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1رسالة جامعية
المؤلفون: 楊振澤, YANG, CHENG-TSE
المساهمون: 醫學科學研究所碩士班, 呂思潔
الوصف: 碩士 ; 指導教授:呂思潔 ; 委員:呂思潔 ; 委員:楊明達 ; 委員:黃文經 ; 目的：探討四週維生素D3增補對於激烈耐力運動誘發氧化傷害與肌肉損傷之影響。方法：本研究以28名健康男性先於功率腳踏車上進行第一次漸增強度測試至力竭，以測量其最大攝氧量 (V?O2max)，並給予實驗參與者連續四週、每日增補5,000 IU的維生素D3或安慰劑；之後進行第二次漸增強度測試至力竭，以作為兩天後65% V?O2max的激烈耐力運動強度。於四週增補前、後抽血採集靜脈血以測量血清25(OH)D濃度，並於激烈耐力運動前 (Pre)、運動後立即 (Post-0)、運動後2小時 (Post-2)、運動後4小時 (Post-4)、運動後24小時 (Post-24) 採集血液樣本以測量氧化傷害指標 (硫代巴比妥酸反應物質與蛋白質羰基)、抗氧化系統活性 (超氧化離子歧化?、麩胱甘?過氧化?與過氧化氫?) 與肌肉損傷指標 (肌酸激?與乳酸脫氫?)。結果：在四週增補後，維生素D3組之血液維生素D濃度顯著高於增補前與安慰劑組 (p < .05)，且安慰劑組之蛋白質羰基、超氧化離子歧化?與肌酸激?於Post-0、Post-2與Post-24皆顯著高於維生素D3組 (p < .05)，而安慰劑組之硫代巴比妥酸反應物質與乳酸脫氫?於Post-24顯著高於維生素D3組 (p < .05)。另外，安慰劑組之過氧化氫?於Post-0顯著高於維生素D3組 (p < .05)。結論：四週維生素D3增補能夠有效改善激烈耐力運動誘發氧化傷害與肌肉損傷。 ; Purpose: To investigate the effects of vitamin D3 supplementation on strenuous endurance exercise (SEE)-induced oxidative stress and muscle damage. Methods: Twenty-eight male subjects conducted a graded exercise test (GXT) on a cycle ergometer to exhaustion to assess their first maximal oxygen uptake (V?O2max). The participants were instructed to take either a daily dose of 5,000 IU of vitamin D3 or a placebo for a duration of four weeks. After four weeks, all participants completed the second GXT to exhaustion. The V?O2max were used to calculate the intensity of 65% V?O2max for the following SEE. Blood samples were collected before and after four weeks supplementation to determine the concentration of serum 25(OH)D. Additionally, venous blood samples were collected at multiple time points: before SEE (Pre), immediately after (Post-0), 2 hours after (Post-2), 4 hours after (Post-4), and 24 hours after (Post-24). These samples were analyzed to assess markers of oxidative damage (thiobarbituric acid reactive substances (TBARS) and protein carbonyls (PC)), antioxidant system activity (superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT)), as well as muscle damage biomarkers (creatine kinase (CK) and lactate dehydrogenase (LDH)). Results: After four-week supplementation, the serum concentration of 25(OH)D in vitamin D3 group ...
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العلاقة: http://libir.tmu.edu.tw/handle/987654321/63330Test; http://libir.tmu.edu.tw/bitstream/987654321/63330/1/index.htmlTest
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2رسالة جامعية
المؤلفون: 陳聖崴, CHEN, SHENG-WEI
المساهمون: 醫學科學研究所碩士班, 呂思潔
مصطلحات موضوعية: 穀胱甘?過氧化物?, 超氧化物歧化?, 過氧化氫?, 肌酸激?, 乳酸脫氫?, glutathione peroxidase, superoxide dismutase, catalase, creatine kinase, lactate dehydrogenase
الوصف: 碩士 ; 指導教授:呂思潔 ; 委員:黃文經 ; 委員:楊明達 ; 目的：本研究旨在探討瑪卡萃取物增補對力竭性耐力運動後氧化壓力、肌肉損傷及運動表現的影響。方法：本研究將20位實驗參與者以最大攝氧量成績配對分成實驗組 (n=9) 及安慰劑組 (n=11)，並給予實驗參與者連續12週、每日早、晚各2250 mg的瑪卡萃取物或安慰劑增補，之後以70% 最大攝氧量的強度進行60分鐘的力竭性耐力運動後，再以90% 最大攝氧量的強度跑至力竭。運動測試期間紀錄運動至力竭時間、平均心跳率、最大心跳率及攝氧量峰值，並於力竭性耐力運動前、運動後立即、運動後2小時、運動後4小時與運動後24小時進行採血以分析氧化傷害指標 (硫化巴比妥酸反應物)、抗氧化系統活性 (穀胱甘?過氧化物?、超氧化物歧化?及過氧化氫?) 及肌肉損傷指標 (肌酸激?及乳酸脫氫?)。結果：增補前二組間各項數值均無顯著差異，而增補後全體實驗參與者在力竭性耐力運動後立即的穀胱甘?過氧化物?、超氧化物歧化?、過氧化氫?的活性、肌酸激?及乳酸脫氫?的濃度皆顯著高於運動前，但硫化巴比妥酸反應物濃度並無顯著差異，且二組在各時間點間的所有依變項皆無顯著差異。結論：本研究證實60分鐘的力竭性耐力運動會誘發肌肉損傷，但能在人體本身的抗氧化系統保護下避免氧化壓力上升，不過補充瑪卡萃取物並無額外增補效益。 ; Purpose: To evaluate the effects of Maca extract supplementation on the oxidative stress, muscle damage, and exercise performance after exhaustive endurance exercise. Methods: Twenty participants were divided into Maca extract group (n=9) or placebo group (n=11) based on the maximal oxygen consumption and were asked to consume Maca extract or placebo (2250 mg twice per day). After 12 weeks of supplementation, all participants completed exhaustive endurance exercise on a treadmill at the intensity of 70% maximal oxygen consumption for 60 minutes, after which intensity was increased to 90% maximal oxygen consumption until exhaustion. The time to exhaustion, average heart rate, maximum heart rate, and the peak of oxygen consumption were recorded during exhaustive endurance exercise. Venous blood samples were drawn before, immediately after, 2-hour after, 4-hour after, and 24-hour after exhaustive endurance exercise to determine the biomarkers of oxidative stress (thiobarbituric acid reactive substances), antioxidant system activity (glutathione peroxidase, superoxide dismutase and catalase), and biomarkers of muscle damage (creatine kinase and lactate dehydrogenase). Results: There were no significant differences in all variables between the two groups before the supplement. After supplementation, the concentrations of glutathione peroxidase, superoxide dismutase, catalase, creatine kinase, and lactate dehydrogenase in all participants at ...
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العلاقة: http://libir.tmu.edu.tw/handle/987654321/63318Test; http://libir.tmu.edu.tw/bitstream/987654321/63318/1/index.htmlTest
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3دورية أكاديمية
المساهمون: 運教所
مصطلحات موضوعية: 固定式腳踏車, 肌酸激酶, 乳酸脫氫酶, Cycle ergometer, Creatine kinase, Lactate dehydrogenase
الوصف: Purpose: The purpose of this study was to examine the effect of branched-chain amino acid (BCAA) supplementation on indices of muscle damage. Methods: Eight healthy active college students participated in a double-blinded crossover study. The subjects ingested either 92 mg/kg BW of BCAA (BCAA) or placebo (PLA) capsules 60 min before exercise respectively. They exercised at 60% VO(subscript 2max) on cycle ergometer for 30 minutes. Blood samples were collected prior to supplementation, immediately prior to exercise, and 0, 15, 60 min after cycling (P0, P15, P60) for analysis of creatine kinase (CK) and lactate dehydrogenase (LDH). The data were analyzed by two-way repeated measures ANOVA and significance was accepted at α=.05. Results: No interactions between treatment and timing were found. Significant main effect was found for treatment and timing on CK and for the main effect of treatment, BCAA's response of CK were significantly lower than PLA (BCAA: 167.30±90.55 U/L; PLA: 200.17±117.46 U/L, p＜.05). Significant main effect was found for timing on LDH. Conclusions: These results indicate that supplementary BCAA 60 min before cycling decreased serum concentrations of the intramuscular enzymes CK after moderate cycling exercise. The effects of BCAA supplementation are suggested to reduce the risk of muscle damage.
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العلاقة: 運動生理暨體能學報 11 2010.12[民99.12] 頁57-67; http://ir.lib.pccu.edu.tw//handle/987654321/40814Test; http://ir.lib.pccu.edu.tw/bitstream/987654321/40814/2/index.htmlTest
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4دورية أكاديمية
المساهمون: 體育系
الوصف: 目的：高強度衰竭運動後代謝性指標恢復速率研究。方法：以15位年滿20歲的大專男性運動選手為受試對象，利用跑步機以80%VO2max的強度跑至衰竭為止，並分別於運動前、衰竭運動後立即、0.5、1、2、24及48小時進行肘窩靜脈採血分析衰竭運動前後不同時間點的BUN、CK及LDH等代謝性指標變化，所得數據以重複量數單因子變異數分析(one-way ANOVA)進行資料處理。結果：BUN、CK、LDH等代謝性指標於衰竭運動後都明顯增加(P>.05)，其中BUN與LDH於運動後2小時達到最高點，於24小時恢復；CK於運動後24小時達到最高點，於48小時恢復。結論：高強度衰竭運動對BUN及LDH影響時間較短，可在24小時內恢復；對CK的影響會持續至24小時以後，於48小時內恢復，因此在實施高強度的衰竭運動時，至少應有一天的間隔時間以利代謝機能恢復。 Purpose: To investigate the recovery rate of metabolic indicators after high-intensity exhaustive exercise. Method: Subjects performed exercise to exhaustion on a motorized treadmill following the Ellestard protocol to determine the maximal aerobic power (VO2max). The speeds for 80% exhausted running was calculated for each subjects as the suggestion of CSM: VO2=(0.2×speed)+(0.9×speed×grade)+3.5. Five milliliters of blood samples were intravenously collected from the subjects before and after the exhaustive exercise. The sampling times were 0, 0.5, 1, 2, 24, 48 hours after the exhaustive exercise, respectively. Analysis: Concentrations of blood urea nitrogen (BUN), creatine kinase (CK), and lactate dehydrogenase (LDH), respectively, were determined as the biomarkers of human metabolism. The data were analyzed by the one-way analysis of variance (ANOVA). Results: It was shown that the concentrations of metabolic indicators BUN, CK, and LDH all increased significantly after the exhaustive exercise (P>.05). Concentrations of both BUN and LDH rose to a maximum 2 hours after the exercise and subsequently gradually recovered till 24 hours after the exercise. Concentration of CK increased with the time, to a maximum at about 24 hours, after the exercise, thereafter decreased with the time till 48 hours after the exercise. Conclusion: High-intensity exhaustive exercise affected the concentrations of metabolic indicators BUN, CK, and LDH, especially for CK till 24 hours after the exercise. It was suggested that the exhaustive exercise should be performed accompanying with a time period, i.e., 24 hours, enough for the recovery of metabolic ...
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العلاقة: 文化體育學刊 (10期) ：p9 -17; http://ir.lib.pccu.edu.tw//handle/987654321/23026Test; http://ir.lib.pccu.edu.tw/bitstream/987654321/23026/2/index.htmlTest
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5دورية أكاديمية
وصف الملف: application/
العلاقة: 屏東教大運動科學學刊第4期; http://140.127.82.166/handle/987654321/1032Test; http://140.127.82.166/bitstream/987654321/1032/1Test/單次無氧運動25-36.pdf
الإتاحة: http://140.127.82.166/handle/987654321/1032Test
http://140.127.82.166/bitstream/987654321/1032/1Test/單次無氧運動25-36.pdf -
6دورية أكاديمية
المؤلفون: 李杰龍, Lee, Jay-Ron
المساهمون: 黃鵬鵬, 臺灣大學：漁業科學研究所
مصطلحات موضوعية: 能量代謝, 乳酸脫氫酶, 鰓, lactate dehydrogenase, energy metabolism, gill
الوصف: 當廣鹽性魚類面對環境鹽度改變時，魚類鰓上皮細胞許多位於富含粒線體細胞 (mitochondria-rich cell, MR cell)的離子通道就必須及時運作以維持魚體內的滲透壓恆定，由於大多數的離子通道都是需要耗能的主動運輸，故鰓是個需要大量能量的器官。而魚類鰓上皮細胞中究竟是以何種物質作為能量的來源，而其又是如何在細胞間運輸的機制至今尚未清楚。相對於哺乳動物中，中樞神經系統需要充足的能量並以肝醣作為細胞內主要能量儲存形式，下游的能量運輸分子則是以乳酸為主而並非是葡萄糖。而星狀細胞(astrocyte)會儲存大量的乳酸再藉由單羧基運輸蛋白(monocarboxylate transpoter, MCT)提供給神經細胞作為能量來源。其中，乳酸脫氫酶(lactate dehydrogenase, LDH)對於乳酸的生成扮演一重要的角色。 本實驗利用莫三比克吳郭魚進行相關研究。首先利用同功異構酶澱粉凝膠電泳觀察乳酸脫氫酶不同的同功異構酶在吳郭魚鰓上皮細胞的表現情形。結果觀察到在鰓上皮細胞以乳酸脫氫酶1(LDH1)的表現為主。進一步利用LDH1、LDH5、glycogen synthase、glycogen、Na+-K+ ATPase α次單元抗體進行免疫細胞螢光染色發現到LDH1以及LDH5分別在 MR cells和富含肝醣細胞(glycogen-rich cell, GR cell)都有分布。之後利用西方墨點法分析吳郭魚在適應不同環境鹽度時LDH1、LDH5以及檸檬酸合成酶(citrate synthase, CS)蛋白質的表現量，發現到LDH1和 CS的蛋白質表現量在轉移海水後1st h都有顯著的增加，而LDH5的蛋白質表現量則是在轉移海水後的1-3rd h 之中都有顯著的增加。藉由上述結果，我們認為在魚類適應不同鹽度過程中，其鰓上皮細胞能量代謝的機制如下：當魚類轉移到海水後1st h時，其鰓上的MR cells會進入檸檬酸循環(TCA cycle)以產生大量的能量給MR cells。而在轉移到海水3rd h時，MR cells則是進行無氧呼吸為主以繼續產生大量的能量給予離子通道進行滲透壓調節。 ; Upon a salinity challenge, euryhaline teleosts immediately regulate the functions of many ion transporters and enzymes in the gill mitochondria-rich (MR) cells for maintaining their internal homeostasis. Large amount of energy is necessary for the operations of these transporters and enzymes, however the mechanism of energy metabolism in fish gills is still unclear. On the other hand, in mammalian central nervous system lactates, instead of glucose, are the main energy substrate transported from astrocyte to neuron via monocarboxylate transporter (MCT). Lactate dehydrogenase 1 (LDH1) is the key enzyme to convert the lactate to pyruvate, and LDH5 is responsible for the reverse reaction. In the present study, we used tilapia (Oreochromis mossambicus) as a model animal to investigate the roles of LDHs in the energy metabolism of fish gills during acclimation to seawater (SW). Results of starch gel electrophoresis and western blot demonstrated that LDH1 is the major form and LDH5 the minor form expressed in tilapia gill epithelial cells. Immunocytochemical experiments indicated that both LDH1 and LDH5 were expressed ...
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Time-course changes in the expression of Na, K-ATPase and the morphometry of mitochondrion-rich cells in gills of euryhaline tilapia (Oreochromis mossambicus) during freshwater acclimation. J Exp Zoolog A Comp Exp Biol 301, 85-96. Lin, L. Y., and Hwang, P. P. (2001). Modification of morphology and function of integument mitochondria-rich cells in tilapia larvae (Oreochromis mossambicus) acclimated to ambient chloride levels. Physiol Biochem Zool 74, 469-76. Lou, F., van Der Laarse, W. J., Curtin, N. A., and Woledge, R. C. (2000). Heat production and oxygen consumption during metabolic recovery of white muscle fibres from the dogfish Scyliorhinus canicula. J Exp Biol 203, 1201-10. Maekawa, M., Inomata, M., Sasaki, M. S., Kaneko, A., Ushiama, M., Sugano, K., Takayama, J., and Kanno, T. (2002). Electrophoretic variant of a lactate dehydrogenase isoenzyme and selective promoter methylation of the LDHA gene in a human retinoblastoma cell line. Clin Chem 48, 1938-45. Magistretti, P. J., Sorg, O., Yu, N., Martin, J. L., and Pellerin, L. (1993). Neurotransmitters regulate energy metabolism in astrocytes: implications for the metabolic trafficking between neural cells. Dev Neurosci 15, 306-12. Mannen, H., Tsoi, S. C., Krushkal, J. S., Li, W. H., and Li, S. S. (1997). The cDNA cloning and molecular evolution of reptile and pigeon lactate dehydrogenase isozymes. Mol Biol Evol 14, 1081-7. Markert, C. L. (1984). Lactate dehydrogenase. Biochemistry and function of lactate dehydrogenase. Cell Biochem Funct 2, 131-4. Marshall, W. S. (2002). Na(+), Cl(-), Ca(2+) and Zn(2+) transport by fish gills: retrospective review and prospective synthesis. J Exp Zool 293, 264-83. Marshall, W. S., Emberley, T. R., Singer, T. D., Bryson, S. E., and McCormick, S. D. (1999). Time course of salinity adaptation in a strongly euryhaline estuarine teleost, fundulus heteroclitus: a multivariable approach. J Exp Biol 202 (Pt 11), 1535-44. McIlwain, H. (1953). The effect of depressants on the metabolism of stimulated cerebral tissues. Biochem J 53, 403-12. McKenna, M. C., Tildon, J. T., Stevenson, J. H., Boatright, R., and Huang, S. (1993). Regulation of energy metabolism in synaptic terminals and cultured rat brain astrocytes: differences revealed using aminooxyacetate. Dev Neurosci 15, 320-9. Medina, J. M., and Tabernero, A. (2005). Lactate utilization by brain cells and its role in CNS development. J Neurosci Res 79, 2-10. Mehrani, H., and Storey, K. B. (1993). Control of glycogenolysis and effects of exercise on phosphorylase kinase and cAMP-dependent protein kinase in rainbow trout organs. Biochem Cell Biol 71, 501-6. Morgan, J. A., Cranwell, P. A., and Pickup, R. W. (1991). Survival of Aeromonas salmonicida in lake water. Appl Environ Microbiol 57, 1777-82. Nakano, K., Tagawa, M., Takemura, A., and Hirano, T. (1998). Temporal changes in liver carbohydrate metabolism associated with seawater transfer in Oreochromis mossambicus. 119, 721-728. Oliveira, G. T., Rossi, I. C., Kucharski, L. C., and Da Silva, R. S. (2004). Hepatopancreas gluconeogenesis and glycogen content during fasting in crabs previously maintained on a high-protein or carbohydrate-rich diet. Comp Biochem Physiol A Mol Integr Physiol 137, 383-90. Ozcan, S., Dover, J., and Johnston, M. (1998). Glucose sensing and signaling by two glucose receptors in the yeast Saccharomyces cerevisiae. Embo J 17, 2566-73. Parker, G., Taylor, R., Jones, D., and McClain, D. (2004). Hyperglycemia and inhibition of glycogen synthase in streptozotocin-treated mice: role of O-linked N-acetylglucosamine. J Biol Chem 279, 20636-42. Pederson, B. A., Cheng, C., Wilson, W. A., and Roach, P. J. (2000). Regulation of glycogen synthase. Identification of residues involved in regulation by the allosteric ligand glucose-6-P and by phosphorylation. J Biol Chem 275, 27753-61. Pellerin, L. (2003). Lactate as a pivotal element in neuron-glia metabolic cooperation. Neurochem Int 43, 331-8. Pellerin, L., and Magistretti, P. J. (2003). How to balance the brain energy budget while spending glucose differently. J Physiol 546, 325. Pellerin, L., Pellegri, G., Martin, J. L., and Magistretti, P. J. (1998). Expression of monocarboxylate transporter mRNAs in mouse brain: support for a distinct role of lactate as an energy substrate for the neonatal vs. adult brain. Proc Natl Acad Sci U S A 95, 3990-5. Perry, S. F. (1997). The chloride cell: structure and function in the gills of freshwater fishes. Annu Rev Physiol 59, 325-47. Perry, S. F., and Walsh, P. J. (1989). Metabolism of isolated fish gill cells: contribution of epithelial chloride cells. J Exp Biol 144, 507-20. Richards, J. G., Heigenhauser, G. J., and Wood, C. M. (2002). Glycogen phosphorylase and pyruvate dehydrogenase transformation in white muscle of trout during high-intensity exercise. Am J Physiol Regul Integr Comp Physiol 282, R828-36. Roche, T. E., and Reed, L. J. (1974). Monovalent cation requirement for ADP inhibition of pyruvate dehydrogenase kinase. Biochem Biophys Res Commun 59, 1341-8. Sangiao-Alvarellos, S., Laiz-Carrion, R., Guzman, J. M., Martin del Rio, M. P., Miguez, J. M., Mancera, J. M., and Soengas, J. L. (2003). Acclimation of S aurata to various salinities alters energy metabolism of osmoregulatory and nonosmoregulatory organs. Am J Physiol Regul Integr Comp Physiol 285, R897-907. Shambaugh, G. E., 3rd, Koehler, R. A., and Freinkel, N. (1977). Fetal fuels II: contributions of selected carbon fuels to oxidative metabolism in rat conceptus. Am J Physiol 233, E457-61. Shaw, C. R., and Barto, E. (1963). Genetic Evidence for the Subunit Structure of Lactate Dehydrogenase Isozymes. Proc Natl Acad Sci U S A 50, 211-4. Skurat, A. V., Dietrich, A. D., and Roach, P. J. (2000). Glycogen synthase sensitivity to insulin and glucose-6-phosphate is mediated by both NH2- and COOH-terminal phosphorylation sites. Diabetes 49, 1096-100. Skurat, A. V., and Roach, P. J. (1995). Phosphorylation of sites 3a and 3b (Ser640 and Ser644) in the control of rabbit muscle glycogen synthase. J Biol Chem 270, 12491-7. Steffensen, J. F. (2002). Metabolic cold adaptation of polar fish based on measurements of aerobic oxygen consumption: fact or artefact? Artefact! Comp Biochem Physiol A Mol Integr Physiol 132, 789-95. Tabernero, A., Vicario, C., and Medina, J. M. (1996). Lactate spares glucose as a metabolic fuel in neurons and astrocytes from primary culture. Neurosci Res 26, 369-76. Tseng, Y. C., (2004). Role of glycogen phosphorylase in energy supplying for osmoregulation in gills of tilapia (Oreochromis mossambicus). Master thesis. Institute of Fisheries Science, National Taiwan University. Vicario, C., and Medina, J. M. (1992). Metabolism of lactate in the rat brain during the early neonatal period. J Neurochem 59, 32-40. Walz, W., and Mukerji, S. (1988a). Lactate production and release in cultured astrocytes. Neurosci Lett 86, 296-300. Walz, W., and Mukerji, S. (1988b). Lactate release from cultured astrocytes and neurons: a comparison. Glia 1, 366-70. Wilson, J. M., and Laurent, P. (2002). Fish gill morphology: inside out. J Exp Zool 293, 192-213. Yuan, M., Shao, H., Geng, Z., Liu, J., and Deng, A. (1998). Regulating function of enzymization and deenzymization of the lactate dehydrogenase isozymes in the mouse tissues during hypoxia. Zhongguo Yi Xue Ke Xue Yuan Xue Bao 20, 449-53.; zh-TW; http://ntur.lib.ntu.edu.tw/handle/246246/59349Test; http://ntur.lib.ntu.edu.tw/bitstream/246246/59349/1/ntu-95-R93b45011-1.pdfTest
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7دورية أكاديمية
المساهمون: 體育學系
مصطلحات موضوعية: 24小時超級馬拉松, 肝膽功能, 膽紅素, 肝臟酵素, 乳酸脫氫酶, 24 hours ultramarathon, Liver function, BIL, GOT, GPT, LDH
الوصف: The purpose of this study was to investigate the effects of a 24 hours ultramarathon race on the runner's liver function. Eleven participants' (average age 45.1±8.77 yr, height 166.8±6.23cm, weight 60.6±6.96kg) blood samples were obtained before, at the end, after 48 hours, and 9 days after the 2002 International 24h Race IAU Asia 24-Hour Championship for standard blood biochemical test. The results showed that at the end of race, runners' total-bilirubin (BIL-T) and direct-bilirubin (BIL-D) increased significantly (p＜.05), alkaline (ALP), GOT, GPT, LDH significantly increased 1.2, 14.5, 3.4, 3.8 folds respectively, total protein (TP), ALB, GLO, γ-GT did not change significantly. Forty-eight hours after the race, GOT, GPT, LDH were a little decreased but still 7.3, 3.6, 3.1 times higher than the original level. TP, ALB and GLO were decreased significantly, BIL-T, BIL-D, and ALP recovered to the original level before the race. Nine days after the race, most of the functional indexes recovered to standard levels, but the TP and ALB were still significantly lower than the original level. Working amounts were positively related to liver damage level. According to the results we concluded that after 24 hours ultramarathon race, runners' increasing liver enzyme level revealed the damage of liver cells, but the increasing BIL should be due to the higher removal rate of declined red blood cells and not due to the mean blockage of bile duct. More working amount induced more damage to the liver, but it could recover after approximately 9 days.
وصف الملف: 155 bytes; text/html
العلاقة: 大專體育學刊 6:1 民93.02 頁275-283; http://ir.lib.pccu.edu.tw//handle/987654321/40632Test; http://ir.lib.pccu.edu.tw/bitstream/987654321/40632/2/index.htmlTest
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8دورية أكاديمية
مصطلحات موضوعية: 紫草萘醌類化合物, 共價修飾作用, 乳酸脫氫酶, 乙醇脫氫酶, alkannin derivatives, covalent modification, LDHase, ADHase
الوصف: 為研究紫草萘醌類化合物的細胞毒性作用機制 ,從新疆軟紫草根中分離出四種紫草萘醌類化合物 β ,β 二甲基丙烯酰阿卡寧 (1) ,乙酰阿卡寧 (2 ) ,β 乙酰氧基異戊酰阿卡寧 (3)和阿卡寧 (4)。研究了四種天然紫草萘醌類化合物對乳酸脫氫酶和乙醇脫氫酶的共價修飾作用。酶活力測定結果表明 ,這四種紫草萘醌類化合物對兩種脫氫酶都具有不同程度的抑制作用 ;酶分子中游離氨基和巰基修飾率的測定結果表明 ,紫草萘醌類化合物對兩種酶的抑制作用主要是通過與酶分子中的巰基共價結合產生的。 Covalent modification of four isolated alkannin derivatives ( alkannin, acetylalkannin, β, β-dimethylacrylalkannin and β-acetoxyisovalerylalkannin, respectively) on rabbit muscle latate dehydrogenase ( LDHase) and yeast Alcohol Dehydrogenase ( ADHase) has been studied .The quinone concentration curves show that the two enzymes are inhibited to different extents by the four alkannin derivatives .Assays of free amino groups and thiol groups in the enzymes indicate that the catalytic activities of LDHase and ADHase are mainly inhibited by covalent reaction of alkannin derivatives with thiol groups in enzymes .These results could be useful for investigating the biological mechanism of alkannin derivatives′cytotoxicity .
العلاقة: http://repository.ust.hk/ir/Record/1783.1-107462Test; 有機化學=Chinese Journal of Organic Chemistry, v. 21, (9), 2001, p. 668-671
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9
المساهمون: 國立臺灣師範大學人類發展與家庭學系
مصطلحات موضوعية: 馬拉松, 不同年齡, 乳酸脫氫酶, 肌酸激酶, 飯前血糖, 乳酸, marathon, age, lactate dehydrogenase, creatine kinase, glucose, lactate
الوصف: 本研究主要目的是瞭解完成馬拉松賽前及賽後生化值之變化；以及不同年齡層完成馬拉松賽生化值之比較。本研究以參加2001年台北市國際馬拉松賽(42.195 km)選手中，自願參與本研究者為實驗對象，共計30人，最後跑完全程者有26人，依年齡分為青年（20-39歲）、壯年（40-49歲）及中老年（50-70歲）三組。於比賽前12小時及比賽後立即抽血，以t考驗比較受試者在馬拉松比賽前後的乳酸脫氫酶、肌酸激酶、飯前血糖及乳酸等四種血液生化值。結果發現全體受試者完成馬拉松後的生化值均顯著高於跑步前(P<.05)，其完成馬拉松的生化值分別為，乳酸脫氫酶(239.46±34.42 U/L)、肌酸激酶(307.65±141.07 U/L)、飯前血糖(113.46±28.76 mg/dL)及乳酸(3.52±1.53 mmol/L)；跑步前的生化值分別為，乳酸脫氫酶(177.96±0.35 U/L)、肌酸激酶(184.4±120.78 U/L)、飯前血糖(100.08±12.02 mg/dL))及乳酸(1.25±0.50 mmol/L)。以單因子變異數分析不同年齡層完成馬拉松的生化值之比較，僅在乳酸脫氫酶差異達顯著水準(P<.05) ，經進一步事後比較，僅有青年組(263.5±33.0 U/L)與壯年組(225.7±32.78 U/L)間有所差異。因此，本研究獲得下列結論：(l)從事長時問的耐力性運動會造成肌酸激酶、乳酸脫氫酶、飯前血糖及乳酸值的上升；(2)參與馬拉松運動容易對身體組織造成某種程度的傷害，而這些損傷程度並不因年齡不同而有所差異。 ; The purpose of the study was to investigate the effect of prolonged endurance exercise on the biomarkers of marathon runner as well as the effect of age on the plasma biomarkers of marathon runner. Thirty athletes of the 2001 Taipei International Marathon volunteered to participate in the study, and 26 finished the race (42.195 km). Based on the age, 26 participates were divided into three groups: Young (20-39), Adult (40-49), and Senior (50-70). Blood samples were taken 12 hours before and immediately after the race, and then analyzed for lactate dehydrogenase (LDH), creatine kinase (CK), glucose, and lactate. After the race, all the biomarkers measured were significantly increased (P<.05). The concentrations of each biomarker measured after the race were: LDH (239.46�34.42 U/L), CK (307.65�141.07 U/L), glucose (113.46�28.76 mg/dL), and lactate (3.52�1.53 mmol/L), whereas those measured before the race were: LDH (177.96�30.35 UIL), CK (184.46�120.78 U/L), glucose (100.08�12.02 mg/dL), and lactate (1.25�0.50 mmol/L). After one-way ANOVA, the significant difference (P<.05) was found in the concentration of LDH between Young (263.5�33.0 U/L) and Adult (225.7�32.8 U/L) groups only. In conclusion, prolonged endurance exercise would significantly increase the concentrations of LDH, CK, glucose, and lactate. Tissue damage could be induced by a ...
وصف الملف: application/pdf
العلاقة: 大專體育學刊，4(2)，157-164; ntnulib_tp_A0303_01_008; http://rportal.lib.ntnu.edu.tw/handle/20.500.12235/41189Test
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10رسالة جامعية
المؤلفون: 張皓竣, Chang, Hao-Chun
المساهمون: 生物化學暨分子生物學研究所, 張文粲, Chang, Wen-Tsan
مصطلحات موضوعية: 瓦氏效應, 乳酸脫氫?乙型, 惡性轉型, 白藜蘆醇, 六碳醣磷酸?甲型, Warburg effect, lactate dehydrogenase B, malignant tranformation, resveratrol, hexokinase I
الوصف: 惡性的腫瘤細胞會將其生長代謝的方式由傳統的檸檬酸循環 (TCA cycle)，轉變成較快速的糖解作用 (Glycolysis) 來獲取能量；這個現象稱為瓦氏效應 (Warburg effect)。過去研究指出代謝酵素的表現異常、有氧呼吸電子傳遞鏈的缺失、缺氧、酸性的微環境，都會使腫瘤細胞能量代謝轉移到糖解作用變得更惡性。乳酸脫氫? (Lactate dehydrogenase) 的主要?能為丙酮酸 (Pyruvate) 與乳酸 (Lactate) 之間的轉換，這個反應會伴隨著菸鹼醯胺腺嘌呤 (NADH) 的氧化與還原，進而去調控細胞能量代謝與抑癌基因p53的表現。乳酸脫氫?是由兩種基因乳酸脫氫?甲型與乙型 (LDHA LDHB) 轉譯出五種不同的異構物。乳酸脫氫?甲型常在腫瘤細胞中被大量表現，被認為與維持腫瘤細胞生長有關係；乳酸脫氫?乙型在近幾年研究指出在腫瘤細胞中會有默化的現象，但詳細的機制則不清楚。為了解乳酸脫氫?乙型在腫瘤細胞中扮演的角色、以及對其能量代謝的影響，本研究在子宮頸癌HeLa細胞株中穩定抑制乳酸脫氫?乙型的表現。由實驗結果可發現，缺失乳酸脫氫?乙型表現的細胞株不論增生或爬行的能力都獲得了提高。在表現變得更惡性得同時，我透過西方墨點法 (Western blot) 分析發現，該細胞株檸檬酸循環與電子傳遞鏈 (OHPHOS) 的酵素表現量皆有異常。經由流式細胞儀分析也可發現氧化代謝物 (ROS) 及H2O2的產生減少且粒線體膜電位 (Membrane potential) 大幅降低。暗示著這株細胞株能量代謝偏向利用糖解作用來獲得能量；限制細胞培養基裡的葡萄糖濃度 (Glucose deprivation)，也可以發現喪失乳酸脫氫?乙型表現的細胞株對此改變較為敏感，而大量走向細胞凋亡 (Apoptosis)。為了更進一步了解乳酸脫氫?乙型是透過什麼作用機制導致腫瘤細胞的癌化，我利用了各種不同的化癌藥物 (2-Deoxyglucose Etoposide)、放射線治療 (Radiation) 等方法處理該細胞株，皆發現較為惡性的抑制乳酸脫氫?乙型的細胞株有較好的生存能力。處理白藜蘆醇 (Resveratrol) 可發現該細胞株對此藥物較為敏感，在極低濃度下細胞就會大量走向細胞凋亡。經由西方墨點法可發現，白藜蘆醇能抑制該細胞株六碳醣磷酸?1（Hexokinase I）的作用，使細胞株無法進行糖解作用而死亡。本篇研究證實在子宮頸癌細胞株抑制乳酸脫氫?乙型的表現，可以造成腫瘤細胞的惡化，也透過西方墨點法及藥物處理的實驗解釋了該細胞株透過瓦式效應促使腫瘤細胞轉型 (Transformation) 的機制。並且也提供了一個新穎的藥物治療標地去專一性地殺死此種類型的腫瘤細胞。 ; Malignant tumor obtains energy by Warburg effect shifting its energy metabolism from traditional Tricarboxylic acid cycle (TCA cycle) to aerobic glycolysis Dysregulation in metabolic enzymes control defects in oxidative phosphorylation hypoxia and acidic microenvironment are some of the possible factors that could cause Warburg effect Lactate dehydrogenase (LDH) is a tetrameric enzyme composed by two different genes transcribes LDHA and LDHB LDH catalyzes the reversible conversion of pyruvate and lactate with NADH and NAD+ oxidoreduction Recent studies show that LDHA favors converting pyruvate to lactate and produces NAD+ Under this condition the tumor suppressor gene p53 would be no longer stable and the microenvironment would become acidic which benefits tumor growth On the opposite of that LDHB seems to play a distinct role in tumor development Previous research has ...
العلاقة: http://ir.lib.ncku.edu.tw/handle/987654321/122979Test; http://ir.lib.ncku.edu.tw/bitstream/987654321/122979/-1/index.htmlTest
