检索结果-内蒙古大学图书馆

The energy landscape for ubihydroquinone oxidation at the Q_o site of the bc₁ complex in Rhodobacter sphaeroides

JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第48期274卷 33931-33944页

作者： Hong, SJ Ugulava, N Guergova-Kuras, M Crofts, AR Univ Illinois Ctr Biophys & Computat Biol Urbana IL 61801 USA Univ Illinois Dept Biochem Urbana IL 61801 USA Univ Illinois Dept Microbiol Urbana IL 61801 USA

Activation energies for partial reactions involved in oxidation of quinol by the bc(1) complex were independent of pH in the range 5.5-8.9. Formation of enzyme-substrate complex required two substrates, ubihydroquinone binding from the lipid phase and the extrinsic domain of the iron-sulfur protein. The activation energy for ubihydroquinone oxidation was independent of the concentration of either substrate, showing that the activated step was in a reaction after formation of the enzyme-substrate complex. At all pH values, the partial reaction with the limiting rate and the highest activation energy was oxidation of bound ubihydroquinone. The pH dependence of the rate of ubihydroquinone oxidation reflected the pK on the oxidized iron-sulfur protein and requirement for the deprotonated form in formation of the enzyme-substrate complex. We discuss different mechanisms to explain the properties of the bifurcated reaction, and we preclude models in which the high activation barrier is in the second electron transfer or is caused by deprotonation of QH(2). Separation to products after the first electron transfer and movement of semiquinone formed in the Q(o) site would allow rapid electron transfer to heme b(L). This would also insulate the semiquinone from oxidation by the iron-sulfur protein, explaining the efficiency of bifurcation.

关键词：抗霉素A/类似物和衍生物抗霉素A/药理学结合部位细胞色素b组/代谢电子转运电子传递复合物Ⅲ/代谢电生理学能量代谢血红素/代谢氢离子浓度动力学氧化还原/药物作用醌类/代谢球形红杆菌/酶学温度泛醌/代谢

来源：评论

学校读者我要写书评

暂无评论

Protection against radiation-induced degradation of DNA bases by polyamines

引用

RADIATION RESEARCH 2000年第1期153卷 29-35页

作者： Douki, T Bretonniere, Y Cadet, J CEA Grenoble Dept Rech Fondamentale Mat Condensee Serv Chim Inorgan & Biol Lab Les Acides Nucl F-38054 Grenoble 9 France

Polyamines have been reported to protect DNA against the formation of radiation-induced strand breaks and crosslinks to proteins. The present study was aimed at investigating the protective effect of spermine, spermidine and putrescine against the degradation of DNA bases upon exposure to gamma rays in aerated aqueous solution. The yield of 8-oxo-7,8-dihydroguanine and 5-hydroxycytosine was found to decrease for concentrations of spermine and spermidine greater than 0.1 mM, A protection factor of 10 was observed for a concentration of 1 mM of the latter two polyamines. Putrescine afforded a lower protection, In addition, the formation yield of a series of radiation-induced degradation products of the purine and pyrimidine bases was determined within DNA in the presence or absence of spermine. The protection factor was within the same range for all the lesions measured. The latter observation ruled out the possibility of degradation of DNA by radiation-induced polyamine peroxyl radicals. This was confirmed by studies involving radiolysis of DMSO and decomposition of 2,2'-azobis(2-methyl-propionamidine) as sources of alkylperoxyl radicals. Therefore, it is likely that the polyamine-mediated protection against the radiation-induced degradation of DNA bases is due to the compaction of the DNA structure and the reduction in the accessibility of DNA to (OH)-O-. rather than by scavenging (OH)-O-. in the bulk solution or in the vicinity of the DNA, (C) 2000 by Radiation Research Society.

关键词：脒类/药理学胞嘧啶/类似物和衍生物胞嘧啶/分析胞嘧啶/化学合成 DNA/化学 DNA/代谢 DNA/辐射效应 DNA损伤/药物作用脱氧腺苷类/代谢脱氧腺苷类/辐射效应脱氧胞苷/类似物和衍生物脱氧胞苷/分析脱氧胞苷/化学合成脱氧鸟苷/类似物和衍生物脱氧鸟苷/分析脱氧鸟苷/化学合成二甲亚砜/代谢二甲亚砜/辐射效应剂量效应关系药物 γ射线气相色谱-质谱法鸟嘌呤/类似物和衍生物鸟嘌呤/分析鸟嘌呤/化学合成羟自由基/药理学氧化还原/药物作用聚胺类/药理学嘌呤类/化学嘌呤类/辐射效应腐胺/药理学嘧啶类/化学嘧啶类/辐射效应辐射防护剂/药理学溶液精脒/药理学精胺/药理学

来源：评论

学校读者我要写书评

暂无评论

Mechanistic studies of phosphoserine phosphatase, an enzyme related to P-type ATPases

引用

JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第48期274卷 33985-33990页

作者： Collet, JF Stroobant, V Van Schaftingen, E Christian de Duve Inst Cellular Pathol Chim Physiol Lab B-1200 Brussels Belgium Catholic Univ Louvain B-1200 Brussels Belgium Ludwig Inst Canc Res B-1200 Brussels Belgium

Phosphoserine phosphatase belongs to a new class of phosphotransferases forming an acylphosphate during catalysis and sharing three motifs with P-type ATPases and haloacid dehalogenases, The phosphorylated residue was identified as the first aspartate in the first motif (DXDXT) by mass spectrometry analysis of peptides derived from the phosphorylated enzyme treated with NaBH4 or alkaline [O-18]H2O. Incubation of native phosphoserine phosphatase with phosphoserine in [O-18]H2O did not result in O-18 incorporation in residue Asp-20, indicating that the phosphoaspartate is hydrolyzed, as in P-type ATPases, by attack of the phosphorus atom. Mutagenesis studies bearing on conserved residues indicated that four conservative changes either did not affect (S109T) or caused a moderate decrease in activity (G178A, D179E, and D183E), Other mutations inactivated the enzyme by >80% (S109A and G180A) or even by greater than or equal to 99% (D179N, D183N, K158A, and K158R), Mutations G178A and D179N decreased the affinity for phosphoserine, suggesting that these residues participate in the binding of the substrate. Mutations of Asp-179 decreased the affinity for Mg2+, indicating that this residue interacts with the cation, Thus, investigated residues appear to play an important role in the reaction mechanism of phosphoserine phosphatase, as is known for equivalent residues in P-type ATPases and haloacid dehalogenases.

关键词：腺苷三磷酸酶类/化学腺苷三磷酸酶类/遗传学腺苷三磷酸酶类/代谢氨基酸序列氨基酸取代天冬氨酸/代谢氢硼化物/药理学催化作用氢离子浓度水解作用动力学质谱分析法/方法诱变定点氧化还原/药物作用氧同位素磷蛋白类/代谢磷酸单酯水解酶类/化学磷酸单酯水解酶类/遗传学磷酸单酯水解酶类/代谢磷酰化重组蛋白质类/化学重组蛋白质类/遗传学重组蛋白质类/代谢序列同源性氨基酸胰蛋白酶/代谢水/代谢人类

来源：评论

学校读者我要写书评

暂无评论

Hexamminecobalt(III) chloride inhibits glucose-induced insulin secretion at the exocytotic process

引用

JOURNAL OF BIOLOGICAL CHEMISTRY 2001年第5期276卷 2979-2985页

作者： Tsubamoto, Y Eto, K Noda, M Daniel, S Suga, S Yamashita, S Kasai, H Wakui, M Sharp, GWG Kimura, S Kadowaki, T Univ Tokyo Grad Sch Med Dept Metab Dis Bunkyo Ku Tokyo 1138655 Japan Univ Tokyo Grad Sch Med Dept Physiol Bunkyo Ku Tokyo 1138655 Japan Cornell Univ Coll Vet Med Dept Mol Med Ithaca NY 14853 USA Hirosaki Univ Sch Med Dept Physiol Hirosaki Aomori 0368562 Japan

Hexamminecobalt(III) (HAC) chloride was found to have a potent inhibitory effect on glucose-induced insulin secretion from pancreatic islets, HAC at 2 mM inhibited the secretion in response to 22.2 mM glucose by 90% in mouse islets, Perifusion experiments revealed that the first phase of insulin secretion was severely suppressed and that the second phase of secretion was completely abrogated. Removal of HAC from the perifusate immediately restored insulin secretion with a transient overshooting above the normal level. However, BAC failed to affect glucose-induced changes in D-[6-C-14]glucose oxidation, levels of reduced forms of NAD and NADP, mitochondrial membrane potential, ATP content, cytosolic calcium concentration, or calcium influx into mitochondria, Furthermore, HAC inhibited 50 mM potassium-stimulated insulin secretion by 77% and 10 muM mastoparan-stimulated insulin secretion in the absence of extracellular Ca2+ by 80%. The results of a co-immunoprecipitation study of lysates from insulin-secreting beta HC9 cells using anti-syntaxin and anti-vesicle-associated membrane protein antibodies for immunoprecipitation or Western blotting suggested that HAC inhibited disruption of the SNARE complex, which is normally observed upon glucose challenge. These results suggest that the inhibitory effect of HAC on glucose-induced insulin secretion is exerted at a site(s) distal to the elevation of cytosolic [Ca2+], possibly in the exocytotic machinery per se;and thus, HAC may serve as a useful tool for dissecting the molecular mechanism of insulin exocytotic processes.

关键词：腺苷三磷酸/代谢生物转运/药物作用钙/代谢细胞培养的氯化物/药理学钴/药理学环AMP/代谢胞质溶胶/药物作用胞质溶胶/代谢药物相互作用胞吐作用/药物作用胞吐作用/生理学葡萄糖/代谢葡萄糖/药理学胰岛素/代谢胰岛/药物作用胰岛/代谢小鼠近交C57BL 线粒体/药物作用线粒体/代谢氧化还原/药物作用肽类氯化钾/药理学黄蜂毒液类/药理学动物男(雄)性小鼠

来源：评论

学校读者我要写书评

暂无评论

Nadolol inhibits reactive oxygen species generation by leukocytes and linoleic acid oxidation

引用

AMERICAN JOURNAL OF CARDIOLOGY 2000年第4期86卷 443-448页

作者： Magsino, CH Hamouda, W Bapna, V Ghanim, H Abu-Reish, IA Aljada, A Dandona, P SUNY Buffalo Kaleida Hlth Div Endocrinol Diabet & Metab Dept Med Buffalo NY USA

We studied the effect of short-term nadolol administration on the reactive oxygen species (ROS) generation by polymorphonuclear leukocytes and mononuclear cells in 8 normal subjects. At a oral dose of 40 mg/day for 5 days, nadolol produced a decrease in the ROS generation by leukocytes, ROS generation by polymorphonuclear leukocytes decreased by 38% from 134 +/- 44 mV at baseline to 83 +/- 34 mV after 5 days (p = 0.005), and ROS generation by mononuclear cells decreased by 33% from 174 +/- 69 mV at baseline to 117 +/- 55 mV after 5 days (p = 0.015), There was also a significant reduction in linoleic acid oxidation as reflected by the lower levels of 9- and 13- hydroxy-octadecadienoic acid after 5 days. There was no change in the plasma thiobarbituric acid-reacting substances, a less sensitive index of oxidative damage to lipids. There was also no significant change in the levels of metatyrosine and orthotyrosine, which are known indexes of oxidative damage to amino acids and proteins. The absence of a significant change in metatyrosine, orthotyrosine, and thiobarbituric acid-reacting substances may reflect the short duration of nadolol administration and the decreased ROS load. Because ROS may induce lipid peroxidation, this inhibitory effect of nadolol on ROS generation by leukocytes and linoleic acid oxidation may inhibit low-density lipoprotein oxidation and thus atherogenesis, This effect may partly explain the favorable outcomes observed in patients with coronary artery disease on long-term p-blocker therapy, (C)2000 by Excerpta Medica, Inc.

关键词：投药口服肾上腺素能β受体拮抗剂/药理学色谱法高压液相白细胞单核/药物作用白细胞单核/代谢亚油酸/代谢纳多洛尔/药理学中性白细胞/药物作用中性白细胞/代谢氧化还原/药物作用苯丙氨酸/血液活性氧/代谢硫巴比妥酸反应物/代谢酪氨酸/血液成年人女(雌)性人类男(雄)性

来源：评论

学校读者我要写书评

暂无评论

Effects of surfactant mixtures, including Corexit 9527, on bacterial oxidation of acetate and alkanes in crude oil

引用

APPLIED AND ENVIRONMENTAL MICROBIOLOGY 1999年第4期65卷 1658-1661页

作者： Bruheim, P Bredholt, H Eimhjellen, K Norwegian Univ Sci & Technol Fac Chem & Biol Dept Biotechnol N-7491 Trondheim Norway

Mixtures of nonionic and anionic surfactants, including Corexit 9527, were tested to determine their effects on bacterial oxidation of acetate and alkanes in crude oil by cells pregrown on these substrates, Corexit 9527 inhibited oxidation of the alkanes in crude oil by Acinetobacter calcoaceticus ATCC 31012, while Span 80, a Corexit 9527 constituent, markedly increased the oil oxidation rate. Another Corexit 9527 constituent, the negatively charged dioctyl sulfosuccinate (AOT), strongly reduced the oxidation rate. The combination of Span 80 and AOT increased the rate, but not as much as Span 80 alone increased it, which tentatively explained the negative effect of Corexit 9527, The results of acetate uptake and oxidation experiments indicated that the nonionic surfactants interacted with the acetate uptake system while the anionic surfactant interacted with the oxidation system of the bacteria. The overall effect of Corexit 9527 on alkane oxidation by A. calcoaceticus ATCC 31012 thus seems to be the sum of the independent effects of the individual surfactants in the surfactant mixture. When Rhodococcus sp, strain 094 was used, the alkane oxidation rate decreased to almost zero in the presence of a mixture of Tergitol 15-S-7 and AOT even though the Tergitol 15-S-7 surfactant increased the alkane oxidation rate and AOT did not affect it. This indicated that there was synergism between the two surfactants rather than an additive effect like that observed for ii. calcoaceticus ATCC 31012.

关键词：乙酸盐类/代谢不动杆菌乙酸钙/药物作用不动杆菌乙酸钙/生长和发育不动杆菌乙酸钙/代谢烷烃类/代谢脂类氧化还原/药物作用石油/代谢红球菌属/药物作用红球菌属/生长和发育红球菌属/代谢表面活性剂/药理学

来源：评论

学校读者我要写书评

暂无评论

Why is glycated LDL more sensitive to oxidation than native LDL? A comparative study

引用

PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS 2000年第4期63卷 177-186页

作者： Sobal, G Menzel, J Sinzinger, H Univ Vienna Radiopharmacol Unit Dept Nucl Med A-1090 Vienna Austria Univ Vienna Inst Immunol A-1090 Vienna Austria

It is well established that oxidative modification of low-density lipoprotein (LDL) plays a causal role in human atherogenesis and the risk of atherosclerosis is increased in patients with diabetes mellitus. To examine the influence of different agents which may influence LDL-glycation and oxidation, experiments including glycation with glucose, glucose 6-phosphate, metal chelators (EDTA) and antioxidants (BHT) were perfomed. The influence of time dependence on the glycation process and the alteration of the electrophoretic mobility of LDL under diverse glycation and/or oxidation conditions was also investigated. The formation of conjugated dienes and levels of lipid peroxides in these different LDL-modifications were estimated. The copper-induced oxidation of LDL in vitro was determined by measurement of thiobarbituric acid reactive substances (TBARS) and expressed as nmol MDA/mg of LDL protein. We found that glycated LDL is more prone to oxidation than native LDL. Using native LDL, the maximal oxidation effect was found to reach a value of 49.72 nmol MDA/mg protein after 8 h. The maximum oxidation of the 31 days, glycated LDL with glucose was 71.76 nmol MDA/mg protein amounting to 144.33 % of the value found for native LDL. In the case of glucose 6-phosphate glycation, the maximum oxidation under the same conditions amounted to 173.77 % of the value found for native LDL. To measure the extent of glycation, fluorescence of advanced glycation end products (AGEs) was determined (370 nm excitation and 440 nm emission). The most potent glycation agent was glucose 6-phosphate leading to the formation of very high amounts of AGEs. This process was promoted in the absence of EDTA, which prevents the oxidative cleavage of modified Amadori products (ketoamines) to AGEs. We therefore conclude that both processes, glycation and oxidation, result in the modification of LDL, The lower the glycation-rate (+/ - EDTA) as measured by relative fluorescence units RFU (generation of A

关键词：抗氧化剂/药理学动脉硬化/代谢螯合剂/药理学铜/药理学依地酸/药理学电泳琼脂凝胶荧光葡萄糖/代谢葡糖-6-磷酸盐/代谢糖基化动力学脂质过氧化作用/药物作用脂蛋白类 LDL/血液脂蛋白类 LDL/代谢氧化还原/药物作用氧化性应激/药物作用硫巴比妥酸反应物/分析成年人女(雌)性人类男(雄)性中年人

来源：评论

学校读者我要写书评

暂无评论

Dichloroacetate improves postischemic function of hypertrophied rat hearts

引用

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 2000年第4期36卷 1378-1385页

作者： Wambolt, RB Lopaschuk, GD Brownsey, RW Allard, MF Univ British Columbia St Pauls Hosp Dept Pathol & Lab Med McDonald Res Labs Vancouver BC V6Z 1Y6 Canada Univ Alberta Cardiovasc Res Grp Edmonton AB Canada Univ British Columbia Dept Biochem & Mol Biol Vancouver BC V6Z 1Y6 Canada

OBJECTIVES We sought to determine whether improving coupling between glucose oxidation and glycolysis by stimulating glucose oxidation during reperfusion enhances postischemic recovery of hypertrophied hearts. BACKGROUND Low rates of glucose oxidation and high glycolytic rates are associated with greater postischemic dysfunction of hypertrophied as compared with nonhypertrophied hearts. METHODS Heart function, glycolysis and glucose oxidation were measured in isolated working control and hypertrophied rat hearts for 30 min before 20 min of global, no-flow ischemia and during 60 min of reperfusion. Selected control and hypertrophied hearts received 1.0 mmol/liter dichloroacetate (DCA), an activator of pyruvate dehydrogenase, at the time of reperfusion to stimulate glucose oxidation. RESULTS In the absence of DCA, glycolysis was higher and glucose oxidation and recovery of function were lower in hypertrophied hearts than in control hearts during reperfusion. Dichloroacetate stimulated glucose oxidation during reperfusion approximately twofold in both groups, while significantly reducing glycolysis in hypertrophied hearts. It also improved function of both hypertrophied and control hearts. In the presence of DCA, recovery of function of hypertrophied hearts was comparable to or better than that of untreated control hearts. CONCLUSIONS Dichloroacetate, given at the time of reperfusion, normalizes postischemic function of hypertrophied rat hearts and improves coupling between glucose oxidation and glycolysis by increasing glucose oxidation and decreasing glycolysis. These findings support the hypothesis that low glucose oxidation rates and high glycolytic rates contribute to the exaggerated postischemic dysfunction of hypertrophied hearts. (J Am Coll Cardiol 2000;36:1378-85) (C) 2000 by the American College of Cardiology.

关键词：心脏扩大/药物疗法心脏扩大/代谢心脏扩大/病理生理学疾病模型动物葡萄糖/代谢糖原/代谢糖酵解/药物作用糖酵解/生理学心肌再灌注损伤/药物疗法心肌再灌注损伤/代谢心肌再灌注损伤/病理生理学心肌/代谢氧化还原/药物作用丙酮酸脱氢酶复合物/药物作用丙酮酸脱氢酶复合物/代谢大鼠 Sprague-Dawley 心室功能/药物作用心室功能/生理学动物男(雄)性大鼠

来源：评论

学校读者我要写书评

暂无评论

Activation of c-Ha-ras by benzo(a)pyrene in vascular smooth muscle cells involves redox stress and aryl hydrocarbon receptor

引用

MOLECULAR PHARMACOLOGY 2000年第1期58卷 152-158页

作者： Kerzee, JK Ramos, KS Texas A&M Univ Coll Vet Med Dept Physiol & Pharmacol College Stn TX 77843 USA

Repeated cycles of vascular injury by benzo(a)pyrene (BaP) increase the onset and progression of atherosclerotic lesions in laboratory animals. This atherogenic response is partly mediated by activation of cis-acting antioxidant/electrophile response elements that enhance c-Ha-ras transcription in vascular smooth muscle cells (vSMCs). Activation of antioxidant/electrophile responsive cis-acting elements may depend on metabolism of BaP by cytochrome P450s to intermediates that induce oxidative stress and modulate gene expression. To test this hypothesis, we evaluated mitogen-activated c-Ha-ras expression in vSMCs treated with BaP or its metabolic intermediates alone, and in combination with agents that modulate cellular redox status. BaP (0.3 and 3 mu M), BaP-3,6-quinone (0.3 mu M), or hydrogen peroxide (50 mu M) enhanced serum-activated c-Ha-ras. Ellipticine (0.01 nM), a known inhibitor of cytochrome P450 metabolism and aryl hydrocarbon receptor (AhR) antagonist, inhibited c-Ha-ras induction by BaP (3 mu M). Serum challenge of G(o) synchronized cultures of vSMCs with DL-buthionine-( S,R)-sulfoximine (0.1 mM), a depletor of cellular glutathione, increased c-Ha-ras mRNA levels during the early phase of the mitogenic response. Combined BaP/DL-buthionine-(S,R)-sulfoximine challenge was cytotoxic to the cells and inhibited c-Ha-ras expression, whereas up-regulation of antioxidant capacity by N-acetylcysteine (0.5 mM) precluded BaP-induced ras expression. BaP increased formation of reactive oxygen species and depleted cellular glutathione, but these changes did not correlate with the kinetics of c-Ha-ras induction. BaP did not enhance c-Ha-ras expression in vSMCs from AhR knockout mice, although aryl hydrocarbon hydroxylase activity was constitutively expressed in these cells. These results suggest that c-Ha-ras activation in vSMCs by BaP involves a redox-sensitive mechanism that is coupled to AhR receptor-dependent functions.

关键词：苯并芘/药理学细胞培养的基因表达调控/药物作用基因 ras 小鼠近交C57BL 肌平滑血管/药物作用肌平滑血管/代谢氧化还原/药物作用受体芳基烃/药物作用受体芳基烃/代谢动物女(雌)性小鼠

来源：评论

学校读者我要写书评

暂无评论

EFFECT OF ACETALDEHYDE ON FATTY-ACID OXIDATION AND KETOGENESIS BY HEPATIC MITOCHONDRIA

引用

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS 1975年第1期169卷 29-41页

作者： CEDERBAUM, AI LIEBER, CS RUBIN, E CITY UNIV NEW YORK MT SINAI SCH MEDDEPT PATHOLNEW YORKNY 10029 VET ADM HOSP SECT LIVERDIS & NUTRBRONXNY 10468 CITY UNIV NEW YORK MT SINAI SCH MEDDEPT BIOCHEMNEW YORKNY 10029 CITY UNIV NEW YORK MT SINAI SCH MEDDEPT MEDNEW YORKNY 10029

Acetaldehyde inhibited the oxidation of fatty acids by rat liver mitochondria as assayed by oxygen consumption and CO2 production. ADP-stimulated oxygen uptake was more sensitive to inhibition by acetaldehyde than was uncoupler-stimulated oxygen uptake, suggesting an effect of acetaldehyde on the electron transport-phosphorylation system. This conclusion is supported by the decrease in the respiratory control ratio, associated with fatty acid oxidation. Acetaldehyde depressed ketone body production as well as the content of acetyl CoA during palmitoyl-1-carnitine oxidation. Acetaldehyde was considerably more inhibitory toward fatty acid oxidation than was acetate. Therefore, the inhibition by acetaldehyde is not mediated by acetate, the direct product of acetaldehyde oxidation by the mitochondria. Oxygen uptake was depressed by acetaldehyde to a slightly, but consistently, greater extent in the absence of fluorocitrate, than in its presence. This suggests inhibition of oxygen consumption from β-oxidation to acetyl CoA and that which arises from citric acid cycle activity. The inhibition of fatty acid oxidation is not due to any effect on the activation or translocation of fatty acids into the mitochondria. The depression of the end products of fatty acid oxidation (CO2 , ketones, acetyl CoA) as well as the greater sensitivity of palmitate oxidation compared to acetate oxidation, suggests inhibition by acetaldehyde of β-oxidation, citric acid cycle activity, and the respiratory-phosphorylation chain. Neither the activities of palmitoyl CoA synthetase nor carnitine palmitoyltransferase appear to be rate limiting for fatty acid oxidation.

关键词：乙醛/药理学乙酸盐类/代谢乙酰辅酶A/代谢钙/药理学辛酸盐类/代谢二氧化碳/代谢肉碱/代谢肉碱O-软脂酰转移酶/代谢柠檬酸盐类/代谢柠檬酸循环/药物作用辅酶A/代谢辅酶A连接酶类/代谢二硝基酚类/药理学乙醇/代谢脂肪酸类/代谢氟/代谢酮体类/生物合成线粒体肝/药物作用线粒体肝/代谢油酸类/代谢氧化还原/药物作用氧耗量/药物作用棕榈酸盐类/代谢动物大鼠

来源：评论

学校读者我要写书评

暂无评论

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

请选择保存的检索档案：

请选择收藏分类：

通借通还

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：