• BMB Reports
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• v.39 no.6
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• pp.696-702
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• 2006

Recently three proteins, playing central roles in the bidirectional transport of urate in renal proximal tubules, were identified: two members of the organic anion transporter (OAT) family, OAT1 and OAT3, and a protein that designated renal urate-anion exchanger (URAT1). Antibodies against these transporters are very important for investigating their expressions and functions. With the cytokine gene as a molecular adjuvant, genetic immunization-based antibody production offers several advantages including high specificity and high recognition to the native protein compared with current methods. We fused high antigenicity fragments of the three transporters to the plasmids pBQAP-TT containing T-cell epitopes and flanking regions from tetanus toxin, respectively. Gene gun immunization with these recombinant plasmids and two other adjuvant plasmids, which express granulocyte/macrophage colony-stimulating factor and FMS-like tyrosine kinase 3 ligand, induced high level immunoglobulin G antibodies, respectively. The native corresponding proteins of URAT1, OAT1 and OAT3, in human kidney can be recognized by their specific antibodies, respectively, with Western blot analysis and immunohistochemistry. Besides, URAT1 expression in Xenopus oocytes can also be recognized by its corresponding antibody with immuno-fluorescence. The successful production of the antibodies has provided an important tool for the study of UA transporters.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.2
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• pp.195-200
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• 1997

Water transport in highly-permeable membranes is facilitated by some specialized pathways, which are called aquaporins (AQP). AQP1 (AQP-CHIP) is the first recognized aquaporin identified from red cells and renal proximal tubules. Up until now 4 other aquaporin homologs have been reported. Each aquaporin has its unique tissue distribution and regulatory mechanims. To elucidate molecular mechanisms for their transcription regulation and tissue-specific expression isolation of aquaporin genes is required. To clone promoters of the AQP family mouse genomic library was screened by the 1st exon-specific probe of AQP4, and 5 different plaques were positively hybridized. Phage DNAs were purified and characterized by restriction mapping and sequencing. One of them is the mouse AQP-CD gene. The gene was consisted of 4 exons and the exon-intron boundaries of mouse AQP-CD gene were identified at identical positions in other related genes. The 5'-flanking region of AQP-CD gene contains one classic TATA box, a GATA consensus sequence, an E-box and a cyclic AMP-responsive element. The cloning of the mouse AQP-CD gene, of which product is expressed in the collecting duct and is responsible for antidiuresis by vasopressin, will contribute to understand the molecular mechanisms of tissue-specific expression and regulation of AQP-CD gene under various conditions.

• Journal of Marine Bioscience and Biotechnology
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• v.13 no.2
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• pp.86-93
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• 2021

A high salt diet contributes to kidney damage by causing hypoxia and oxidative stress. Recently, an increase in dietary salt has been reported to induce an inflammatory phenotype in immune cells, further contributing to kidney damage. However, studies on the exact mechanism and role of a high salt diet on the inflammatory response in the kidneys are still insufficient. In this study, a cisplatin-induced acute kidney injury model using C57BL/6 mice was used to analyze the effect of salt intake on kidney injury. Results showed that high salt administration aggravated kidney edema in mice induced by treatment with cisplatin. Moreover, the indicators of kidney and liver function impairment were significantly increased in the group cotreated with high salt compared with that treated with cisplatin alone. Furthermore, the exacerbation of kidney damage by high salt administration was also associated with a decrease in the number of cells in the immune regulatory system. Additionally, high salt administration further decreased renal perfusion functions along with increased cisplatin-induced damage to proximal tubules. This was accompanied by increased expression of T cell immunoglobulin, mucin domain 1 (a biomarker of kidney injury), and Bax (a pro-apoptotic factor). Moreover, cisplatin-induced expression of proinflammatory mediators and cytokines, including cyclooxygenase-2 and tumor necrosis factor-α in kidney tissue, was further increased by high salt intake. Therefore, these results indicate that the kidney's inflammatory response by high salt treatment can further promote kidney damage caused by various pathological factors.

• Applied Microscopy
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• v.30 no.3
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• pp.273-283
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• 2000

To investigate the defensive effect of green tea against the lead toxicity, Sprague-Dewley rats (150 gm) were divided into 5 groups; the control group (A), the group treated with lead for 4 weeks (Group B-1), the group treated with lead and green tea for 4 weeks (Group B-2), the group treated with lead for 8 weeks (Group C-1), and the group treated with lead and green tea for 8 weeks (Group C-2). The lead acetate (500 ppm) was injected two times for one week into the abdomen and green tea solution (3 g/100 ml distilled water) offered freely. The results of histological and biocheical study are as follows; 1. Blood Urea Nitrogen (BUN) were increased in all the tested groups. The Group B-1 was more increased than the Group B-2, and the Group C-1 more than the Group C-2. The values of Alkaline phosphatase (ALP) were also decreased in all the tested groups, as such the former phenomenon. 2 In the Group B-1, some microvilli, mitochondria and rER were modificated on epithelial cell of proximal renal tubules. The cristae of mitochondria were enlarged, microvilli and nucleus were observed normally on the Group B-2. The number of Microvilli, mitochodria and rER were decreased, many lysosomes and irregular nucleus observed in the Group C-1. In the Group C-2, microvilli were modificated slightly and other organelles were observed similary with the Group B-2.

• Journal of fish pathology
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• v.8 no.1
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• pp.57-67
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• 1995

Twenty-four hours, acute toxicity and the histopathological effect of formaline to flounder, Paralichthys olivaceus larvae were examined. The $LC_{50}$ values obtained to farmaline were 2,520 ppm in 1 hour treatment. 1.610 ppm in 2 hours treatment, 868 ppm in 4 hours treatment and 141 ppm in 24 hours treatment. Many pathological features such as hypertrophy of mucous and epithelial cells in secondary gill lamella, hyaline droplet degeneration of tubular epithelial cells in the proximal convoluted segment of renal tubules, focal or massive necrosis in liver cells and pycnotic nucleus in heart cells were recognized. The above results were discussed in relation to the application of formaline as therapeutic agent in flounder disease.

• Journal of Life Science
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• v.29 no.8
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• pp.879-887
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• 2019

This study investigated the localization and changes in the concentration of injected mercury in the kidney, liver, and spleen of mice. To evaluate changes in the concentration of mercury over time, the mice were euthanized 10, 150, and 300 days post-treatment. Localization of accumulated mercury was identified by the autometallography method. Mercury was densely located in the supranuclear cytoplasm of epithelial cells of proximal tubules of the kidney but was not detected in the glomerulus 10 days post-treatment. In the liver, mercury was mainly found in hepatocytes around the portal vein and in sinusoidal Kupffer cells 10 days post-treatment. Mercury was scattered throughout both white and red pulp of the spleen 10 days post-treatment. In terms of changes in the concentration of mercury, the levels were lower in the renal cortex and medulla 150 and 300 days post-treatment as compared with those 10 days post-treatment. Mercury was found at low concentrations in liver hepatocytes 150 and 300 days post-treatment. The mercury concentration was also low in both the white and red pulp of the spleen 150 and 300 days post-treatment. Therefore, the concentrations of accumulated mercury in the kidney, liver, and spleen 150 and 300 days post-treatment were lower than those 10 days post-treatment. We identified the localization of mercury in cells and tissues of several organs and observed that accumulated mercury in organs decreased naturally over time.

• Journal of Radiation Protection and Research
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• v.15 no.2
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• pp.27-39
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• 1990

Appreciable radiation exposures certainly were occurred in the reactor burn-up, the nuelear fall-out and the surroundings of nuclear installations with radioactive effluents. Therefore, radioactive nuclides is not only potentially hazardous to workers of nuclear power plants and related industrials, but also the wokers who handle radioactive nuclides in biochemical research and nuclear medicine diagnostics. And in the case of occurring the nuclear accidents, the early medical treatment of radiation injury should be necessary but little is established medical procedures to decontaminate the victims of internal contamination of radioactive nuclides in korea. Accordingly, to achieve the basic data for protective roles and medical treatment of radiation injury, the present studies were carrid out to evaluate the decontamination of uranium by the chemical drugs. The results observed were summarized as follows: 1. The combined treatmet group of sodium bicarbonate and saline with uranyl nitrate injection simultaneously and the dithiothreitol group that was administered 30 minutes after uranyl nitrate injection were increased significantly in the change of body weight than uranyl nitrate-only group (P<0.005). 2. All the experimental groups were increased the fluid intake and urine volume on the uranyl nitrate-induced acute renal failure. but the combined treatment group of sodium bicarbonate and saline with uranyl nitrate injection simultaneously and the dithiothreitol group that was administered 30 minutes after uranyl nitrate injection have the higher increment of fluid intake and urine volume (P<0.05). 3. When sodium bicarbonate and saline was treated with uranyl nitrate injection simultaneously. and dithiothreitol was administered 30 minutes after uranyl nitrate injection. there was significantly reduced in BUN concentration (P<0.01). 4. When dithiothreitol was administered 30 minutes after uranyl nitrate injection. there was reduced more significantly on the increment of serum creatinine concentration than that observed in uranyl nitrate-only group(P<0.01). but when the combined treatment of sodium bicarbonate and saline with uranyl nitrate simultaneously, there was still. albeit much less marked. decrease in serum creatinine concentration. 5. The sodium bicarbonate and saline was treated with uranyl nitrate simultaneously and dithiothreitol was administered at 30 minutes after uranyl nitrate were excreted markedly higher urine creatinine concentration than the uranyl nitrate-only group. 6. Uranyl nitrate has been used in experimental animals to produce hydropic degeneration and swelling of proximal tubules, disappearance of microvilli and brush border or necrosis in the kidney and centrilobular necrosis, congestion, and telangiectasia of the liver. When the sodium bicarbonate and saline was treated with uranyl nitrate simultaneously, and dithiothreitol was administered. 30 minutes after uranyl nitrate, there was more marked the protective effect than uranyl nitrate-only group. Finally, if the sodium bicarbonate and saline may administered as quickly as possible each time that some risk for internal contamination, with uranium, and dithiothreitol is administered 30 minutes after uranium contamination, there ameliorates the course of uranyl nitrate-induced acute renal failure.and this effect is assocciated with prevention of uranium (heavy metal)-induced alterations in BUN, serum creatinine, urine creatinine, fluid intake, urine volume and body weight.