blockade of RalBP1 by various approaches has been shown to increase sensitivity to radiation and chemotherapeutic drugs, leading to cell apoptosis. In xenograft tumor models in mice, RalBP1 blockade or depletion results in complete and sustained regression across many cancer cell types including lung cancer cells. In addition to its transport function, RalBP1 has many other cellular and physiological functions, based on its domain structure which includes a unique Ral-binding domain and a RhoGAP catalytic domain, as well as docking sites for multiple signaling proteins. Additionally, RalBP1 is also important for stromal cell function in tumors, as it was recently shown to be required for efficient endothelial cell function and angiogenesis in solid tumors. In this review, we discuss the cellular and physiological functions of RalBP1 in normal and lung cancer cells.

• Parasites, Hosts and Diseases
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• v.61 no.4
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• pp.428-438
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• 2023

Clonorchis sinensis is commonly found in East Asian countries. Clonorchiasis is prevalent in these countries and can lead to various clinical symptoms. In this study, we used overlap extension polymerase chain reaction (PCR) and the Xenopus laevis oocyte expression system to isolate a cDNA encoding the choline transporter of C. sinensis (CsChT). We subsequently characterized recombinant CsChT. Expression of CsChT in X. laevis oocytes enabled efficient transport of radiolabeled choline, with no detectable uptake of arginine, α-ketoglutarate, p-aminohippurate, taurocholate, and estrone sulfate. Influx and efflux experiments showed that CsChT-mediated choline uptake was time- and sodium-dependent, with no exchange properties. Concentration-dependent analyses of revealed saturable kinetics consistent with the Michaelis-Menten equation, while nonlinear regression analyses revealed a Km value of 8.3 µM and a Vmax of 61.0 pmol/oocyte/h. These findings contribute to widen our understanding of CsChT transport properties and the cascade of choline metabolisms within C. sinensis.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.1
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• pp.35-43
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• 1997

Cis-dichlorodiammine platin${\mu}M$II (Cisplatin), an effective chemotherapeutic agent, induces acute renal failure by unknown mechanisms. To investigate direct toxic effects of cisplatin on the renal proximal tubular transport system, LLC-$PK_1$ cell line was selected as a cell model and the sugar transport activity was evaluated during a course of cisplatin treatment. Cells grown to confluence were treated with cisplatin for 60 min, washed, and then incubated for up to 5 days. At appropriate intervals, cells were tested for sugar transport activity using ${\alpha}-methyl-D-[^{14}C]glucopyranoside$ (AMG) as a model substrate. In cells treated with 100 ${\mu}M$ cisplatin, the AMG uptake was progressively impaired after 3 days. The viability of cells was not substantially changed with cisplatin of less than 100 ${\mu}M$, but it decreased markedly with 150 and 200 ${\mu}M$. In cisplatin-treated cells, the $Na^+$ -dependent AMG uptake was drastically inhibited with no change in the $Na^+$ -independent uptake. Kinetic analysis indicated that Vmax was suppressed, but Km was not altered. The $Na^+$ -dependent phlorizin binding was also decreased in cisplatin-treated cells. However, the AMG efflux from preloaded cells was not apparently retarded by cisplatin treatment. These data indicate that the cisplatin treatment impairs $Na^+$ -hexose cotransporters in LLC-$PK_1$ cells and suggest strongly that defects in transporter function at the luminal plasma membrane of the proximal tubular cells constitute an important pathogenic mechanism of cisplatin nephrotoxicity.

• Toxicological Research
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• v.29 no.3
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• pp.165-172
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• 2013

Acetaminophen (APAP) known as paracetamol is the main ingredient in Tylenol, which has analgesic and anti-pyretic properties. Inappropriate use of APAP causes major morbidity and mortality secondary to hepatic failure. Overdose of APAP depletes the hepatic glutathione (GSH) rapidly, and the metabolic intermediate leads to hepatocellular death. This article reviews the mechanisms of hepatotoxicity and provides an overview of current research studies. Pharmacokinetics including metabolism (activation and detoxification), subsequent transport (efflux)-facilitating excretion, and some other aspects related to toxicity are discussed. Nuclear factor erythroid 2-related factor 2 (Nrf2)-regulated gene battery plays a critical role in the multiple steps associated with the mitigation of APAP toxicity. The role of Nrf2 as a protective target is described, and potential natural products inhibiting APAP toxicity are outlined. This review provides an update on the mechanism of APAP toxicity and highlights the beneficial role of Nrf2 and specific natural products in hepatoprotection.

• Bulletin of the Korean Chemical Society
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• v.4 no.3
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• pp.128-132
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• 1983

The self-diffusion experiment of water was performed across two series of tactic poly(2-hydroxyethyl methacrylate), P(HEMA) membranes prepared by crosslinking with various amount of hexamethylene diisocyanate (HMDIC). The tagging material was tritium hydroxide (THO) and the efflux of THO was counted on a Liquid Scintillation Counter. The transport data of THO show that the permeability decreases as the amount of HMDIC increased from 2.5 to 10 mole % and the self-diffusions coefficient shows a parallel trend with it. The diffusivity data was discussed in terms of the change of water structural orderliness within membranes. Using the relation between viscosities and diffusivities derived from Eyring's absolute rate theory, the corresponding viscosities of water within two series of tactic P(HEMA) membranes were obtained. From this, it is seen that the viscosity of water within tactic P(HEMA) membranes may have the same values with those of supercooling water whose temperature ranges from -28 to -$36^{\circ}C.$.