The Journal of Trace Elements in Experimental Medicine最新文献_第5页

Oral copper loading test in humans 人体口服铜负荷试验

The Journal of Trace Elements in Experimental Medicine

Pub Date : 2003-01-01 DOI: 10.1002/jtra.10025

Mojgan Rahmaniyan, Kelley E. Johnston, Tsunenobu Tamura

There has been no report of normal responses of plasma copper and/or ceruloplasmin concentrations after an oral loading dose of unlabeled copper in humans. To establish a normal plasma response curve following an oral dose, we performed a copper-loading test (10 mg elemental copper as copper sulfate) in six healthy adult subjects and monitored plasma copper and ceruloplasmin concentrations for 3.5 h. We found that there were no significant changes in plasma copper and ceruloplasmin concentrations following the oral dose in the subjects. The test was originally intended to evaluate whether there was copper malabsorption in a female patient who developed signs of copper deficiency with her plasma copper levels below 3.0 μmol/l after multiple gastrointestinal surgeries. She did not respond to oral copper sulfate administration but responded to a sublingual application of copper glycinate. These findings suggest that she does not have adequate intestinal copper absorption. In conclusion, the use of unlabeled copper, such as copper sulfate, for an oral loading test, seemingly simple and economical, does not appear to be a suitable means to evaluate copper absorption in humans and is discouraged. In case of copper malabsorption, sublingual administration of copper may be worth trying. J. Trace Elem. Exp. Med. 16: 61–66, 2003. © 2003 Wiley-Liss, Inc.

目前还没有关于人类口服负载剂量的未标记铜后血浆铜和/或铜蓝蛋白浓度的正常反应的报告。为了建立口服剂量后的正常血浆反应曲线，我们对6名健康成年受试者进行了铜负荷试验（10 mg元素铜，硫酸铜），并监测了3.5小时的血浆铜和铜蓝蛋白浓度。我们发现，受试者口服剂量后，血浆铜和铜蓝蛋白浓度没有显著变化。该测试最初旨在评估一名女性患者是否存在铜吸收不良，该患者在多次胃肠道手术后出现铜缺乏症状，血浆铜水平低于3.0μmol/l。她对口服硫酸铜没有反应，但对舌下应用甘氨酸铜有反应。这些发现表明她没有足够的肠道铜吸收。总之，使用未标记的铜，如硫酸铜，进行口服负荷试验，看似简单且经济，似乎不是评估人体铜吸收的合适方法，因此不鼓励使用。在铜吸收不良的情况下，舌下给药铜可能值得一试。J.Trace Elem。实验医学。16:61-662003。©2003 Wiley-Liss，股份有限公司。

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引用次数: 0

Structure–activity relationship of insulinomimetic vanadyl–picolinate complexes in view of their clinical use 从临床应用角度看拟胰岛素型吡啶甲酸钒配合物的构效关系

The Journal of Trace Elements in Experimental Medicine

Pub Date : 2003-01-01 DOI: 10.1002/jtra.10036

Hiromu Sakurai, Hiroyuki Yasui

In view of the clinical use of vanadium compounds, we prepared seven analogs of a vanadylpicolinate complex (VO(pic)2) with VO(N2O2) coordination mode, which was found in 1995 to exhibit highly effective and long-term insulinomimetic activity in treating both streptozotocin (STZ)-induced type 1 diabetic rats (STZ rats) and hereditarily type 2 diabetic KK-A y mice by daily intraperitoneal (i.p.) injections and on oral administration, to find the structureactivity relationship of the complexes. Using an in vitro insulinomimetic evaluation of the complexes in terms of their inhibiting effect on free fatty acids release from isolated rat adipocytes treated with epinephrine (adrenaline), we found the activity (IC50 :5 0% inhibitor’s concentration of the complex on the free fatty acid release) to be as follows: VO(5ipa)2 > VO(3mpa)2 > VO(6mpa)2 > VO(3hpa)2 > VO(pic)2 > VO(6hpa)2 » VOSO4, indicating that the introduction of an electron-withdrawing halogen atom or an electron-donating methyl group at the 5th or 3rd position on the picolinate ligand causes stronger insulinomimetic activity than that of the lead complex VO(pic)2. Next we examined the pharmacokinetic features in the blood of the complexes by using the blood circulation-monitoring electron spin resonance method, in which good linear relationships between the pharmacokinetic parameters and the IC50 values were found. Based on the results, we tested the complexes and found that both VO(5ipa)2 and VO(3mpa)2 complexes treat type 1 diabetes in STZ rats. Because the daily oral administration of vanadyl complexes is the only method to treat type 1 diabetes in place of daily insulin injections, the present results will be useful for the development of vanadyl complexes with high safety and long-term activity. J. Trace Elem. Exp. Med. 16:269280, 2003. � 2003 Wiley-Liss, Inc.

鉴于钒化合物的临床应用，我们制备了七种具有VO（N2O2）配位模式的钒基-吡啶甲酸盐络合物（VO（pic）2）的类似物，1995年发现，通过每天腹膜内（i.p.）注射和口服，其在治疗链脲佐菌素（STZ）诱导的1型糖尿病大鼠（STZ大鼠）和遗传性2型糖尿病KK-Ay小鼠方面表现出高效和长期的拟胰岛素活性，以发现复合物的结构-活性关系。使用复合物在其对用肾上腺素（肾上腺素）处理的分离的大鼠脂肪细胞的游离脂肪酸释放的抑制作用方面的体外胰岛素模拟评估，我们发现活性（复合物对游离脂肪酸的IC50:50%抑制剂浓度）如下：VO（5ipa）2>；VO（3mpa）2>；VO（6mpa）2>；VO（3hpa）2>；VO（pic）2>；VO（6hpa）2≈VOSO4，表明在吡啶甲酸配体的第5或第3位引入吸电子的卤素原子或给电子的甲基比铅络合物VO（pic）2具有更强的胰岛素模拟活性。接下来，我们使用血液循环监测电子自旋共振方法检查了复合物在血液中的药代动力学特征，发现药代动力学参数与IC50值之间存在良好的线性关系。在此基础上，我们对复合物进行了测试，发现VO（5ipa）2和VO（3mpa）2复合物均可治疗STZ大鼠的1型糖尿病。由于每天口服钒基复合物是治疗1型糖尿病的唯一方法，而不是每天注射胰岛素，因此本研究结果将有助于开发具有高安全性和长期活性的钒基复合品。J.Trace Elem。Exp.Med.16:269–2802003。©2003 Wiley-Liss，股份有限公司。

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引用次数: 12

Insulin-like actions of vanadium: Potential as a therapeutic agent 钒的胰岛素样作用：作为治疗剂的潜力

The Journal of Trace Elements in Experimental Medicine

Pub Date : 2003-01-01 DOI: 10.1002/jtra.10034

Lucy Marzban, John H. McNeill

Vanadium compounds are glucose-lowering agents that are shown to mimic/enhance most of the metabolic actions of insulin both in vitro and in vivo. Several studies have demonstrated that vanadium treatment lowers plasma glucose levels in experimental models of type 1 diabetes and enhances insulin sensitivity in models of type 2 diabetes. Therefore, these compounds have gained attention as candidates for oral therapy in both types of diabetes. Despite numerous studies, the mechanism(s) by which vanadium mediates its metabolic effects in vivo are still not completely understood. The finding that most of the insulin-like effects of vanadium in vitro are observed in the presence of high concentrations of vanadium that are not usually achieved in vivo suggests that these effects of vanadium may not have therapeutic relevance. Also, a growing body of evidence from in vivo studies indicates that enhancing glucose disposal in the peripheral tissues is not an adequate explanation for the glucose lowering effects of vanadium in vivo. Accordingly, recent studies suggest that suppression of hepatic glucose production through inhibition of key gluconeogenic enzymes might have an important role in mediating the glucoregulatory effects of vanadium. Several potential sites in the insulin-signaling pathways, including both receptor and postreceptor mechanisms, have been proposed for the insulin-like effects of vanadium compounds. In this review, we have attempted to discuss the possible molecular mechanism(s) underlying the metabolic effects of vanadium in vivo. J. Trace Elem. Exp. Med. 16:253–267, 2003. © 2003 Wiley-Liss, Inc.

钒化合物是一种降血糖剂，在体外和体内都能模拟/增强胰岛素的大部分代谢作用。几项研究表明，钒治疗可降低1型糖尿病实验模型中的血糖水平，并增强2型糖尿病模型中的胰岛素敏感性。因此，这些化合物作为两种类型糖尿病的口服治疗候选药物而受到关注。尽管进行了大量研究，但钒介导其体内代谢作用的机制仍不完全清楚。钒在体外的大多数胰岛素样作用是在体内通常无法达到的高浓度钒存在下观察到的，这一发现表明钒的这些作用可能与治疗无关。此外，越来越多的体内研究证据表明，增强外周组织中的葡萄糖处理并不能充分解释钒在体内的降血糖作用。因此，最近的研究表明，通过抑制关键的糖异生酶来抑制肝脏葡萄糖的产生，可能在介导钒的葡萄糖调节作用中发挥重要作用。胰岛素信号通路中的几个潜在位点，包括受体和受体后机制，已经被提出用于钒化合物的胰岛素样作用。在这篇综述中，我们试图讨论钒在体内代谢作用的可能分子机制。J.Trace Elem。《实验医学》，16:253–2672003。©2003 Wiley-Liss，股份有限公司。

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引用次数: 62

Effects of three divalent cations: manganese, zinc, and magnesium on arterial blood pressures in guinea pigs 三种二价阳离子：锰、锌和镁对豚鼠动脉血压的影响

The Journal of Trace Elements in Experimental Medicine

Pub Date : 2003-01-01 DOI: 10.1002/jtra.10027

Nursen Onat, Öner Süzer

Our aim was to compare the effects of the divalent cations, namely magnesium, zinc, and manganese on the arterial blood pressures and heart rate of guinea pigs. Eighteen guinea pigs weighing 500–700 g were divided into three groups (six in each group), and three divalent cations as sulfate salt (MgSO4, ZnSO4, MnSO4) were administered to all animals after 20-min period of stabilization and at three escalating concentrations (10−6, 10−5, 10−4 mol/kg intravenously, respectively) in 25-min intervals. Each animal received only one kind of cation. Arterial pressures and heart rate were measured and their derivatives were calculated (dp/dt). Our study showed that divalent cations lowered the arterial blood pressures. No significant differences were between groups for systolic, diastolic, and mean pressures, except that 10−4 mol/kg ZnSO4 was lethal. The heart rates values of ZnSO4 (202 ± 9) was significantly (P < 0.05) lower after 10−6 mol/kg than MgSO4 (230 ± 7). Three divalent cations caused to decrease on arterial pressures. Zn2+ caused cardiac arrest in the highest dose. Intravenous administration of Mn2+ and Mg2+ seems to have similar effects on arterial blood pressures and heart rate. Further work is needed to relate effects on Mn2+ for their possible use in the emergency department. J. Trace Elem. Exp. Med. 16:75–85, 2003. © 2003 Wiley-Liss, Inc.

我们的目的是比较二价阳离子，即镁、锌和锰对豚鼠动脉血压和心率的影响。18只体重500–700 g的豚鼠被分为三组（每组6只），在稳定20分钟后，以三种递增浓度（分别为10−6、10−5、10−4 mol/kg静脉注射），每隔25分钟给所有动物注射三种二价阳离子硫酸盐（MgSO4、ZnSO4、MnSO4）。每只动物只接受一种阳离子。测量动脉压和心率，并计算其导数（dp/dt）。我们的研究表明，二价阳离子可以降低动脉血压。除了10−4 mol/kg ZnSO4是致命的外，各组的收缩压、舒张压和平均压没有显著差异。ZnSO4的心率值（202±9）在10−6 mol/kg后显著低于MgSO4（230±7）（P<；0.05）。导致动脉压降低的三种二价阳离子。Zn2+在最高剂量下引起心脏骤停。静脉注射Mn2+和Mg2+似乎对动脉血压和心率有相似的影响。还需要进一步的工作来联系对Mn2+的影响，以便在急诊科使用。J.Trace Elem。Exp.Med.16:75-852003。©2003 Wiley-Liss，股份有限公司。

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引用次数: 1

Zinc is essential for brain development and function 锌对大脑发育和功能至关重要

The Journal of Trace Elements in Experimental Medicine

Pub Date : 2003-01-01 DOI: 10.1002/jtra.10042

Harold H. Sandstead

Zinc's roles in brain function are poorly understood. Zinc is essential pre- and postnatally for growth, maturation, and function. In early pregnancy, zinc is essential for cell multiplication and implantation of the embryo and for cell differentiation and organ formation. Deficiency causes teratology in all tissues. Zn deficiency in later pregnancy impairs neuronal replication and migration (as observed in cerebellar external granular cells). Synaptogenesis is impaired (as observed in Purkinje cells). It has been proposed that zinc deficiency impairs calcium channels causing a decrease in intracellular calcium that suppresses gene expression of growth factors and synthesis of nucleic acids and proteins. Whatever the mechanism, effects in experimental animals include poorly reversible impairments in learning and memory later in life, which appears associated with decreased neuronal survival. It is unknown if similar phenomena occur in humans. It is known however that low fetal growth, a process caused by maternal zinc deficiency, is risk factor for coronary heart disease, type 2 diabetes mellitus, chronic lung disease, and obesity. One wonders if fetal growth is related to later neuronal health and function. J. Trace Elem. Exp. Med. 16:165–173, 2003. © 2003 Wiley-Liss, Inc.

锌在大脑功能中的作用尚不清楚。锌在出生前和出生后对生长、成熟和功能至关重要。在妊娠早期，锌对细胞增殖和胚胎植入以及细胞分化和器官形成至关重要。缺乏会导致所有组织畸形。妊娠后期锌缺乏会损害神经元的复制和迁移（如在小脑外部颗粒细胞中观察到的）。突触发生受损（如在浦肯野细胞中观察到的）。有人提出锌缺乏会损害钙通道，导致细胞内钙减少，从而抑制生长因子的基因表达以及核酸和蛋白质的合成。无论是什么机制，实验动物的影响包括晚年学习和记忆的可逆性较差的损伤，这似乎与神经元存活率下降有关。目前还不知道类似的现象是否发生在人类身上。然而，众所周知，母亲缺锌引起的胎儿生长发育迟缓是冠心病、2型糖尿病、慢性肺病和肥胖的危险因素。人们想知道胎儿的生长是否与后来的神经元健康和功能有关。J.Trace Elem。《实验医学》，16:165–1732003。©2003 Wiley-Liss，股份有限公司。

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引用次数: 49

Regulation of tyrosine phosphorylation cascades by phosphatases: What the actions of vanadium teach us 磷酸酶对酪氨酸磷酸化级联反应的调节：钒的作用教会了我们什么

The Journal of Trace Elements in Experimental Medicine

Pub Date : 2003-01-01 DOI: 10.1002/jtra.10040

Philippa Hulley, Allan Davison

Protein phosphorylation and dephosphorylation regulate much of the machinery of the cell. Emphasis in recent years has swung toward regulation by dephosphorylation. Much current research focuses on protein tyrosine phosphatases. Researchers of cellular regulation use vanadium as a probe because of its unparalleled ability to selectively inhibit protein tyrosine phosphatases at submicromolar concentrations. This review focuses on the biological actions of vanadium relevant to cellular regulatory cascades. Recent research has led to identification of control points and possible drug targets in 1) the glucose control mechanisms downstream from insulin receptors; 2) pathways regulating mitogenesis, tumor promotion, and other events downstream from growth factor receptors; 3) regulation of osteogenesis and possibilities for counteracting the bone damaging actions of glucocorticoids. An up-to-date understanding of the mechanisms by which vanadium acts and of its currently identified targets is prerequisite to the intelligent design of experiments of this kind. In this review, we will consider mechanisms at the enzymological level, in cellular regulatory cascades, and events affecting the cell or organism as a whole. J. Trace Elem. Exp. Med. 16:281–290, 2003. © 2003 Wiley-Liss, Inc.

蛋白质磷酸化和去磷酸化调节细胞的许多机制。近年来，重点转向通过去磷酸化进行调节。目前的研究主要集中在蛋白质酪氨酸磷酸酶上。细胞调控研究人员使用钒作为探针，因为它在亚摩尔浓度下具有无与伦比的选择性抑制蛋白质酪氨酸磷酸酶的能力。本文综述了钒与细胞调控级联反应的生物学作用。最近的研究已经确定了以下方面的控制点和可能的药物靶点：1）胰岛素受体下游的葡萄糖控制机制；2）调节有丝分裂、肿瘤促进和生长因子受体下游其他事件的途径；3）成骨的调节以及对抗糖皮质激素的骨损伤作用的可能性。对钒的作用机制及其目前确定的靶点的最新了解是这类实验智能设计的先决条件。在这篇综述中，我们将考虑酶学水平、细胞调控级联中的机制，以及影响细胞或生物体整体的事件。J.Trace Elem。《实验医学》，16:281–2902003。©2003 Wiley-Liss，股份有限公司。

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引用次数: 15

Cadmium and human health: A perspective based on recent studies in China† 镉与人类健康：基于中国最近研究的观点†

The Journal of Trace Elements in Experimental Medicine

Pub Date : 2003-01-01 DOI: 10.1002/jtra.10039

Gunnar Nordberg

Cadmium (Cd) occurs in low concentrations in all human diets and in cigarettes. In contaminated areas and in certain occupations, high human exposures occur. In assessing risk to human health, it is important to identify the adverse effect that occurs at the lowest exposure level, i.e., the critical effect, which is crucial for preventive action. Excessive Cd exposure may give rise to renal, pulmonary, hepatic, skeletal, reproductive effects, and cancer. Previous evaluations (e.g., by WHO) have identified renal dysfunction, occurring in long-term Cd exposure, as the critical effect. However, skeletal and reproductive effects are also discussed as possible critical effects. For preventive action, information is important about exposure levels that give rise to the earliest (critical) effects. To gain new information on this issue, population groups in China exposed to high concentrations of Cd via rice and Cd-exposed workers were studied for possible renal, skeletal, and male reproductive toxicity. Skeletal effects in terms of decreased bone mineral density and an increased occurrence of fractures were found in groups of the general population living in the most Cd-exposed area. Our studies further show that renal effects measured by sensitive biomarkers, such as urinary content of beta-2-microglobulin, calcium, and N-acetyl-beta-D-glucosaminidase, occurs at lower cumulative exposures to Cd than those giving rise to skeletal effects and also at lower exposures than previously estimated, e.g., by WHO. The findings confirm the renal dysfunction as the critical effect of long-term Cd exposure. Metallothionein (MT) gene expression in peripheral blood lymphocytes was measured in Cd exposed workers. A higher prevalence of renal dysfunction was found among Cd exposed workers with low MT gene expression than among those with high MT gene expression, at similar blood and urinary Cd levels. MT gene expression in PBLC thus may be a biomarker for identifying sensitive population groups. J. Trace Elem. Exp. Med. 16:307–319, 2003. © 2003 Wiley-Liss, Inc.

镉（Cd）以低浓度存在于所有人类饮食和香烟中。在受污染的地区和某些职业中，会出现大量的人体暴露。在评估对人类健康的风险时，重要的是要确定在最低暴露水平下发生的不良影响，即临界影响，这对预防行动至关重要。过量接触镉可能导致肾、肺、肝、骨骼、生殖影响和癌症。先前的评估（例如世界卫生组织的评估）已确定长期镉暴露中发生的肾功能障碍是关键影响。然而，骨骼和生殖影响也被讨论为可能的关键影响。对于预防行动而言，关于最早（关键）影响的暴露水平的信息很重要。为了获得有关这一问题的新信息，对中国通过水稻和镉暴露工人暴露于高浓度镉的人群进行了可能的肾脏、骨骼和男性生殖毒性研究。在镉暴露最多地区的普通人群中，发现了骨密度降低和骨折发生率增加的骨骼效应。我们的研究进一步表明，通过敏感生物标志物（如尿中β-2-微球蛋白、钙和N-乙酰基-β-D-葡糖苷酶的含量）测量的肾效应，在累积暴露于镉的情况下发生，低于那些引起骨骼效应的情况，也低于世界卫生组织先前估计的暴露情况。研究结果证实，肾功能障碍是长期镉暴露的关键影响。测定了镉作业工人外周血淋巴细胞中金属硫蛋白（MT）基因的表达。在血液和尿液镉水平相似的情况下，MT基因表达低的镉暴露工人的肾功能障碍发生率高于MT基因表达高的工人。因此，MT基因在PBLC中的表达可能是鉴定敏感群体的生物标志物。J.Trace Elem。Exp.Med.16:307–3192003。©2003 Wiley-Liss，股份有限公司。

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引用次数: 63

Trace elements in human health and disease: An update 人类健康和疾病中的微量元素：最新进展

The Journal of Trace Elements in Experimental Medicine

Pub Date : 2003-01-01 DOI: 10.1002/jtra.10057

Ananda S. Prasad

引用次数: 113

Dietary boron: An overview of the evidence for its role in immune function† 膳食硼：其在免疫功能中作用的证据综述†

The Journal of Trace Elements in Experimental Medicine

Pub Date : 2003-01-01 DOI: 10.1002/jtra.10041

Curtiss D. Hunt

This review summarizes the evidence for boron essentiality across the biological spectrum with special focus on biochemical pathways and biomolecules relevant to immune function. Boron is an essential trace element for at least some organisms in each of the phylogenetic kingdoms Eubacteria, Stramenopila (brown algae and diatoms), Viridiplantae (green algae and familiar green plants), Fungi, and Animalia. Discovery of several of the currently recognized boron-containing biomolecules was achieved because the bound boron formed four coordinate covalent bonds with the ligand, creating a thermodynamically stable complex that is almost undissociable in water. Boron is a constitutive element in three antibiotics and a quorum-sensing signal in bacteria. It enhances Fc receptor expression and interleukin-6 production in cultured mammalian macrophages. Boron binds tightly to the diadenosine polyphosphates and inhibits the in vitro activities of various serine protease and oxidoreductase enzymes. Physiological amounts of dietary boron decrease skinfold thickness after antigen injection in gilts and elevated circulating natural killer cells after adjuvant injection in rats. It is predicted that several boron biomolecules waiting discovery are signaling molecules that interact with the cell surface and are probably composed of two mirror or near-mirror halves stabilized by a single boron atom to form a large circular bio

这篇综述总结了硼在整个生物光谱中的重要性，特别关注与免疫功能相关的生物化学途径和生物分子。硼是系统发育王国中至少一些生物的必需微量元素——真细菌、Stramenopila（褐藻和硅藻）、Viridiplantae（绿藻和常见的绿色植物）、真菌和动物。发现了几种目前公认的含硼生物分子，因为结合的硼与配体形成了四配位共价键，形成了一种热力学稳定的复合物，在水中几乎不可分解。硼是三种抗生素的组成元素，也是细菌的群体感应信号。它增强了培养的哺乳动物巨噬细胞中Fc受体的表达和白细胞介素-6的产生。硼与二腺苷多磷酸盐紧密结合，并抑制各种丝氨酸蛋白酶和氧化还原酶的体外活性。生理量的膳食硼在金边母猪注射抗原后降低了皮褶厚度，在大鼠佐剂注射后提高了循环自然杀伤细胞。据预测，几个等待发现的硼生物分子是与细胞表面相互作用的信号分子，可能由两个镜像或近镜像的半体组成，由一个硼原子稳定，形成一个大的圆形生物分子。J.Trace Elem。Exp.Med.16:291–3062003。出版于2003年，Wiley-Liss，股份有限公司。

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引用次数: 104

Experimental stress-induced changes in trace element levels of various tissues in rats 实验性应激诱导大鼠不同组织微量元素水平的变化

The Journal of Trace Elements in Experimental Medicine

Pub Date : 2003-01-01 DOI: 10.1002/jtra.10023

Yunus Karakoc, Ertan Yurdakos, Tevfik Gulyasar, Murat Mengi, U. Bora Barutcu

In this study, we investigated the effects of acute and chronic immobilization stress on the Zn, Cu, and Fe levels of the temporal lobe, brain stem, spleen, and liver tissues in rats. The animals in the acute stress group were put in the cages, one time only for 120 min. For the chronic stress groups (2h and 4h), the rats were kept in the cages daily for 2 and 4 h, respectively, for 5 consecutive days. Controls and immobilized rats were decapitated, and then tissue samples were taken. Zn, Cu, and Fe levels in the temporal lobe, brain stem, spleen, and liver were measured by flame atomic absorption spectrophotometer. Our results showed that acute immobilization stress causes endogenous Zn and Cu release from the brain tissues. In the 2h chronic stress group, Fe levels markedly increase in the temporal lobe and brain stem whereas they decrease in the spleen and liver. In the 4h chronic stress group, Fe levels increase in the temporal lobe and brain stem while Zn and Cu levels increase in the spleen and liver. In the acute and chronic immobilization stress groups, mobilization of Zn and Cu can be related to the induction of metallothionein (MT) in the liver and spleen but not in the brain. On the other hand, excess Fe in the temporal lobe and brain stem causes us to believe think that the brain iron transport proteins may be involved, and enhanced, by immobilization stress. J. Trace Elem. Exp. Med. 16:55–60, 2003. © 2003 Wiley-Liss, Inc.

在本研究中，我们研究了急性和慢性固定应激对大鼠颞叶、脑干、脾脏和肝组织锌、铜和铁水平的影响。急性应激组动物置于笼中，一次仅120分钟。对于慢性应激组（2小时和4小时），大鼠每天分别在笼中饲养2和4小时，连续5天。将对照组和固定大鼠斩首，然后采集组织样本。用火焰原子吸收分光光度计测定颞叶、脑干、脾脏和肝脏中的Zn、Cu和Fe水平。我们的研究结果表明，急性固定化应激会导致脑组织内源性锌和铜的释放。在2小时慢性应激组中，颞叶和脑干的Fe水平显著升高，而脾脏和肝脏的Fe水平降低。在4小时慢性应激组中，颞叶和脑干的Fe水平增加，而脾脏和肝脏的Zn和Cu水平增加。在急性和慢性固定应激组中，锌和铜的动员可能与肝和脾中金属硫蛋白（MT）的诱导有关，但与脑中的诱导无关。另一方面，颞叶和脑干中过量的铁使我们相信，大脑铁转运蛋白可能参与并增强了固定应激。J.Trace Elem。Exp.Med.16:55-602003。©2003 Wiley-Liss，股份有限公司。

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引用次数: 18