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Glutathione Metabolism in Crohn′s Disease 克罗恩病中的谷胱甘肽代谢
Pub Date : 1994-12-01 DOI: 10.1006/bmmb.1994.1062
Iantomasi T., Marraccini P., Favilli F., Vincenzini M.T., Ferretti P., Tonelli F.

A statistically significant decrease of glutathione (GSH) and an increase of GSH disulfide (GSSG) both in healthy and ill ileum of patients with Crohn′s disease in comparison with the controls (without this pathology) is demonstrated. However, the lowering of these levels was more remarkable in ill ileum in which high levels of GSSG were detected, too. These alterations may be in part explained by the changes obtained in GSH-related enzyme levels. Finally, considering the results that others and we obtained by studies on GSH oral absorption in rat intestine, an oral therapy of GSH in Crohn′s disease is suggested.

与对照组(无这种病理)相比,克罗恩病患者健康和患病回肠中谷胱甘肽(GSH)和谷胱甘肽二硫(GSSG)均有统计学意义的显著下降。然而,这些水平的降低在病态回肠中更为显著,其中也检测到高水平的GSSG。这些变化可以部分解释为谷胱甘肽相关酶水平的变化。最后,结合我们和他人对谷胱甘肽在大鼠肠道内口服吸收的研究结果,建议口服谷胱甘肽治疗克罗恩病。
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引用次数: 61
Enzymatic and Secretory Activities in Pancreatic-Islets of Non-Insulin-Dependent Diabetic Rats after Short-Term Infusion of Succinic Acid Monomethyl Ester 短期输注琥珀酸单甲基酯对非胰岛素依赖型糖尿病大鼠胰岛酶和分泌活性的影响
Pub Date : 1994-12-01 DOI: 10.1006/bmmb.1994.1066
Giroix M.H., Sener A., Portha B., Malaisse W.J.

The monomethyl ester of succinic acid (SME) was recently proposed as a novel tool for stimulation of proinsulin biosynthesis and insulin release in animal models of non-insulin-dependent diabetes mellitus. In the present study, either saline or SME (14 mmol/day) was infused for 3 days to control rats, animals injected with streptozotocin during the neonatal period, and Goto-Kakizaki rats with inherited diabetes. The infusion of SME failed to correct the anomalies found in the islets of diabetic rats, namely, a decreased activity of the mitochondrial FAD-linked glycerophosphate dehydrogenase, a low insulin content, and an impaired secretory response to various nutrient secretagogues including D-glucose, 2-ketoisocaproate, and the combination of L-leucine and L-glutamine. These findings raise the question of whether a more prolonged administration of SME is required to raise the insulin store and improve the secretory potential of the endocrine pancreas in animals with type 2 diabetes.

琥珀酸单甲酯(SME)最近被认为是刺激非胰岛素依赖型糖尿病动物模型中胰岛素原生物合成和胰岛素释放的新工具。本研究采用生理盐水或SME (14 mmol/天)连续3天输注的方法,分别用于对照组大鼠、新生期注射链脲佐菌素的大鼠和遗传糖尿病的后藤- kakizaki大鼠。SME输注未能纠正糖尿病大鼠胰岛中发现的异常,即线粒体fad连接的甘油磷酸脱氢酶活性下降,胰岛素含量低,以及对多种营养分泌剂(包括d -葡萄糖,2-酮异己酸,l -亮氨酸和l -谷氨酰胺的组合)的分泌反应受损。这些发现提出了一个问题,即是否需要更长时间的SME管理来提高2型糖尿病动物的胰岛素储存和改善内分泌胰腺的分泌潜力。
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引用次数: 3
Methylated Purine Bases in Hepatic and Colonic RNA of Rats Treated with 1,2-Dimethylhydrazine 1,2-二甲基肼处理大鼠肝脏和结肠RNA中嘌呤碱基的甲基化
Pub Date : 1994-10-01 DOI: 10.1006/bmmb.1994.1057
Kang J.O.

Administration of 1,2-dimethylhydrazine (DMH) to rats produces colon cancer. The mechanism by which this agent induces colon cancer is unclear. This investigation was conducted to assess the effect of DMH on the hepatic RNA and the colonic RNA of rats. DMH (300 mg/kg body wt) was administered to rats by ip injections. After 24 h, the hepatic RNA and the colonic RNA were isolated and their component purine bases were analyzed by HPLC. DMH treatment resulted in the formation of 1-methyladenine, 1-methylguanine, N2-methylguanine, O6-methylguanine, and 7-methylguanine in RNA. These methylated products may play a role in cellular injury produced by DMH.

大鼠服用1,2-二甲基肼(DMH)可产生结肠癌。这种药物诱发结肠癌的机制尚不清楚。本实验旨在探讨DMH对大鼠肝脏RNA和结肠RNA的影响。DMH (300 mg/kg体wt)通过腹腔注射给药。24 h后,分离肝脏RNA和结肠RNA,用高效液相色谱法分析其组成嘌呤碱基。DMH处理导致RNA中形成1-甲基腺嘌呤、1-甲基鸟嘌呤、n2 -甲基鸟嘌呤、o6 -甲基鸟嘌呤和7-甲基鸟嘌呤。这些甲基化产物可能在DMH引起的细胞损伤中起作用。
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引用次数: 7
Homozygous Presence of the Crossover (Fusion Gene) Mutation Identified in a Type II Gaucher Disease Fetus: Is This Analogous to the Gaucher Knock-out Mouse Model? 在II型戈谢病胎儿中发现纯合子存在交叉(融合基因)突变:这与戈谢病小鼠模型类似吗?
Pub Date : 1994-10-01 DOI: 10.1006/bmmb.1994.1052
Strasberg P.M., Skomorowski M.A., Warren I.B., Hilson W.L., Callahan J.W., Clarke J.T.R.

Gaucher disease (GD) is an inherited deficiency of β-glucocerebrosidase (EC 3.1.2.45, gene symbol GBA). In type I GD, the CNS is not involved (nonneuronopathic), whereas in type II GD (acute neuronopathic) CNS involvement is early and rapidly progressive, while in type III GD (subacute neuronopathic) CNS involvement occurs later and is slowly progressive. The T6433C (L444P) substitution is prevalent in type GD II. It may occur alone as a single base-pair mutation but often is found as part of a complex allele containing additional GBA nucleotide substitutions, G6468C (A456P) and G6482C (V460V), without (recNciI) or with (recTL) G5957C (D409H). This complex allele is presumed to have formed by recombination (crossover, fusion) of the structural gene with the pseudogene, which contains the mutated sequences. Two complex alleles have never been demonstrated to coexist in any individual. We devised a selective PCR method for the specific amplification of the normal and/or fusion gene. Using this procedure we demonstrated the fusion gene in homozygous form for the first time, in a Macedonian/Ashkenazi Jewish GD type II fetus. Both parents were carriers of the recombination. This was confirmed by direct sequence analysis. A previous conceptus in this family was stillborn at 36 weeks, with features of severe type II GD. Neonates showing a severe clinical phenotype, analogous to the early neonatal lethal disease occurring in mice homozygous for a null allele produced by targeted disruption of GBA, have been described elsewhere, but the specific mutations in these cases have not yet been characterized. We suggest that this genotype is lethal, as in the mice, and may account for some or all of the mutations in the neonates.

戈谢病(GD)是一种遗传性β-葡萄糖脑苷酶(EC 3.1.2.45,基因符号GBA)缺乏症。在I型GD中,中枢神经系统不受累(非神经性),而在II型GD(急性神经性)中,中枢神经系统受累是早期和快速进展的,而在III型GD(亚急性神经性)中,中枢神经系统受累发生较晚且缓慢进展。T6433C (L444P)取代在GD II型中普遍存在。它可以单独作为单个碱基对突变发生,但通常作为包含额外的GBA核苷酸替换的复杂等位基因的一部分被发现,G6468C (A456P)和G6482C (V460V),没有(recNciI)或与(recTL) G5957C (D409H)。这个复杂的等位基因被认为是由结构基因与含有突变序列的假基因重组(交叉、融合)而形成的。两个复杂的等位基因从未被证明在任何个体中共存。我们设计了一种选择性PCR方法来特异性扩增正常和/或融合基因。利用这种方法,我们首次在马其顿/德系犹太人GD II型胎儿中证实了融合基因的纯合子形式。父母双方都是基因重组的携带者。直接序列分析证实了这一点。这个家庭以前的一个孕妇在36周时死产,具有严重的II型GD的特征。新生儿表现出严重的临床表型,类似于由GBA靶向破坏产生的空等位基因纯合的小鼠中发生的早期新生儿致命性疾病,已经在其他地方描述过,但这些病例中的特定突变尚未被表征。我们认为这种基因型是致命的,就像在老鼠身上一样,并且可能解释了新生儿的部分或全部突变。
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引用次数: 24
Effect of Protein Kinase C on the Plasma Membrane Calcium Pump in Purified Beta Cells 蛋白激酶C对纯化β细胞质膜钙泵的影响
Pub Date : 1994-10-01 DOI: 10.1006/bmmb.1994.1060
Hoenig M., Knutson K.L.

The effect of protein kinase C activation on (Ca2+-Mg2+)-ATPase and 45Ca2+ uptake in purified plasma membranes and membrane vesicles from beta cells was examined. PKC activation was achieved by incubating cells for 10 or 30 min in 100 nM or 1 μM of the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) and evident by translocation of the α-isoform from the cytosolic to the membrane fraction. (Ca2+-Mg2+)-ATPase had a Km for Ca2+ of 0.56 ± 0.17 μM and the Vmax was 120 ± 12 nmol/min*mg protein in membranes from cells treated with TPA, while it was 0.66 ± 0.14 μM and 135 ± 19 nmol/min*mg protein, respectively, in its absence. In inside-out vesicles 45Ca2+ uptake had a Km for Ca2+ of 79 ± 19 nM and a Vmax of 1.68 ± 0.43 nmol/min*mg protein in the presence of TPA. In the absence of TPA, the Km was 71 ± 17 mM, and the Vmax was 1.59 ± 0.39 nmol/min*mg mg protein, respectively. It is concluded that in beta cells PKC activation does not regulate (Ca2+-Mg2+)-ATPase activity or Ca2+ transport directly.

研究了蛋白激酶C活化对β细胞纯化质膜和膜囊中(Ca2+-Mg2+)- atp酶和45Ca2+摄取的影响。PKC活化是通过细胞在100 nM或1 μM的12- o -十四烷酰13-乙酸磷酯(TPA)中孵育10或30 min实现的,并且通过α-异构体从细胞质转移到膜部分来证明。(Ca2+-Mg2+)-ATPase对Ca2+的Km为0.56±0.17 μM, Vmax为120±12 nmol/min*mg蛋白,而对TPA未处理的细胞膜的Vmax为0.66±0.14 μM, Vmax为135±19 nmol/min*mg蛋白。在TPA存在的情况下,45Ca2+的吸收Km为79±19 nM, Vmax为1.68±0.43 nmol/min*mg蛋白。无TPA时,Km为71±17 mM, Vmax为1.59±0.39 nmol/min*mg mg protein。由此可见,在β细胞中,PKC激活并不直接调节(Ca2+-Mg2+)- atp酶活性或Ca2+转运。
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引用次数: 0
Myocardial Adaptation to Long-Term Action of Substances Associated with Decreased Intensity of Cardiac Function 心肌对与心功能强度降低相关物质长期作用的适应
Pub Date : 1994-10-01 DOI: 10.1006/bmmb.1994.1051
Veksler V.I., Levitskaya E.L., Khatkevich A.N., Orekhova I.V., Khuchua Z.A., Kapelko V.I.

The effect of prolonged treatment of rats with 6-n-propyl-2-thiouracil (PTU), verapamil, or propranolol on cardiac pump function and the properties of myofibrils and mitochondria was studied. After 6-8 weeks of treatment, the heart rate and maximal cardiac output of the isolated heart of rats treated with verapamil or propranolol were higher than those in the control group. The PTU treatment was followed by lower heart rate and maximal work. Calcium sensitivity (pCa50 value) of skinned ventricular fibers was higher in all experimental groups compared to the control by 0.07-0.15 units. Myofibrillar Mg2+, Ca2+-ATPase activity measured in isolated Triton-skinned cardiomyocytes was considerably lower after PTU treatment than that in respective controls (0.128 ± 0.013 vs 0.178 ± 0.010 μmol Pi/min/mg protein). In contrast, long-term treatment with verapamil or propranolol was accompanied by increased activity to 0.223 ± 0.018 and 0.254 ± 0.015 μmol Pi/min/mg protein, respectively. Neither the basal mitochondrial respiration rate of saponin-skinned cardiac fibers nor its enhancement after addition of low ADP concentration or creatine was significantly altered in any experimental group. Also no difference between control and experimental groups was observed in the total activity of creatine kinase or relative percentage of its isoenzymes extracted from cardiac tissue. Thus the changes in cardiac pump function after prolonged treatment with agents decreasing cardiac function may be attributed to concomitant alterations of myofibrils while mitochondria remain relatively intact.

研究了6-n-丙基-2-硫脲嘧啶(PTU)、维拉帕米和心得安对大鼠心脏泵功能及肌原纤维和线粒体特性的影响。治疗6 ~ 8周后,维拉帕米和心得安组大鼠离体心脏心率和最大心输出量均高于对照组。PTU治疗后,心率降低,运动量最大。各实验组剥皮心室纤维钙敏感性(pCa50值)均较对照组提高0.07 ~ 0.15个单位。PTU处理后,肌纤维Mg2+、Ca2+- atp酶活性明显低于对照组(0.128±0.013 vs 0.178±0.010 μmol Pi/min/mg蛋白)。与此相反,长期使用异拉帕米或心得安可使活性增加,分别达到0.223±0.018和0.254±0.015 μmol Pi/min/mg蛋白。在任何实验组中,皂苷皮心脏纤维的基础线粒体呼吸速率及其添加低浓度ADP或肌酸后的增强均未发生显著变化。在心肌组织中肌酸激酶的总活性或其同工酶的相对百分比方面,对照组和实验组之间也没有差异。因此,长期使用降低心功能的药物治疗后心脏泵功能的变化可能归因于肌原纤维的伴随改变,而线粒体保持相对完整。
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引用次数: 5
Protective Action of Succinic Acid Monomethyl Ester Against the Impairment of Glucose-Stimulated Insulin Release Caused by Glucopenia or Starvation: Metabolic Determinants 琥珀酸单甲基酯对葡萄糖减少症或饥饿引起的葡萄糖刺激胰岛素释放损伤的保护作用:代谢决定因素
Pub Date : 1994-10-01 DOI: 10.1006/bmmb.1994.1055
Eizirik D.L., Welsh N., Sener A., Malaisse W.J.

The monomethyl ester of succinic acid (SME) was recently found to protect pancreatic islet B-cells against the impairment of glucose-stimulated insulin release caused by either glucopenia or starvation. The possible metabolic determinants of such a protective action are now scrutinized. After 180 min preincubation at 2.8 mM D-glucose in the presence of SME (10 mM), the oxidation of D-[U-14C]glucose, relative to either the utilization of D-[5-3H]glucose or the generation of 14C-labeled acidic metabolites, was higher than that after preincubation in the absence of SME, and became close to that otherwise found after preincubation at 16.7 mM D-glucose. Likewise, after 3 days of culture at a low concentration of D-glucose (2.8 nM), the presence of SME in the culture medium tended to increase the subsequent oxidation of D-[6-14C]glucose and utilization of D-[5-3H]glucose. These two variables increased as a function of the concentration of D-glucose in the culture medium, this coinciding with a modest increase in hexokinase activity and a more pronounced increase in glucokinase activity. The presence of SME in the culture medium failed, however, to exert any obvious effect upon the respiration of the islets, suggesting that the protective action of the ester against glucopenia may also involve variables distinct from the metabolism of either endogenous or exogenous nutrients. Likewise, the fact that SME infusion to starved rats prevents the impairment of glucose-induced insulin release otherwise attributable to starvation may involve enzymatic determinants, such as a less severe decrease in glucokinase activity, metabolic variables, such as a greater relative increase in D-[U-14C]glucose oxidation relative to D-[5-3H]glucose utilization in response to a rise in extracellular D-glucose concentration, and other factors yet to be identified that-participate in the secretory sequence at a site distal to those metabolic events triggered by D-glucose in the islet cells.

琥珀酸单甲基酯(SME)最近被发现可以保护胰岛b细胞免受葡萄糖减少症或饥饿引起的葡萄糖刺激的胰岛素释放损伤。这种保护作用的可能的代谢决定因素现在正在仔细研究。在存在SME (10 mM)的2.8 mM D-葡萄糖条件下预孵育180 min后,D-[U-14C]葡萄糖的氧化,相对于D-[5-3H]葡萄糖的利用率或14c标记的酸性代谢物的生成,都高于不存在SME的预孵育后,接近于在16.7 mM D-葡萄糖条件下预孵育后的结果。同样,在低浓度(2.8 nM) D-葡萄糖培养3天后,培养基中SME的存在倾向于增加D-[6-14C]葡萄糖的后续氧化和D-[5-3H]葡萄糖的利用。这两个变量随着培养基中d -葡萄糖浓度的增加而增加,这与己糖激酶活性的适度增加和葡萄糖激酶活性的更明显的增加相一致。然而,培养基中SME的存在未能对胰岛的呼吸产生任何明显影响,这表明酯对葡萄糖减少症的保护作用也可能涉及不同于内源性或外源性营养物质代谢的变量。同样,饥饿大鼠输注SME可防止葡萄糖诱导的胰岛素释放损伤,否则可归因于饥饿,这一事实可能涉及酶决定因素,如葡萄糖激酶活性较轻的下降,代谢变量,如D-[U-14C]葡萄糖氧化相对于D-[5-3H]葡萄糖利用相对于细胞外D-葡萄糖浓度上升的相对增加。以及其他尚未确定的因素,这些因素参与胰岛细胞中d -葡萄糖引发的代谢事件远端的分泌序列。
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引用次数: 9
Nonkallikrein Arginine Endopeptidase in the Human Submaxillary Gland: Purification and Characterization of the Enzyme 人颌下腺非钾化肽精氨酸内肽酶:酶的纯化和特性
Pub Date : 1994-10-01 DOI: 10.1006/bmmb.1994.1056
Watanabe Y., Suzuki M., Fujimoto Y.

The two major species of arginine endopeptidase present in the soluble fraction of human submaxillary gland are glandular kallikrein and another enzyme tentatively named nonkallikrein arginine endopeptidase. In this study, we purified the latter enzyme to homogeneity and examined its catalytic properties. The newly found enzyme was clearly distinguishable from human tissue kallikrein in its molecular nature, action toward various synthetic substrates, and kinin-generated activity. The specificity of the action of the enzyme was further investigated using various basic amino acid-containing peptides as model substrates. HPLC analysis of peptide fragments produced, followed by their amino acid analysis, revealed that the enzyme preferentially hydrolyzed the Arg-Arg or Arg-Lys bonds in dynorphins A 1-10, 1-9, and 1-8, β-neoendorphin, adenorphin, and neurotensin.

存在于人颌下腺可溶性部分的两种主要精氨酸内肽酶是腺体钾化酶和另一种暂定名为非钾化酶的精氨酸内肽酶。在本研究中,我们将后者酶纯化到均匀性,并对其催化性能进行了研究。新发现的酶在分子性质、对各种合成底物的作用和激肽生成活性方面与人组织激肽素明显不同。以多种含碱性氨基酸肽为模型底物,进一步研究了该酶的特异性作用。HPLC分析产生的肽片段,然后进行氨基酸分析,表明该酶优先水解促啡肽A 1-10、1-9和1-8、β-新内啡肽、肾上腺素和神经紧张素中的Arg-Arg或Arg-Lys键。
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引用次数: 0
Insulinotropic Action of Formycin A Formycin A的胰岛素调节作用
Pub Date : 1994-10-01 DOI: 10.1006/bmmb.1994.1053
Malaisse W.J., Sener A., Gruber H.E., Erion M.D.

The adenosine analogue formycin A is phosphorylated to its triphosphate ester in a sequence of reactions catalyzed by adenosine kinase and adenylate kinase. Formycin A triphosphate is an ATP analogue that is currently used to probe for ATP binding sites. Considering the key role ascribed to ATP in the coupling of metabolic to cationic events in the process of glucose-stimulated insulin release, we investigated whether formycin A displays insulinotropic action in rat pancreatic islets. Formycin A (10 μM to 1.0 mM) caused a concentration-related increase of insulin release evoked by 8.3 mM D-glucose and prevented the fall in insulin output otherwise observed over two successive incubations of 90 min each. Formycin A (1.0 mM) also augmented insulin secretion at low (5.6 mM) and high (16.7 mM) concentrations of D-glucose. At the low hexose concentration, the secretory response to formycin A was comparable to that evoked by either glibenclamide or glipizide. At higher concentrations of D-glucose, however, formycin A was more potent than the hypoglycemic sulfonylureas in enhancing insulin output. These findings support the role of ATP in glucose-stimulated insulin release and, therefore, suggest that ATP mimetics represent a new class of insulinotropic agents that have potential utility in the treatment of non-insulin-dependent diabetes mellitus.

腺苷类似物福霉素A在一系列由腺苷激酶和腺苷酸激酶催化的反应中被磷酸化成三磷酸酯。Formycin A triphosphate是一种ATP类似物,目前用于探测ATP结合位点。考虑到ATP在葡萄糖刺激胰岛素释放过程中代谢与阳离子事件耦合中的关键作用,我们研究了福霉素A是否在大鼠胰岛中表现出促胰岛素作用。Formycin A (10 μM至1.0 mM)引起8.3 mM d -葡萄糖引起的胰岛素释放浓度相关增加,并防止胰岛素输出下降,否则在两次连续孵育中观察到每次90分钟。Formycin A (1.0 mM)在低(5.6 mM)和高(16.7 mM) d -葡萄糖浓度下也能增强胰岛素分泌。在低己糖浓度下,对formycin A的分泌反应与格列本脲或格列吡嗪引起的反应相当。然而,在较高浓度的d -葡萄糖下,福霉素A在提高胰岛素输出方面比降糖磺脲类药物更有效。这些发现支持ATP在葡萄糖刺激胰岛素释放中的作用,因此表明ATP模拟物代表了一类新的胰岛素促胰岛素药物,在治疗非胰岛素依赖型糖尿病方面具有潜在的效用。
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引用次数: 6
Immunochemical Characterization of Feline and Human N-Acetylgalactosamine 4-Sulfatase 猫和人n -乙酰半乳糖胺4-硫酸酯酶的免疫化学特性
Pub Date : 1994-10-01 DOI: 10.1006/bmmb.1994.1058
Brooks D.A., Gibson G.J., Hopwood J.J.

Maroteaux-Lamy syndrome (mucopolysaccharidosis type VI; MPS VI) is a disorder which results from a deficiency in the lysosomal associated enzyme N-acetylgalactosamine 4-sulfatase (4-sulfatase). A feline model of human MPS VI has previously been described and provides a system for the evaluation of enzyme replacement therapy protocols. As a preliminary study to human 4-sulfatase enzyme replacement therapy in feline we have compared the immunochemical properties of human and feline 4-sulfatase. By SDS-PAGE the molecular mass of purified feline and human 4-sulfatase were similar under both reducing and nonreducing conditions. There was, however, a detectable conformation difference between human and feline 4-sulfatase indicating some structural variation. Feline 4-sulfatase reacted weakly with a panel of monoclonal antibodies in an immunobinding assay (interacting with 4-sulfatase in free solution), but the same monoclonal antibodies reacted strongly with feline 4-sulfatase in an immunoquantification assay where the feline 4-sulfatase was bound to a polyclonal antibody (which presumably induces a conformation change in the feline 4-sulfatase to closer approximate the structure of human 4-sulfatase). A monoclonal antibody which selectively reacts with human 4-sulfatase has been used to develop an assay suitable for evaluating human 4-sulfatase enzyme replacement in cat tissues.

马罗托-拉米综合征(粘多糖病VI型);MPS VI)是一种由溶酶体相关酶n -乙酰半乳糖胺4-硫酸酯酶(4-硫酸酯酶)缺乏引起的疾病。先前已经描述了人类MPS VI的猫模型,并为酶替代治疗方案的评估提供了一个系统。作为人4-硫酸酯酶在猫体内替代治疗的初步研究,我们比较了人和猫4-硫酸酯酶的免疫化学性质。通过SDS-PAGE分析,纯化猫和人4-硫酸酯酶在还原和非还原条件下的分子质量相似。然而,人类和猫的4-硫酸酯酶之间存在可检测到的构象差异,表明存在一些结构差异。在免疫结合实验中,猫4-硫酸酯酶与一组单克隆抗体反应较弱(在游离溶液中与4-硫酸酯酶相互作用),但在免疫定量实验中,同样的单克隆抗体与猫4-硫酸酯酶反应强烈,其中猫4-硫酸酯酶与多克隆抗体结合(这可能导致猫4-硫酸酯酶的构象改变,更接近人类4-硫酸酯酶的结构)。一种单克隆抗体选择性地与人4-硫酸酯酶反应,建立了一种适合于评价猫组织中人4-硫酸酯酶替代的测定方法。
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引用次数: 11
期刊
Biochemical medicine and metabolic biology
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