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        발레수행시 Pyridoxine섭취가 골단백 및 아미노산 대사에 미치는 영향

        신말연(Mal Ryun Shin) 한국무용과학회 2006 한국무용과학회지 Vol.13 No.-

        본 연구는 발레수행시 Pyridoxine의 적정 섭취량과 섭취 기간의 타당성을 골단백 및 아미노산 대사와 연관하여 분석함으로서 발레무용수들에게 추가적인 Pyridoxine섭취의 효용성에 관한 실험적 자료를 제시 하는데 목적을 두었다. 본 연구의 대상자들은 14명의 발레전공 여대생으로 실험기간 30일 동안 전원에게 흡연, 음주, 각종 영양제 및 약물 복용을 금지시켰으며 발레 활동은 일주일에 3회-5회 실시하였다. GroupI은 Placebo 2.4㎎, GroupII는 Pyridoxine 1.6㎎, GroupIII는 Pyridoxine 2.4㎎을 섭취하도록 하였으며, Double Blind 방법에 의해 실험이 진행되었다. 본 연구의 분석항목은 Osteocalcin(OS), Calcium(CA), Isoleucine, Leucine, Lysine, Phenylaianine, Methionire, Threonine, Tryptophan, Valine 등을 분석하였다. 자료 분석방법에 있어서 Analysis of Covariance(ANCOVA)를 적용하였고, 유의한 차가 나타난 경우 Multiple Range Test(Scheffe)를 실시하였다. 분석한 결과 발레수행 시의 Pyridoxine섭취가 칼슘 농도에 통계적으로 유의한 차이(p<.05)를 나타났으며, Osteocalcin 및 아미노산 등에 통계적으로 유의한 차이를 나타내지 않았다. 종합적으로 본 연구결과는 Pyridoxine섭취가 발레와 같은 신체활동수행에 Ergogenic Aids로서 긍정적인 영향을 미친다는 주장을 지지하고 있지는 않다. 그러나 발레무용수와 영양과의 관계뿐만 아니라 Pyridoxine의 생화학적 대사과정에 관한 불명확한 연구 논제들은 Pyridoxine섭취와 신체활동수행 사이의 상호 작용을 직접적으로 규명할 수 있는 실험 설계 방법 및 기자재들을 사용하여 향후에 긍정적으로 연구되어 질 수 있다. 발레수행 동안 혈장에서 발생하는 피리독설 기질 재분포 구조의 중요성, 골격근에서 Pyridoxine대사 작용에 관여하는 집단특정 프로테아제(GSP)의 역할, 발레동작들이 심혈관 질환에 미치는 보호 효과에서 Pyridoxine 의 관련 가능성 등의 논제들이 향후 연구에서 수반 되어야 한다. The purpopse of this study was to determine the effect of pyridoxine supplementation with ballet exercise on bone lipoprotein and amino-acid metabolism. 14 college female ballet dancers were participated in 30 days study for a double blind and subjects were randomly assigned to one of the three groups, i.e., GroupⅠ(n=4): placebo (2.4mg/day); GroupⅡ(n=5): pyridoxine (1.6mg/day); GroupⅢ(n=5): pyridoxine(2.4mg/day) with ballet exercise 3-5 times per week. Study subjects measured osteocalcin(OS), calcium(CA), isoleucine, leucine, lysine, phenylaianine, methionire, threonine, tryptophan, valine, before and after the treatment. Analysis of Covariance (ANCOVA), Multiple Range Test(Scheffe) were used to determine the statistical significance. There were no group differences in the osteocalcin(OS) and essential amino acids, but calcium were significantly changed(p<.05). The result of this study does not lend support to the contention that pyridoxine intake has much practical impact on ballet exercise performance as a ergogenic acid. However, it does appear that several significant research topics in pyridoxine biochemistry metabolism as well as ballet dancer and nutrition can be explored profitably in the future using experimental designs involving interaction between pyridoxine status and exercise performance.

      • Detoxifying effect of pyridoxine on acetaminophen-induced hepatotoxicity via suppressing oxidative stress injury

        Roh, Taehyun,De, Umasankar,Lim, Seong Kwang,Kim, Min Kook,Choi, Seul Min,Lim, Duck Soo,Yoon, Sungpil,Kacew, Sam,Kim, Hyung Sik,Lee, Byung-Mu Elsevier 2018 Food and chemical toxicology Vol.114 No.-

        <P><B>Abstract</B></P> <P>The detoxifying effect of pyridoxine against acetaminophen (APAP)-induced hepatotoxicity was investigated. HepG2 cells were co-treated with APAP and pyridoxine to compare with betaine or methionine for 24 h. LDH, ALT and AST activities were measured to determine direct cells damage <I>in vitro</I> and in vivo. Lipid peroxidation, antioxidant enzymes activity, and glutathione level were measured. Cytochrome c releaseand procaspase-3, cleaved caspase-3, Bcl-2, or Bax protein levels were measured to determine APAP-induced apoptotic cell death. Pyridoxine treatment significantly increased cell viability and decreased leakage of LDH activity against APAP-induced hepatotoxicity in HepG2 cells. ALT and AST activities were dose-dependently reduced by pyridoxine treatment compared to APAP-treated group. Significant increases in activities of GST and GPx were observed after co-treatment with APAP and pyridoxine. Although APAP-induced Nrf2 and HO-1 expression levels were gradually reduced in HepG2 cells by pyridoxine treatment, induction of antioxidant enzymes activities were dose-dependently increased. These protected effects of pyridoxine against APAP-induced hepatoxicity were closely associated with suppression of APAP-induced oxidative stress and apoptotic cell death in HepG2 cells. These data indicated that the protective action of pyridoxine against hepatic cell injuries was involved in the direct antioxidant activity which provides a pivotal mechanism for its potential hepatoprotective action.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Pyridoxine decreased LDH, ALT and AST activities against APAP-induced hepatotoxicity <I>in vitro</I> and in vivo. </LI> <LI> Increases in antioxidant enzymes (GST and GPx) and GSH levels were observed after co-treatment with APAP and pyridoxine. </LI> <LI> Cytochrome c and procaspase-3, Bcl-2, or Bax protein levels were measured to determine APAP-induced apoptotic cell death. </LI> <LI> The protective action of pyridoxine against hepatic cell injuries was involved in the direct antioxidant activity. </LI> <LI> Pyridoxine showed protective activity via HO-1 induction serving as a key player in APAP-induced cell survival pathway. </LI> </UL> </P>

      • High-Dosage Pyridoxine-Induced Auditory Neuropathy and Protection with Coffee in Mice

        Hong, Bin Na,Yi, Tae Hoo,Kim, Sun Yeou,Kang, Tong Ho Pharmaceutical Society of Japan 2009 BIOLOGICAL & PHARMACEUTICAL BULLETIN Vol.32 No.4

        <P>Auditory neuropathy (AN) is a hearing disorder characterized by an abnormal auditory brainstem response (ABR). This study examined experimental AN model induced in mice following increased dosages of pyridoxine. Induced AN was examined for ≤10 weeks following the last pyridoxine treatment. To assess AN, we evaluated the ABR, auditory middle latency response (AMLR), otoacoustic emission (OAE), and histochemical morphology of the auditory nerve. Pyridoxine-treated mice exhibited an increase in the hearing threshold shift and delayed latency of both ABR and AMLR in proportion to pyridoxine dosage. Additionally, the extent of auditory nerve fiber loss increased in a dose-dependent manner following pyridoxine intoxication. Coffee or trigonelline treatment ameliorated the hearing threshold shift, delayed latency of the auditory evoked potential, and improved sensory fiber loss induced by pyridoxine intoxication. The present findings demonstrate that high-dose pyridoxine administration can be used to produce a new mouse model for AN, and coffee or trigonelline as a main active compound of coffee extract can potentially facilitate recovery from pyridoxine-induced auditory neuropathy.</P>

      • Tat-mediated Protein Transduction of Human Brain Pyridoxine-5-P Oxidase into PC12 Cells

        Kim, So-Young,An, Jae-Jin,Kim, Dae-Won,Choi, Soo-Hyun,Lee, Sun-Hwa,Hwang, Seok-Il,Kwon, Oh-Shin,Kang, Tae-Cheon,Won, Moo-Ho,Cho, Sung-Woo,Park, Jin-Seu,Eum, Won-Sik,Lee, Kil-Soo,Choi, Soo-Young Korean Society for Biochemistry and Molecular Biol 2006 Journal of biochemistry and molecular biology Vol.39 No.1

        Pyridoxine-5-P oxidase catalyses the terminal step in the biosynthesis of pyridoxal-S-P, the biologically active form of vitamin $B_6$ Which acts as an essential cofactor. Here, a human brain pyridoxine-5-P oxidase gene was fused with a gene fragment encoding the HIV-1 Tat protein transduction domain (RKKRRQRRR) in a bacterial expression vector to produce a genetic in-frame Tat-pyridoxine-5-P oxidase fusion protein. Expressed and purified Tat-pyridoxine-5-P oxidase fusion protein transduced efficiently into PC12 cells in a time- and dose-dependent manner when added exogenously to culture media. Once inside the cells, the transduced Tat-pyridoxine-5-P oxidase protein showed catalytic activity and was stable for 48 h. Moreover, the formation of pyridoxal-5-P was increased by adding exogenous Tat-pyridoxine-5-P oxidase to media pre-treated with the vitamin $B_6$ precursor pyridoxine. In addition, the intracellular concentration of pyridoxal-S-P was markedly increased when Tat-pyridoxal kinase was transduced together with Tat-pyridoxine-5-P oxidase into cells. These results suggest that the transduction of Tat-pyridoxine-5-P oxidase fusion protein presents a means of regulating the level of pyridoxal-5-P and of replenishing this enzyme in various neurological disorders related to vitamin $B_6$.

      • SCIESCOPUSKCI등재

        Effects of Pyridoxine on Growth Performance and Plasma Aminotransferases and Homocysteine of White Pekin Ducks

        Xie, Ming,Tang, Jing,Wen, Zhiguo,Huang, Wei,Hou, Shuisheng Asian Australasian Association of Animal Productio 2014 Animal Bioscience Vol.27 No.12

        A dose-response experiment with seven supplemental pyridoxine levels (0, 0.66, 1.32, 1.98, 2.64, 3.30, and 3.96 mg/kg) was conducted to investigate the effects of pyridoxine on growth performance and plasma aminotransferases and homocysteine of White Pekin ducks and to estimate pyridoxine requirement for these birds. A total of 336 one-day-old male White Pekin ducks were divided to 7 experimental treatments and each treatment contained 8 replicate pens with 6 birds per pen. Ducks were reared in raised wire-floor pens from hatch to 28 d of age. At 28 d of age, the weight gain, feed intake, feed/gain, and the aspartate aminotransferase, alanine aminotransferase, and homocysteine in plasma of ducks from each pen were all measured. In our study, the pyridoxine deficiency of ducks was characterized by growth depression, decreasing plasma aspartate aminotransferase activity and increasing plasma homocysteine. The ducks fed vitamin $B_6$-deficient basal diets had the worst weight gain and feed/gain among all birds and this growth depression was alleviated (p<0.05) when pyridoxine was supplemented to basal diets. On the other hand, plasma aspartate aminotransferase and homocysteine may be the sensitive indicators for vitamin $B_6$ status of ducks. The ducks fed basal diets had much lower aspartate aminotransferase activity and higher homocysteine level in plasma compared with other birds fed pyridoxine-supplemented diets (p<0.05). According to quadratic regression, the supplemental pyridoxine requirements of Pekin ducks from hatch to 28 days of age was 2.44 mg/kg for feed/gain and 2.08 mg/kg for plasma aspartate aminotransferase and the corresponding total requirements of this vitamin for these two criteria were 4.37 and 4.01 mg/kg when the pyridoxine concentration of basal diets was included, respectively. All data suggested that pyridoxine deficiency could cause growth retardation in ducks and the deficiency of this vitamin could be indicated by decreasing plasma aspartate aminotransferase activity and increasing plasma homocysteine.

      • Pyridoxine improves hippocampal cognitive function via increases of serotonin turnover and tyrosine hydroxylase, and its association with CB1 cannabinoid receptor-interacting protein and the CB1 cannabinoid receptor pathway

        Jung, H.Y.,Kim, D.W.,Nam, S.M.,Kim, J.W.,Chung, J.Y.,Won, M.H.,Seong, J.K.,Yoon, Y.S.,Yoo, D.Y.,Hwang, I.K. Elsevier/North-Holland 2017 Biochimica et biophysica acta, General subjects Vol.1861 No.12

        Background: In the present study, we investigated the effects of pyridoxine on hippocampal functions and changes in protein profiles based on the proteomic approach. Methods: Eight-week-old mice received intraperitoneal injections of physiological saline (vehicle) or 350mg/kg pyridoxine twice a day for 21days. Results: Phosphoglycerate mutase 1 was up-regulated, while CB1 cannabinoid receptor-interacting protein 1 (CRIP1) was down-regulated, in the pyridoxine-treated group. Additionally, the serotonin and tyrosine hydroxylase was increased in the hippocampus of the pyridoxine-treated group than in that of the vehicle-treated group. Furthermore, discrimination indices based on the novel object recognition test were significantly higher in the pyridoxine-treated group than in the vehicle-treated group. Administration of CRIP1a siRNA significantly increases the discrimination index as well as cell proliferation and neuroblast differentiation in the dentate gyrus. In addition, the administration of rimonabant, a CB1 cannabinoid receptor antagonist, for 3weeks significantly decreased the novel object recognition memory, the tyrosine hydroxylase level, the amount of cell proliferation, and neuroblast differentiation in the dentate gyrus. Treatment with pyridoxine significantly increased novel object recognition memory, but slightly ameliorated rimonabant-induced reduction in serotonin, the tyrosine hydroxylase level, the amount of cell proliferation, and neuroblast differentiation in the dentate gyrus. Conclusion: These results suggest that pyridoxine promotes hippocampal functions by increasing serotonin and tyrosine hydroylase immunoreactivity in the hippocampus. This positive effect may be associated with CRIP1a and CB1 cannabinoid receptor function. General significance: Vitamin-B<SUB>6</SUB> enhances hippocampal functions and this is closely associated with CRIP1a and CB1 cannabinoid receptors.

      • KCI등재

        Pyridoxine섭취가 발레무용수의 혈액성분, Osteocalcin 및 TC/HDL-C ratio에 미치는 영향

        신말연(Shin, Mal-Ryun),조정호(Cho, Jung-Ho) 한국체육과학회 2015 한국체육과학회지 Vol.24 No.3

        The purpose of this study was to determine the effect of pyridoxine supplementation with ballet exercise on cell blood components osteocalcin(Os), and total cholesterol/high density lipoprotein cholesterol ration(TC/HDL-C ratio) in female ballet dancers. 14 female ballet dancers were participated in 30days study for a double blind and subjects were randomly assigned to one of the three groups, i.e., Group I (n=4): placebo(2.4mg/day); group Ⅱ (n=5): pyridoxine(1.6mg/day); Group Ⅲ(n=5): pyridoxine(2.4mg/day) with ballet exercise 3-5 times per week. Study subjects measured white blood cells(WBC), red blood cells(RBC), hemoglobin(Hb), osteocalcin(Os), and total cholesterol/high density lipoprotein chloesterol ration(TC/HDL-C ratio), before and after the treatment. Analysis of Covariance (ANCOVA), Multiple Range Test(Scheffe), and anaysis of simple regression were used to determine the statistical significance. There were no group differences in the osteocalcin(Os), and total cholesterol/high density lipoprotein cholesterol ratio, and hemoglobin. but WBC and RBC were significantly changed(p〈.05). The result of this study does not lend support to the contention that pyridoxal phosphate intake has much practical impact on ballet exercise performance as a ergogenic acid. However, it does appear that several significant research topics in pyridoxine biochemistry metabolism as well as ballet exercise and nutrition can be explored profitably in the future using experimental designs involving interaction between pyridoxine status and exercise performance.

      • KCI등재

        Negligible Effect of Oral Garlic Oil on the Oral Absorption of Pyridoxine in Metadoxine in Rats

        Dae Young Lee,강희은,김상건,Myung Gull Lee 대한약학회 2010 Archives of Pharmacal Research Vol.33 No.7

        Metadoxine [an ion-pair between pyridoxine and pyrrolidone carboxylate (PCA)] plus garlic oil treatment synergistically reduces alcoholic steatosis compared to each agent alone. We evaluated the effect of garlic oil on the pharmacokinetics of pyridoxine. After the oral administration of metadoxine, the total area under the plasma concentration-time curve from time zero to time infinity (AUC) and the peak plasma concentration (Cmax) of pyridoxine were significantly greater (by 40.6%) and higher (by 63.9%), respectively, than after oral administration of pyridoxine plus PCA. Oral metadoxine plus garlic oil also gave larger AUC (31.8%) and higher Cmax (64.9%) than pyridoxine plus PCA. However, garlic oil did not change the AUC or Cmax of pyridoxine in metadoxine. Thus, garlic oil does not enhance the metadoxine activity by affecting the absorption of pyridoxine.

      • KCI등재

        Paper Microfluidics Based on rGO/Polyaniline Nanofibers for Sensing Pyridoxine

        Santhosh Mallesh,박두산 한국농업기계학회 2024 바이오시스템공학 Vol.49 No.1

        Purpose This study aims to develop a simple, low-cost, highly disposable paper-based electrochemical device to determine pyridoxine (vitamin B6). Methods Dual-layer paper-based electrochemical devices (PEDs) were fabricated using wax and screen-printing techniques. The electrochemical sensing layer towards pyridoxine detection is prepared by modifying the working electrode with reduced graphene oxide (rGO) and electrodeposited polyaniline (PANI) nanofi bers. Optimization of electrodeposition time was carried out to uniformly coat PANI nanofi bers over rGO-modifi ed PEDs. Surface morphologies of modifi ed electrodes were examined by fi eld emission scanning electron microscopy (FESEM), and PEDs were electrochemically characterized by cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS). Chronoamperometric responses of the modifi ed electrode against pyridoxine were utilized for its quantifi cation. Results Morphological characterization of the modifi ed FESEM indicates PANI’s porous and nanofi ber network over rGO. The electrochemical characterization of the PEDs with CV and EIS reveals that the synergetic combination of PANI and rGO nanostructure possesses excellent electrochemical performance and enhanced electrocatalytic activity towards the oxidation of pyridoxine. The chronoamperometric (CA) responses of the PANI-rGO/PEDs towards pyridoxine showed a broader linear range from 5 to 1100 μM ( R 2 = 0.97) and showed a lower detection limit of 1.43 μM at 0.50 V vs. pseudo-Ag/AgCl. Conclusion The proposed multi-layer PEDs modifi ed with a uniformly formed nanofi ber network of PANI-rGO nanocomposite have the potential to be applied in developing a sensitive sensor for monitoring pyridoxine in a low-cost and disposable way. They are appropriate to be utilized in resource-limited settings.

      • KCI등재

        Postprandial anti-hyperglycemic effect of vitamin B6 (pyridoxine) administration in healthy individuals

        김혁화,강유리,최황용,이정윤,오정배,Justin S. Kim,Young-Cheul Kim,이기원,권영인 한국식품과학회 2019 Food Science and Biotechnology Vol.28 No.3

        Postprandial blood glucose lowering effect ofvitamin B6 (pyridoxine) was evaluated in healthy individualswith normal blood glucose levels. Blood glucoselevels were measured every 30 min for 2 h after oral sugaradministration with or without 50 mg of pyridoxine. Pyridoxinesignificantly lowered the postprandial blood glucoselevels at 30 min (from 165.95 ± 17.19 to 138.36 ± 20.43,p\0.01) and 60 min (from 131.40 ± 17.20 to118.50 ± 15.95) after administration. In addition, the areaunder the concentration–time curve (AUCt) was reducedby about 8.3% (from 257.08 ± 22.38 to 235.71 ± 12.33,p\0.05) and the maximum concentration of blood glucose(Cmax) was reduced by about 13.8% (from165.95 ± 17.19 to 143.07 ± 11.34, p\0.01) when comparedwith those of the control group. Our findings suggestthat pyridoxine supplementation may be beneficial forcontrolling postprandial hyperglycemia.

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