• Journal of Plant Biotechnology
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• 제43권4호
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• pp.422-431
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• 2016

Plants utilize cytochrome P450, a large superfamily of heme-containing mono-oxygenases, in the synthesis of lignins, UV protectants, pigments, defense compounds, fatty acids, hormones, and signaling molecules. Despite the overwhelming assortment of rice P450 accession numbers in the database, their functional studies are lacking. So far, there is no evidence involving rice P450 in disease immunity. Most of our understanding has been based on other plant systems that are mostly dicot. In this study, we isolated the cytochrome P450 (OsCYP71) in rice, and screened the gene using gain-of-function technique. The full-length cDNA of OsCYP71 was constitutively overexpressed using the 35S promoter. We then explored the functions of OsCYP71 in the rice - Xanthomonas oryzae pv. oryzae pathosystem. Using the gene expression assays, we demonstrate the interesting correlation of PR gene activation and the magnitude of resistance in P450-mediated immunity.

• BMB Reports
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• 제29권1호
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• pp.58-62
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• 1996

The structural changes in the electron donor side of the PSII reaction center have been monitored since heat treatment ($45^{\circ}C$ for 5 min) of thylakoids is known to decrease the oxygen evolving activity. In heat-treated spinach chloroplast thylakoids, the inhibitory effect of 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU) on the electron transport activity of the PSII reaction center from diphenyl carbazide to dichlorophenolindophenol became reduced approximately 3.8 times and [$^{14}C$]-labeled DCMU binding on the D1 polypeptide decreased to 25~30% that of intact thylakoid membranes, implying that the conformational changes of the DCMU binding pocket, residing on the D1 polypeptide, occur by heat treatment. The accessibility of trypsin to the $NH_2$-terminus of the cytochrome b-559 ${\alpha}$-subunit, assayed with Western blot using an antibody generated against the synthetic peptide (Arg-68 to Arg-80) of the COOH-terminal domain, was also increased, indicating that heat-treatment caused changes in the structural environments near the stromal side of the cytochrome b-559 ${\alpha}$-subunit, allowing trypsin more easily to cleave the $NH_2$-terminal domain. Therefore, the structural changes in the electron donor side of the PSII reaction center complexes could be one of the reasons why the oxygen evolving activity of the heat-treated thylakoid membranes decreased.

• Advances in Traditional Medicine
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• 제7권3호
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• pp.311-320
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• 2007

The present study was designed to estimate the protective effect of (-) epigallocatechin gallate (EGCG) on ethanol-induced liver injury in rats. Chronic ethanol administration (6 g/kg/day ${\times}$ 60 days) caused liver damage that was manifested by the elevation of markers of liver dysfunction - aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, bilirubin and ${\gamma}$-glutamyl transferase in plasma and reduction in liver glycogen. The activities of alcohol metabolizing enzymes such as alcohol dehydrogenase and aldehyde dehydrogenase were found to be altered in alcohol-treated group. Ethanol administration resulted in the induction of cytochrome p450 and cytochrome-$b_{5}$ activities and reduction of cytochrome-c reductase and glutathione-S-transferase, a phase II drug metabolizing enzyme. Further, ethanol reduced the viability of isolated hepatocytes (ex vivo) as assessed by trypan blue exclusion test and induced hepatocyte apoptosis as assessed by propidium iodide staining. Treatment of alcoholic rats with EGCG restored the levels of markers of liver injury and mitigated the alterations in alcohol metabolizing and drug metabolizing enzymes and cyt-c-reductase. Increased hepatocyte viability and reduced apoptotic nuclei were observed in alcohol + EGCG-treated rats. These findings suggest that EGCG acts as a hepatoprotective agent against alcoholic liver injury.

• 혜화의학회지
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• 제8권1호
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• pp.643-657
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• 1999

Through observing effect of BOPEASAN(BPT) on an aging white rat's metabolic enzyme system, the following conclusions were addressed 1. The quantity of the lipid peroxide in lung of was decreased meaningfully in all of experimental subject groups, relatively to counterpart groups. 2. Cytochrome P-450, Cytochrome b5, NADPH-Cytochrome P45, was decreased meaningfully in the experimental subject groups B,C and D. 3. superoxide dismutase, catarase, grutathione peroxidase, was increased meaningfully in the experimental subject groups B.C and D. 4. glutathione, glutathione S-transferase, glutathione redutase, ${\gamma}$-Glutamylcytein synthetase, had no meaningful change in the experimental subject groups. Regarding the above conclusions, the Bopeasan was affecting positively on both lipid peroxide a nd the enzyme system, as well as it has efficacy of suppressing the phenomena of aging, Therefore, the Bopeasan is, hereafter, expected to be applied clinically.

• Archives of Pharmacal Research
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• 제18권3호
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• pp.179-182
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• 1995

Previous study showed that $CCl_4$ administration evoked a rapid decrease in cytochrome $P_{450}$ 2E1 protein soon after the exposure due to posttranslational inhibition(Biochem. Biophys. Res. Commun. 179:449-454, 1991). In this report, aniline hydroxylase and the amounts of immunoreactive $P_{450}$ 2E1 were rapidly decreased during day 1 to 2 and recovered during day 3 to 4 after a single dose of $CCl_4$. The activity of pentoxyresorufin-O-dealkylase was also suppressed at day 1 and began to repair from day 2. However, the decrease in immunoreactive $P_{450}$ 2C content was not observed. The decreases in $P_{450}$ 2E1 enzyme activity and immunoreactive protein by acute $CCl_4$ treatment were accompanied by a decline in $P_{450}$ 2E1 mRNA level. The data thus suggested a pretranslational reduction of $P_{450}$ 2E1 during day 1 to 2 after acute $CCl_4$ treatment.

• 한국전기화학회:학술대회논문집
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• 한국전기화학회 2005년도 춘계총회 및 학술발표회
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• pp.31-31
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• 2005

• 한국전기화학회:학술대회논문집
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• 한국전기화학회 2002년도 춘계총회 및 학술발표회
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• pp.7-7
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• 2002

• Bulletin of the Korean Chemical Society
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• 제16권12호
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• pp.1139-1141
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• 1995

• 약학회지
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• 제39권4호
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• pp.450-460
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• 1995

The acute toxicity of fthalide in rat was studied in vivo by the observations of the changes in hematogram, serological parameters, content of cytochrome p-450, activities of NADPH-cytochrom c reductase, glucose-6-phosphatase, and the contents of cholinesterase and carboxylesterase in liver. Fthabde is a practically non-toxic substance(LD50 is 3.86g/kg), but rats were intoxicated with fthabde at a oral dose of 100 mg/kg for 12 days. WBC were significantly decreased and activities of ALT and LDH, on the cotrary, the content of glucose in serum were slightly increased. Cytochrome p-450 and lipid peroxide in liver were significantly increased in the fthalide-intoxicated rats. The longer administration of fthalide showed further increase of carboxylesterase activity in liver and serum, but decrease of activities of glucose-6-phosphatase and cholinesterase in liver and serum. These results show that fthatide can induce the hepatocellular injury and neurotoxicity.

• Toxicological Research
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• 제13권3호
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• pp.183-186
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• 1997

Acute toxicity of pectenotoxin 2 (PTX2) was examined in mice. Treatment of mice with a toxic dose of PTX2 resulted in clinical signs such as ataxia, cyanosis and an abrupt decrease in body temperature. Histopathological studies revealed that the liver is the major target organ for PTX2. Activities of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and sorbitol dehydrogenase (SDH) were significantly elevated by PTX2 administration. Glucose-6-phosphatase activities were not changed by the treatment. The PTX2 treatment decreased relative liver weight without changing the body weight. The effect of PTX2 on hepatic drug metabolizing enzyme system was determined. An ip dose of PTX2 (200 $\mu$g/kg) induced a significant decrease in the hepatic microsomal protein content. Cytochrome P-450 content, cytochrome b$_5$ content, NADPH cytochrome c reductase, aminopyrine N-demethylase activities, or hepatic glutathione content were not altered by PTX2 treatment.