• Toxicological Research
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• v.12 no.2
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• pp.277-281
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• 1996

To evaluate the renal toxicity of the antitumor agent, 5-(piperidonomethylphenyl)-2,3-dihydroimidazo[2,1-a]isoquinoline (SDZ-62-434), rats were treated with SDZ-62-434 of 50 mg/Kg, i.p., once and 10 mg/Kg, i.p., daily for 7 days. The kidney weights and urine volume after and during the treatment were observed. The concentrations of urinary creatinine, protein, and the activities of N-acetyl-$\beta $D-glucosaminidase (NAG), alanine aminopeptidase (AAP), $\gamma$-glutamyl transpeptidase (GGT) and lactate dehydrogenase (LDH) in 24 hr urine were also determined. The kidney weights after acute and subacute administration was not affected. The urine excretions were increased 5 days after the acute administration and increased after the daily 3rd day-administration. The excretion of creatinine was similar as that of urine excretion. The excretion of creatinine was increased 5 days after the acute and subacute administration. However, the protein excretion didn't changed in both treatment. Those indicate that SDZ-62-434 might induce the diuresis and also suggest that diuresis might be due to the some metabolites rather than the compound itself. The urinary activities of NAG and LDH were not affected after the acute treatment. However, the urinary activities of AAP and GGT were slightly increased 3 days after the acute administration but, returned to the control value. In subacute treatment, the activities of GGT was not changed. And the activities of NAG were declined after the 7th day-administration. However, the activities of AAP were significantly increased after the 5th day-administration. Furthermore, the urinary activities of LDH were continuously increased during the subacute administration. These results indicate that the high and subacute administration might induce a weak damage on the kidney cells. Furtherrnore, the present results suggest that SDZ-62-434 might have relatively slow-emerging and mild toxicity to the kidney.

• Microbiology and Biotechnology Letters
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• v.47 no.1
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• pp.78-86
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• 2019

Recombinant Corynebacterium glutamicum producing N-acetylglucosamine (GlcNAc) was constructed by metabolic engineering. To construct a basal strain producing GlcNAc, the genes nagA, nagB, and nanE encoding N-acetylglucosamine-6-phosphate deacetylase, glucosamine-6-phosphate deaminase, and N-acetylmannosamine-6-phosphate epimerase, respectively, were sequentially deleted from C. glutamicum ATCC 13032, yielding strain KG208. In addition, the genes glmS and gna1 encoding glucosamine-6-phosphate synthase and glucosamine-6-phosphate N-acetyltransferase, which originated from C. glutamicum and Saccharomyces cerevisiae, respectively, were expressed in several expression vectors. Among several combinations of glmS and gna1 expression, recombinant cells expressing glmS and gna1 under control of the ilvC promoter produced 1.77 g/l of GlcNAc and 0.63 g/l of glucosamine in flask cultures.

• Journal of Life Science
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• v.19 no.8
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• pp.1073-1080
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• 2009

A number of studies have demonstrated that the regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) can reduce the risks of colorectal, oesophageal and lung cancers. NSAIDs have been shown to exert their anti-cancer effects through inducing apoptosis in cancer cells. The susceptibility of tumor cells to anti-tumor drug-induced apoptosis appears to depend on the balance between pro-apoptotic and anti-apoptotic programs such as nuclear factor kB (NF-kB), phosphatidylinositol 3-kinase (PI3K)-Akt/protein kinase B (PKB) and MEK1/2-ERK1/2 pathways. We examined the effects of pro-survival PI3K and ERK1/2 signal pathways on cell cycle arrest and apoptosis in response to NSAIDs including sulindac sulfide and NS398. We show that simultaneous inhibition of the Akt/PKB and ERK1/2 signal cascades could synergistically enhance the potential pro-apoptotic activities of sulindac sulfide and NS398. Similar enhancement was observed in cells treated with sulindac sulfide or NS398 and 100 ${\mu}$M genistein, an inhibitor of receptor tyrosine kinases (RTKs) that are upstream of PI3K and MEK1/2 signaling. We further demonstrate that NAG-1 is induced and plays a critical role(s) in apoptosis by NSAIDs-based combined treatment. In sum, our results show that combinatorialtreatment of sulindac sulfide or NS398 and genistein results in a highlysynergistic induction of apoptotic cell death to increase the chemopreventive effects of the NSAIDs, sulindac sulfide and NS398.

• Toxicological Research
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• v.16 no.1
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• pp.47-52
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• 2000

To evaluate the renal toxicity of the antitumor agent, 1-(N-methyl) piperazinyl-3-phenyl-isoquinoline(CWJ-$\alpha$-5), rats were terated with CWJ-$\alpha$-5 (acute : 100mg/kg, i.p., single and subacute : 10mg/kr, i.p., daily for 7 days). The changes in the body weights, water consumption, kidney weights and urine volume after and during the treatment were observed. The concentrations of urinary creatinine, the activities of N-acetyl-$\beta$-D-glucosaminidase (NAG), alanine aminopeptidase (AAP), $\gamma$-glutamyl transpeptidase ($\gamma$-GT) and lactate dehydrogenase (LDH) in 24 hr urine were also determined. The body weight and water consumption were decreased after the acute and subacute administration. However, the excretion of urine was not changed except the 1 day after the acute treatment. The excretion of creatinine was significantly decreased from 1 day after acute administration and continuously decreased. Also the excretion of creatinine was decreased during subacute administration. However, the protein excretion did not changed in both treatment. Those indicate that CWJ-$\alpha$-5 might decrease the metabolic rate of muscle. The urinary activities of NAG, AAP, $\gamma$-GT, and LDH were significantly affected by the drug treatment. The urinary activities of NAG, AAP and $\gamma$-GT were significantly increased 1 and 3 days after the acute administration and then returned to the control value. However, the urinary activities of LDH were increased 7 days after acute treatment. During subacute treatment, the urinary activities of $\gamma$-GT were not changed. However, the urinary activities of NAG, AAP and LDH were only significantly increased after the third administration. These results indicate that either the high acute dose or the subacute administration with low dose of the compound might induce a temporal damage in the kidney cells.

• Journal of Life Science
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• v.20 no.2
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• pp.213-218
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• 2010

In the present study, we investigated anti-proliferative activities of capsaicin and gene expression changes in response to capsaicin treatment in human colorectal HCT116 cells. The results showed that capsaicin decreased cell viabilities in a dose dependent manner and induced global gene expression changes. We found that 103 genes were up-regulated more than twofold, whereas 153 genes were down-regulated more than twofold by $100\;{\mu}M$ capsaicin treatment. Among the up-regulated genes, we selected 4 genes (NAG-1, DDIT3, GADD45A and PCK2) and performed RT-PCR to confirm the microarray data. We found that $100\;{\mu}M$ of capsaicin increased tumor suppressor p53 gene expression. In addition, the results showed that NAG-1, DDIT3 and GADD45A expressions were not dependent on p53 presence, whereas PCK2 expression. The results of this study may help to increase our understandings of the molecular mechanism of anti-proliferative activity mediated by capsaicin in human colorectal cancer cells.

• Proceedings of the Korean Society of Crop Science Conference
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• 1993.10a
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• pp.10-11
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• 1993

• Proceedings of the Korean Society of Crop Science Conference
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• 2005.10b
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• pp.132-133
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• 2005

• Magazine of the Korea Concrete Institute
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• v.23 no.3
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• pp.39-43
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• 2011

• Proceedings of the Korean Society for Noise and Vibration Engineering Conference
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• 2011.04a
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• pp.161-162
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• 2011

• Proceedings of the Korean Society of Crop Science Conference
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• 2003.05a
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• pp.49-49
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• 2003