首页 > 最新文献

The Journal of Trace Elements in Experimental Medicine最新文献

英文 中文
Side effects of lithium on rat cranial arachnoid and dura mater collagen: A quantitative ultrastructural study 锂对大鼠颅骨蛛网膜和硬脑膜胶原的副作用:定量超微结构研究
Pub Date : 2003-01-01 DOI: 10.1002/jtra.10022
Margaret Tzaphlidou
Lithium is widely used in medicine as an antidepressive drug. Despite abundant literature on the subject, questions on the effects of lithium on collagen, which is one of the major components of tissues and organs, are far from being answered. We have examined the effects of lithium chloride (1.5 meq/kg of body weight) on rat cranial arachnoid and dura mater collagen fibrils by electron microscopy and image analysis. Animals were sacrificed 1 day, 2, 6, and 12 months after the end of a 30-consecutive days experimental period. In all cases investigated, severe structural abnormalities in collagen fibrils, at the ultrastructural level, were found. These abnormalities consist of decreased mean diameter and irregularity of shape of collagen fibrils (when viewed in cross sections) as well as marked disorganization in the packing of the fibrils. The observed alterations seem to be permanent. J. Trace Elem. Exp. Med. 16:17–26, 2003. © 2003 Wiley-Liss, Inc.
锂作为一种抗抑郁药物被广泛应用于医学。尽管有大量关于这一主题的文献,但关于锂对胶原蛋白的影响的问题远未得到回答,胶原蛋白是组织和器官的主要成分之一。我们通过电子显微镜和图像分析研究了氯化锂(1.5meq/kg体重)对大鼠颅骨蛛网膜和硬脑膜胶原纤维的影响。在连续30天的实验期结束后1天、2个月、6个月和12个月处死动物。在所有研究的病例中,发现胶原原纤维在超微结构水平上存在严重的结构异常。这些异常包括胶原原纤维的平均直径减小和形状不规则(当在横截面中观察时),以及原纤维的堆积明显紊乱。观察到的变化似乎是永久性的。J.Trace Elem。Exp.Med.16:17-262003。©2003 Wiley-Liss,股份有限公司。
{"title":"Side effects of lithium on rat cranial arachnoid and dura mater collagen: A quantitative ultrastructural study","authors":"Margaret Tzaphlidou","doi":"10.1002/jtra.10022","DOIUrl":"https://doi.org/10.1002/jtra.10022","url":null,"abstract":"Lithium is widely used in medicine as an antidepressive drug. Despite abundant literature on the subject, questions on the effects of lithium on collagen, which is one of the major components of tissues and organs, are far from being answered. We have examined the effects of lithium chloride (1.5 meq/kg of body weight) on rat cranial arachnoid and dura mater collagen fibrils by electron microscopy and image analysis. Animals were sacrificed 1 day, 2, 6, and 12 months after the end of a 30-consecutive days experimental period. In all cases investigated, severe structural abnormalities in collagen fibrils, at the ultrastructural level, were found. These abnormalities consist of decreased mean diameter and irregularity of shape of collagen fibrils (when viewed in cross sections) as well as marked disorganization in the packing of the fibrils. The observed alterations seem to be permanent. J. Trace Elem. Exp. Med. 16:17–26, 2003. © 2003 Wiley-Liss, Inc.","PeriodicalId":101243,"journal":{"name":"The Journal of Trace Elements in Experimental Medicine","volume":"16 1","pages":"17-26"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/jtra.10022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72324476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Zinc status (plasma and hair zinc concentrations) during pregnancy: A longitudinal study† 妊娠期锌状况(血浆和头发锌浓度):一项纵向研究†
Pub Date : 2003-01-01 DOI: 10.1002/jtra.10046
A.O. Çavdar, F. Söylemez, B. Cengiz, F. Aydemir
A longitudinal study of plasma and hair zinc concentration analysis was performed in 51 and 38 pregnant women, respectively. Plasma zinc levels were followed from first trimester to the end of second trimester, whereas hair zinc concentrations were measured in all trimesters. They were all measured by atomic absorption spectrophotometer. Both plasma and hair zinc levels declined significantly during the second trimesters There was also a significant difference in plasma zinc levels between the “well-nourished” and “poorly nourished” groups (P < 0.001 and P < 0.05)Similar changes could not be observed for hair zinc concentrations, probably because of the fact that all pregnant women were from Ankara rather than from villages, where the dietary habit is frequently associated with zinc deficiency. J. Trace Elem. Exp. Med. 16:175–179, 2003. © 2003 Wiley-Liss, Inc.
分别对51名和38名孕妇进行了血浆和头发锌浓度分析的纵向研究。从妊娠早期到妊娠中期结束,对血浆锌水平进行跟踪,而在所有妊娠期测量头发锌浓度。它们都是用原子吸收分光光度计测量的。血浆和头发锌水平在孕中期都显著下降。“营养良好”组和“营养不良”组的血浆锌水平也有显著差异(P<;0.001和P<;0.05)头发锌浓度没有观察到类似的变化,可能是因为所有孕妇都来自安卡拉,而不是村庄,因为那里的饮食习惯经常与缺锌有关。J.Trace Elem。Exp.Med.16:175-1792003。©2003 Wiley-Liss,股份有限公司。
{"title":"Zinc status (plasma and hair zinc concentrations) during pregnancy: A longitudinal study†","authors":"A.O. Çavdar,&nbsp;F. Söylemez,&nbsp;B. Cengiz,&nbsp;F. Aydemir","doi":"10.1002/jtra.10046","DOIUrl":"https://doi.org/10.1002/jtra.10046","url":null,"abstract":"A longitudinal study of plasma and hair zinc concentration analysis was performed in 51 and 38 pregnant women, respectively. Plasma zinc levels were followed from first trimester to the end of second trimester, whereas hair zinc concentrations were measured in all trimesters. They were all measured by atomic absorption spectrophotometer. Both plasma and hair zinc levels declined significantly during the second trimesters There was also a significant difference in plasma zinc levels between the “well-nourished” and “poorly nourished” groups (P < 0.001 and P < 0.05)Similar changes could not be observed for hair zinc concentrations, probably because of the fact that all pregnant women were from Ankara rather than from villages, where the dietary habit is frequently associated with zinc deficiency. J. Trace Elem. Exp. Med. 16:175–179, 2003. © 2003 Wiley-Liss, Inc.","PeriodicalId":101243,"journal":{"name":"The Journal of Trace Elements in Experimental Medicine","volume":"16 4","pages":"175-179"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/jtra.10046","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72362791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 7
An overview of the role of iron in T cell activation 铁在T细胞活化中的作用综述
Pub Date : 2003-01-01 DOI: 10.1002/jtra.10047
Solo Kuvibidila, Raj P. Warrier, B. Surendra Baliga
Iron, an essential growth trace element, is required for proliferation of all living cells, including T lymphocytes. Many, though not all, immune responses require lymphocyte proliferation. Iron deficiency, a worldwide public health problem for children and for women of childbearing age, is associated with impaired lymphocyte proliferative responses to mitogens and cell-mediated immunity. However, the mechanisms have not been fully elucidated. Our data on certain early key events in the T cell activation pathways, obtained from iron-deficient murine splenic T lymphocytes, show reductions in hydrolysis of cell membrane phosphatidyl inositol 4,5 bisphosphate, protein kinase C activation, and interleukin-2 secretion. Although the expression of CD3 molecule (a component of the T cell-receptor/CD3 complex, required for T cell activation) is not decreased by iron deficiency in splenocytes and thymocytes, the expression of the co-stimulatory molecule, CD28, is. Iron-deficiency increases the percentage of CD3+/CD28− thymocytes but decreases that of CD3−/CD28+ cells. Iron deficiency and iron chelation by deferoxamine decrease CD28 fluorescence intensity but tends to increase that of CD3. Progression of activated spleen cells through the cell cycle (Go/G1, S, G2/M phases) is also altered by iron deficiency independently of differences in the percentages of CD3+ T cells between groups, probably through impaired transition of G1 to S phase. Data suggest that the role of iron in T cell proliferation is not limited to the regulation of ribonucleotide reductase activity, but also involves other steps in the T cell activation pathways. J. Trace Elem. Exp. Med. 16:219–225, 2003. © 2003 Wiley-Liss, Inc.
铁是一种重要的生长微量元素,是包括T淋巴细胞在内的所有活细胞增殖所必需的。许多(尽管不是全部)免疫反应需要淋巴细胞增殖。缺铁是世界范围内儿童和育龄妇女的公共卫生问题,与淋巴细胞对有丝分裂原的增殖反应和细胞介导的免疫受损有关。然而,其机制尚未完全阐明。我们从缺铁的小鼠脾脏T淋巴细胞获得的关于T细胞激活途径中某些早期关键事件的数据显示,细胞膜磷脂酰肌醇4,5二磷酸的水解、蛋白激酶C激活和白细胞介素-2分泌减少。尽管脾细胞和胸腺细胞中CD3分子(T细胞受体/CD3复合物的一种成分,T细胞活化所需)的表达不会因缺铁而降低,但共刺激分子CD28的表达是。缺铁会增加CD3+/CD28−胸腺细胞的百分比,但会降低CD3+/CD28+细胞的百分比。铁缺乏和去铁胺的铁螯合降低了CD28的荧光强度,但倾向于增加CD3的荧光强度。活化的脾细胞在细胞周期(Go/G1、S、G2/M期)中的进展也因缺铁而改变,与各组间CD3+T细胞百分比的差异无关,可能是由于G1期向S期的过渡受损。数据表明,铁在T细胞增殖中的作用不仅限于核糖核苷酸还原酶活性的调节,还涉及T细胞激活途径中的其他步骤。J.Trace Elem。Exp.Med.16:219–2252003。©2003 Wiley-Liss,股份有限公司。
{"title":"An overview of the role of iron in T cell activation","authors":"Solo Kuvibidila,&nbsp;Raj P. Warrier,&nbsp;B. Surendra Baliga","doi":"10.1002/jtra.10047","DOIUrl":"https://doi.org/10.1002/jtra.10047","url":null,"abstract":"Iron, an essential growth trace element, is required for proliferation of all living cells, including T lymphocytes. Many, though not all, immune responses require lymphocyte proliferation. Iron deficiency, a worldwide public health problem for children and for women of childbearing age, is associated with impaired lymphocyte proliferative responses to mitogens and cell-mediated immunity. However, the mechanisms have not been fully elucidated. Our data on certain early key events in the T cell activation pathways, obtained from iron-deficient murine splenic T lymphocytes, show reductions in hydrolysis of cell membrane phosphatidyl inositol 4,5 bisphosphate, protein kinase C activation, and interleukin-2 secretion. Although the expression of CD3 molecule (a component of the T cell-receptor/CD3 complex, required for T cell activation) is not decreased by iron deficiency in splenocytes and thymocytes, the expression of the co-stimulatory molecule, CD28, is. Iron-deficiency increases the percentage of CD3+/CD28− thymocytes but decreases that of CD3−/CD28+ cells. Iron deficiency and iron chelation by deferoxamine decrease CD28 fluorescence intensity but tends to increase that of CD3. Progression of activated spleen cells through the cell cycle (Go/G1, S, G2/M phases) is also altered by iron deficiency independently of differences in the percentages of CD3+ T cells between groups, probably through impaired transition of G1 to S phase. Data suggest that the role of iron in T cell proliferation is not limited to the regulation of ribonucleotide reductase activity, but also involves other steps in the T cell activation pathways. J. Trace Elem. Exp. Med. 16:219–225, 2003. © 2003 Wiley-Liss, Inc.","PeriodicalId":101243,"journal":{"name":"The Journal of Trace Elements in Experimental Medicine","volume":"16 4","pages":"219-225"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/jtra.10047","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72362800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 12
Pre- and post-transcriptional regulation of the Menkes disease gene Menkes病基因的转录前和转录后调控
Pub Date : 2003-01-01 DOI: 10.1002/jtra.10037
Edward D. Harris, Sudeep Majumdar
Menkes disease is testament to a copper (Cu)-ATPase (ATP7A) playing a dominant role in the absorption and homeostasis of Cu. Significantly, the proximal promoter region of the Menkes disease gene (MNK) has cis-active elements that relate to binding sites for transcription factors which in yeast are known to be activated by a low Cu status. A response to low Cu has not been rationalized into the control of Menkes gene expression, but seems important in light of recent Cu absorption studies in humans. The ATP7A gene gives rises to alternative transcripts, one of which has an insert at the 5′ end with sequence information for a protein with a structural domain similar to a Golgi tethering protein. This has opened speculation that one alternative transcript product may have an important biological function in regulating the entrance of ATP7A laded vesicles into the secretory pathway. This paper presents evidence supporting promoter activation and alternative splicing, pre- and post-transcription events respectively, in the control of Menkes disease gene expression. J. Trace Elem. Exp. Med. 16:181–189, 2003. © 2003 Wiley-Liss, Inc.
Menkes病证明了铜(Cu)-ATP酶(ATP7A)在Cu的吸收和稳态中发挥主导作用。值得注意的是,Menkes病基因(MNK)的近端启动子区具有顺式活性元件,这些元件与转录因子的结合位点有关,已知酵母中的转录因子会被低Cu状态激活。对低铜的反应尚未被合理化为对Menkes基因表达的控制,但鉴于最近对人类铜吸收的研究,这似乎很重要。ATP7A基因产生了替代转录物,其中一种在5′端有一个插入物,其中包含一种结构域类似于高尔基体系留蛋白的蛋白质的序列信息。这引发了人们的猜测,即一种替代转录产物可能在调节ATP7A修饰的囊泡进入分泌途径方面具有重要的生物学功能。本文提供的证据支持启动子激活和选择性剪接,分别在转录前和转录后事件,在控制门氏病基因表达。J.Trace Elem。《实验医学》,16:181–1892003。©2003 Wiley-Liss,股份有限公司。
{"title":"Pre- and post-transcriptional regulation of the Menkes disease gene","authors":"Edward D. Harris,&nbsp;Sudeep Majumdar","doi":"10.1002/jtra.10037","DOIUrl":"https://doi.org/10.1002/jtra.10037","url":null,"abstract":"Menkes disease is testament to a copper (Cu)-ATPase (ATP7A) playing a dominant role in the absorption and homeostasis of Cu. Significantly, the proximal promoter region of the Menkes disease gene (MNK) has cis-active elements that relate to binding sites for transcription factors which in yeast are known to be activated by a low Cu status. A response to low Cu has not been rationalized into the control of Menkes gene expression, but seems important in light of recent Cu absorption studies in humans. The ATP7A gene gives rises to alternative transcripts, one of which has an insert at the 5′ end with sequence information for a protein with a structural domain similar to a Golgi tethering protein. This has opened speculation that one alternative transcript product may have an important biological function in regulating the entrance of ATP7A laded vesicles into the secretory pathway. This paper presents evidence supporting promoter activation and alternative splicing, pre- and post-transcription events respectively, in the control of Menkes disease gene expression. J. Trace Elem. Exp. Med. 16:181–189, 2003. © 2003 Wiley-Liss, Inc.","PeriodicalId":101243,"journal":{"name":"The Journal of Trace Elements in Experimental Medicine","volume":"16 4","pages":"181-189"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/jtra.10037","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72362804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
High dietary fructose compared with corn starch does not heighten changes in copper absorption, retention, or status indicators in men fed low dietary copper†‡ 与玉米淀粉相比,高膳食果糖不会增加摄入低膳食铜的男性对铜的吸收、保留或状态指标的变化††
Pub Date : 2003-01-01 DOI: 10.1002/jtra.10021
David B. Milne, Forrest H. Nielsen
In experimental animals, high dietary fructose exacerbates signs of copper deficiency in rats. Thus, an experiment was performed to determine whether high dietary fructose affected copper metabolism and copper status indicators in healthy men who were fed low dietary copper. Six men aged 27 to 37 years completed a metabolic unit study divided into four 7-week dietary periods with a randomized, double-blind, 2 × 2 factorial design with variables of 0.6 or 2.6 mg Cu/2500 kcal and fructose or corn starch as 20% of energy. Twice during each dietary period the men consumed a standardized breakfast meal labeled with 2.5 μCi 67Cu, then were counted daily in a whole-body counter for 3 weeks after each meal. At the end of each dietary period, blood was collected to assess copper status. Neither type of dietary carbohydrate nor intake of copper significantly affected 67Cu absorption, but copper deprivation resulted in a negative copper balance. The source of dietary carbohydrate did not affect the biological half-life of copper, but it was significantly (P < 0.001) longer when dietary copper was low (35 ± 11 d; mean ± SD) than when supplemented (20 ± 5 days). The natural log of the biological half-life directly correlated with plasma copper (r = 0.498; P = 0.001) and immunoreactive, or radial immunodiffusion, ceruloplasmin (RID Cp; r = 0.394; P = 0.013), and was inversely related to glutathione (r = −0.510, P = 0.03). When high dietary fructose was fed, erythrocyte superoxide dismutase activity and RID Cp was lower, and the enzymatic ceruloplasmin/RID Cp ratio was higher during copper depletion than during repletion; just the opposite occurred when corn starch was fed. No other copper status indicator was affected by an interaction between dietary carbohydrate and copper or was heightened by high dietary fructose. The results indicate that men fed approximately 0.6 mg Cu/d for 7 weeks attempted to adapt to this low intake by retaining absorbed copper longer. The adaptation was inadequate because copper balance became negative. However, although copper status was decreased, the response of men to short-term dietary copper deprivation was not heightened by high dietary fructose. J. Trace Elem. Exp. Med. 16:27–38, 2003. © 2003 Wiley-Liss, Inc.
在实验动物中,高果糖会加重大鼠铜缺乏的症状。因此,进行了一项实验,以确定高膳食果糖是否影响摄入低膳食铜的健康男性的铜代谢和铜状态指标。六名年龄在27至37岁之间的男性完成了一项代谢单位研究,该研究采用随机、双盲、2×2析因设计,分为四个7周饮食期,变量为0.6或2.6 mg Cu/2500 kcal,果糖或玉米淀粉占能量的20%。在每个饮食期间,男性两次食用标有2.5μCi 67Cu的标准化早餐,然后在每餐后3周内每天在全身计数器中计数。在每个饮食期结束时,采集血液以评估铜的状况。无论是碳水化合物类型还是铜的摄入都不会显著影响67Cu的吸收,但铜缺乏会导致负铜平衡。膳食碳水化合物的来源不影响铜的生物半衰期,但当膳食铜较低时(35±11天;平均值±SD)比补充时(20±5天)明显(P<;0.001)长。生物半衰期的自然对数与血浆铜(r=0.498;P=0.001)和免疫反应性或放射免疫扩散性铜蓝蛋白(RID Cp;r=0.394;P=0.013)直接相关,与谷胱甘肽呈负相关(r=−0.510,P=0.03),并且酶促铜蓝蛋白/RID Cp比率在铜耗竭期间高于补充期间;当玉米淀粉被喂养时,情况正好相反。没有其他铜状态指标受到膳食碳水化合物和铜之间的相互作用的影响,或者被高果糖提高。结果表明,连续7周喂食约0.6mg/d铜的男性试图通过保持吸收的铜更长时间来适应这种低摄入量。由于铜平衡变为负,因此调整不充分。然而,尽管铜含量有所下降,但高果糖并没有提高男性对短期饮食铜缺乏的反应。J.Trace Elem。Exp.Med.16:27-382003。©2003 Wiley-Liss,股份有限公司。
{"title":"High dietary fructose compared with corn starch does not heighten changes in copper absorption, retention, or status indicators in men fed low dietary copper†‡","authors":"David B. Milne,&nbsp;Forrest H. Nielsen","doi":"10.1002/jtra.10021","DOIUrl":"https://doi.org/10.1002/jtra.10021","url":null,"abstract":"In experimental animals, high dietary fructose exacerbates signs of copper deficiency in rats. Thus, an experiment was performed to determine whether high dietary fructose affected copper metabolism and copper status indicators in healthy men who were fed low dietary copper. Six men aged 27 to 37 years completed a metabolic unit study divided into four 7-week dietary periods with a randomized, double-blind, 2 × 2 factorial design with variables of 0.6 or 2.6 mg Cu/2500 kcal and fructose or corn starch as 20% of energy. Twice during each dietary period the men consumed a standardized breakfast meal labeled with 2.5 μCi 67Cu, then were counted daily in a whole-body counter for 3 weeks after each meal. At the end of each dietary period, blood was collected to assess copper status. Neither type of dietary carbohydrate nor intake of copper significantly affected 67Cu absorption, but copper deprivation resulted in a negative copper balance. The source of dietary carbohydrate did not affect the biological half-life of copper, but it was significantly (P < 0.001) longer when dietary copper was low (35 ± 11 d; mean ± SD) than when supplemented (20 ± 5 days). The natural log of the biological half-life directly correlated with plasma copper (r = 0.498; P = 0.001) and immunoreactive, or radial immunodiffusion, ceruloplasmin (RID Cp; r = 0.394; P = 0.013), and was inversely related to glutathione (r = −0.510, P = 0.03). When high dietary fructose was fed, erythrocyte superoxide dismutase activity and RID Cp was lower, and the enzymatic ceruloplasmin/RID Cp ratio was higher during copper depletion than during repletion; just the opposite occurred when corn starch was fed. No other copper status indicator was affected by an interaction between dietary carbohydrate and copper or was heightened by high dietary fructose. The results indicate that men fed approximately 0.6 mg Cu/d for 7 weeks attempted to adapt to this low intake by retaining absorbed copper longer. The adaptation was inadequate because copper balance became negative. However, although copper status was decreased, the response of men to short-term dietary copper deprivation was not heightened by high dietary fructose. J. Trace Elem. Exp. Med. 16:27–38, 2003. © 2003 Wiley-Liss, Inc.","PeriodicalId":101243,"journal":{"name":"The Journal of Trace Elements in Experimental Medicine","volume":"16 1","pages":"27-38"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/jtra.10021","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72324473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 5
Effect of sodium selenite on lipids and lipid-metabolizing enzymes in N-nitrosodiethylamine-induced hepatoma-bearing rats 亚硒酸钠对N-亚硝基二乙胺诱导肝癌大鼠脂质及脂质代谢酶的影响
Pub Date : 2003-01-01 DOI: 10.1002/jtra.10018
C. Thirunavukkarasu, K. Selvedhiran, J. Prince Vijaya Singh, P. Senthilnathan, D. Sakthisekaran
As part of a substantial effort to curtail the adverse health effects posed by hepatoma, studies have been conducted to elucidate the possible mechanism for the anticarcinogenic action of sodium selenite against N-nitrosodiethylamine-induced hepatoma. Several investigations recognize selenium as potent antioxidant, as well as an anticarcinogen, in both animal and human systems. Sodium selenite was administered to Wistar rats bearing hepatoma induced by N-nitrosodiethylamine to study the alterations in the concentration of lipid profiles and in activities of some lipid-metabolizing enzymes. Control and tumor-bearing animals were fed 4 ppm of sodium selenite before initiation or during initiation and/or during promotion phases of carcinogenesis. Hepatic total cholesterol, free cholesterol, triglycerides, free fatty acids, and phospholipids were significantly lowered, whereas cholesterol esters was greater because of selenite administration in N-nitrosodiethylamine-induced tumor-bearing rats. Total lipase, lipoprotein lipase, lecithin: cholesterol acyl transferase, and cholesterol ester synthetase registered greater activities in hepatoma of selenite administered rats with tumor whereas the activity of cholesterol ester hydrolase in hepatoma-bearing animals was lower as a result of selenite administration. These observations clearly indicate the effect of selenite in correcting the abnormalities of lipid metabolism in tumor-induced animals. Previous evidence from this laboratory and present observations it can be concluded that the anticancer property of selenite my also be by its strong hypolipidemic capacity in vivo system. J. Trace Elem. Exp. Med. 16:1–15, 2003. © 2003 Wiley-Liss, Inc.
作为减少肝癌对健康造成的不良影响的实质性努力的一部分,已经进行了研究,以阐明亚硒酸钠对N-亚硝基二乙胺诱导的肝癌的抗癌作用的可能机制。几项研究表明,硒在动物和人类系统中都是一种强效抗氧化剂和抗癌原。用亚硒酸钠对N-亚硝基二乙胺诱发的Wistar大鼠肝癌进行研究,以研究脂质浓度和某些脂质代谢酶活性的变化。对照和荷瘤动物在致癌作用开始前、开始期间和/或促进阶段喂食4ppm的亚硒酸钠。在N-亚硝基二乙胺诱导的荷瘤大鼠中,肝脏总胆固醇、游离胆固醇、甘油三酯、游离脂肪酸和磷脂显著降低,而胆固醇酯更高,因为亚硒酸盐给药。总脂肪酶、脂蛋白脂肪酶、卵磷脂:胆固醇酰基转移酶和胆固醇酯合成酶在亚硒酸盐给药的肿瘤大鼠的肝癌中表现出更高的活性,而携带肝癌的动物的胆固醇酯水解酶的活性由于亚硒酸酯给药而较低。这些观察结果清楚地表明亚硒酸盐在纠正肿瘤诱导的动物脂质代谢异常中的作用。该实验室先前的证据和目前的观察结果可以得出结论,亚硒酸盐的抗癌特性也可能是由于其在体内系统中具有强大的降血脂能力。J.Trace Elem。Exp.Med.16:1–152003。©2003 Wiley-Liss,股份有限公司。
{"title":"Effect of sodium selenite on lipids and lipid-metabolizing enzymes in N-nitrosodiethylamine-induced hepatoma-bearing rats","authors":"C. Thirunavukkarasu,&nbsp;K. Selvedhiran,&nbsp;J. Prince Vijaya Singh,&nbsp;P. Senthilnathan,&nbsp;D. Sakthisekaran","doi":"10.1002/jtra.10018","DOIUrl":"https://doi.org/10.1002/jtra.10018","url":null,"abstract":"As part of a substantial effort to curtail the adverse health effects posed by hepatoma, studies have been conducted to elucidate the possible mechanism for the anticarcinogenic action of sodium selenite against N-nitrosodiethylamine-induced hepatoma. Several investigations recognize selenium as potent antioxidant, as well as an anticarcinogen, in both animal and human systems. Sodium selenite was administered to Wistar rats bearing hepatoma induced by N-nitrosodiethylamine to study the alterations in the concentration of lipid profiles and in activities of some lipid-metabolizing enzymes. Control and tumor-bearing animals were fed 4 ppm of sodium selenite before initiation or during initiation and/or during promotion phases of carcinogenesis. Hepatic total cholesterol, free cholesterol, triglycerides, free fatty acids, and phospholipids were significantly lowered, whereas cholesterol esters was greater because of selenite administration in N-nitrosodiethylamine-induced tumor-bearing rats. Total lipase, lipoprotein lipase, lecithin: cholesterol acyl transferase, and cholesterol ester synthetase registered greater activities in hepatoma of selenite administered rats with tumor whereas the activity of cholesterol ester hydrolase in hepatoma-bearing animals was lower as a result of selenite administration. These observations clearly indicate the effect of selenite in correcting the abnormalities of lipid metabolism in tumor-induced animals. Previous evidence from this laboratory and present observations it can be concluded that the anticancer property of selenite my also be by its strong hypolipidemic capacity in vivo system. J. Trace Elem. Exp. Med. 16:1–15, 2003. © 2003 Wiley-Liss, Inc.","PeriodicalId":101243,"journal":{"name":"The Journal of Trace Elements in Experimental Medicine","volume":"16 1","pages":"1-15"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/jtra.10018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72324475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 5
Association between oxidative stress and selenium levels in patients with breast cancer at different clinical stages 癌症不同临床阶段患者氧化应激与硒水平的关系
Pub Date : 2003-01-01 DOI: 10.1002/jtra.10030
Banu Sancak, Adem Ünal, Sakine Candan, Uḡur Coşkun, Nazan Günel
Oxidative stress has been suggested to play a role in some physiological conditions and in many disease processes, including carcinogenesis. The aim of the study was to investigate the association between the oxidative stress and selenium levels in the erythrocytes of breast cancer patients at different clinical stages. The extent of lipid peroxidation was assessed by measuring thiobarbituric acid reactive substances (TBARS), called malondialdehyde (MDA), in erythrocytes. Glutathione peroxidase activity (GPx) in erythrocyte and serum selenium levels were determined in patients and controls. Thirty-three female breast cancer patients at different clinical stages were divided into four groups. Ten control subjects were also included in this study. Atomic absorption, spectrophotometry, and colorimetric methods were used to obtain serum selenium and erythrocyte MDA levels, respectively. GPx activities were assessed with kinetic method described by Paglia and Valentine (J Lab Clin Med 1967; 70(1):158–169). All cancer patients (groups A, B, and C) showed significant increases in erythrocyte GPx activities compared with those in control subjects (P 0.05). Although plasma selenium levels did not change among the groups A, B, and C, it was demonstrated that breast cancer patients have lower serum selenium levels than healthy controls (P 0.05). Erythrocyte MDA levels were significantly lower (P < 0.05) in breast cancer patients who had had surgery within 1 month (group A) when compared with those levels in breast cancer patients who had just been diagnosed and had not had any surgery yet (group C). Although clinical stage in breast cancer does not have any effect on serum selenium levels or erythrocyte GPx activity, erythrocyte MDA levels changed among the patients at different clinical stages. Increased MDA levels in untreated patients show us increased oxidative stress. If we removed malignant breast tissue by surgery and gave adjuvant therapy, lipid peroxidation product MDA levels in erythrocyte would decrease. Increased GPx enzyme activity in erythrocytes may be a result of a protective mechanism that develops in breast cancer patients against free radical damage. Although an inverse correlation between the serum selenium levels and erythrocyte GPx activity in patients with breast cancer is suggested, there is no correlation at different clinical stages of patients. J Trace Elem. Exp. Med. 16:87–94, 2003. © 2003 Wiley-Liss, Inc.
氧化应激已被认为在一些生理条件和许多疾病过程中发挥作用,包括致癌作用。本研究旨在探讨癌症患者不同临床阶段红细胞氧化应激与硒水平之间的关系。通过测量红细胞中的硫代巴比妥酸反应物质(TBARS),即丙二醛(MDA)来评估脂质过氧化的程度。测定患者和对照组红细胞谷胱甘肽过氧化物酶活性(GPx)和血清硒水平。将33例处于不同临床阶段的女性癌症患者分为四组。本研究还包括10名对照受试者。采用原子吸收法、分光光度法和比色法分别测定血清硒和红细胞MDA水平。使用Paglia和Valentine描述的动力学方法评估GPx活性(J Lab Clin Med 1967;70(1):158-169)。与对照组相比,所有癌症患者(A、B、C组)红细胞GPx活性均显著升高(P<0.05)。不同临床阶段癌症患者之间无显著差异(P>0.05),结果发现癌症患者血清硒水平低于健康对照组(P<0.05),与对照组相比(P<0.05)。A组和B组在MDA水平方面没有差异(P>0.05)。与刚接受手术的癌症患者相比,在1个月内接受手术的癌症患者(A组)红细胞MDA水平显着降低(P<0.01)确诊且尚未进行任何手术(C组)。虽然癌症的临床分期对血清硒水平和红细胞GPx活性没有任何影响,但不同临床分期的患者红细胞MDA水平发生了变化。未经治疗的患者的MDA水平升高表明氧化应激增加。如果我们通过手术切除恶性乳腺组织并给予辅助治疗,红细胞中脂质过氧化产物MDA水平会降低。红细胞中GPx酶活性的增加可能是癌症患者对自由基损伤的保护机制的结果。尽管癌症患者血清硒水平与红细胞GPx活性呈负相关,但在患者的不同临床阶段没有相关性。J Trace Elem。Exp.Med.16:87-942003。©2003 Wiley-Liss,股份有限公司。
{"title":"Association between oxidative stress and selenium levels in patients with breast cancer at different clinical stages","authors":"Banu Sancak,&nbsp;Adem Ünal,&nbsp;Sakine Candan,&nbsp;Uḡur Coşkun,&nbsp;Nazan Günel","doi":"10.1002/jtra.10030","DOIUrl":"https://doi.org/10.1002/jtra.10030","url":null,"abstract":"Oxidative stress has been suggested to play a role in some physiological conditions and in many disease processes, including carcinogenesis. The aim of the study was to investigate the association between the oxidative stress and selenium levels in the erythrocytes of breast cancer patients at different clinical stages. The extent of lipid peroxidation was assessed by measuring thiobarbituric acid reactive substances (TBARS), called malondialdehyde (MDA), in erythrocytes. Glutathione peroxidase activity (GPx) in erythrocyte and serum selenium levels were determined in patients and controls. Thirty-three female breast cancer patients at different clinical stages were divided into four groups. Ten control subjects were also included in this study. Atomic absorption, spectrophotometry, and colorimetric methods were used to obtain serum selenium and erythrocyte MDA levels, respectively. GPx activities were assessed with kinetic method described by Paglia and Valentine (J Lab Clin Med 1967; 70(1):158–169). All cancer patients (groups A, B, and C) showed significant increases in erythrocyte GPx activities compared with those in control subjects (P 0.05). Although plasma selenium levels did not change among the groups A, B, and C, it was demonstrated that breast cancer patients have lower serum selenium levels than healthy controls (P 0.05). Erythrocyte MDA levels were significantly lower (P < 0.05) in breast cancer patients who had had surgery within 1 month (group A) when compared with those levels in breast cancer patients who had just been diagnosed and had not had any surgery yet (group C). Although clinical stage in breast cancer does not have any effect on serum selenium levels or erythrocyte GPx activity, erythrocyte MDA levels changed among the patients at different clinical stages. Increased MDA levels in untreated patients show us increased oxidative stress. If we removed malignant breast tissue by surgery and gave adjuvant therapy, lipid peroxidation product MDA levels in erythrocyte would decrease. Increased GPx enzyme activity in erythrocytes may be a result of a protective mechanism that develops in breast cancer patients against free radical damage. Although an inverse correlation between the serum selenium levels and erythrocyte GPx activity in patients with breast cancer is suggested, there is no correlation at different clinical stages of patients. J Trace Elem. Exp. Med. 16:87–94, 2003. © 2003 Wiley-Liss, Inc.","PeriodicalId":101243,"journal":{"name":"The Journal of Trace Elements in Experimental Medicine","volume":"16 2-3","pages":"87-94"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/jtra.10030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72316363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 11
Human exposure to mercury: The three modern dilemmas 人类汞暴露:现代三大困境
Pub Date : 2003-01-01 DOI: 10.1002/jtra.10050
Thomas W. Clarkson, Laszlo Magos, Gary J. Myers
{"title":"Human exposure to mercury: The three modern dilemmas","authors":"Thomas W. Clarkson,&nbsp;Laszlo Magos,&nbsp;Gary J. Myers","doi":"10.1002/jtra.10050","DOIUrl":"https://doi.org/10.1002/jtra.10050","url":null,"abstract":"","PeriodicalId":101243,"journal":{"name":"The Journal of Trace Elements in Experimental Medicine","volume":"16 4","pages":"321-343"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/jtra.10050","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72362799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 77
Zinc and immunity: Molecular mechanisms of zinc action on T helper cells† 锌与免疫:锌对T辅助细胞作用的分子机制†
Pub Date : 2003-01-01 DOI: 10.1002/jtra.10056
Ananda S. Prasad
The essentiality of zinc for humans was recognized in 1963. It is now evident that nutritional deficiency of zinc in human populations throughout the developing world is common. The major factor responsible for this deficiency is the consumption of mainly cereal proteins rich in phytate. The clinical manifestations of zinc deficiency include growth retardation and male hypogonadism in the adolescents, rough skin, poor appetite, mental lethargy, delayed wound healing, cell-mediated immune dysfunctions, and abnormal neurosensory disorders. A conditioned deficiency of zinc has been observed in many diseased states. In this work I have summarized our current knowledge concerning the molecular mechanisms of zinc action on T helper cells. Our studies showed that in zinc-deficient HUT-78 cells, phosphorylated IκB and Iκk, ubiquitinated IκB, and binding of nuclear factor (NF)-κB to DNA were significantly decreased. Zinc increased the translocation of NF-κB from cytosol to nucleus. These data show that zinc plays an important role in the activation of NF-κB in HUT-78 cells. We showed a significant effect of zinc on gene expression of interleukin (IL)-2 and IL-2 receptors α and β. We also showed that a decrease in gene expression of IL-2 and its receptors in zinc-deficient HUT-78 cells may be the result of decreased activation of NF-κB in zinc-deficient cells. J. Trace Elem. Exp. Med. 16:139–163, 2003. © 2003 Wiley-Liss, Inc.
锌对人类的重要性在1963年得到承认。现在很明显,在整个发展中世界的人口中,锌的营养缺乏是很常见的。造成这种缺乏的主要因素是主要消耗富含植酸酶的谷物蛋白质。缺锌的临床表现包括青少年生长迟缓和男性性腺功能减退、皮肤粗糙、食欲差、精神嗜睡、伤口愈合延迟、细胞介导的免疫功能障碍和异常神经感觉障碍。在许多患病状态下,已经观察到锌的条件性缺乏。在这项工作中,我总结了我们目前关于锌对T辅助细胞作用的分子机制的知识。我们的研究表明,在缺锌的HUT-78细胞中,磷酸化的IκB和Iκk、泛素化的I NF-κB以及核因子(NF)-κB与DNA的结合显著降低。锌增加了NF-κB从胞质溶胶向细胞核的移位。这些数据表明,锌在HUT-78细胞中的NF-κB活化中起着重要作用。我们发现锌对白细胞介素(IL)-2和IL-2受体α和β的基因表达有显著影响。我们还发现,锌缺乏的HUT-78细胞中IL-2及其受体基因表达的减少可能是锌缺乏细胞中NF-κB活化减少的结果。J.Trace Elem。《实验医学》,16:139-1632003。©2003 Wiley-Liss,股份有限公司。
{"title":"Zinc and immunity: Molecular mechanisms of zinc action on T helper cells†","authors":"Ananda S. Prasad","doi":"10.1002/jtra.10056","DOIUrl":"https://doi.org/10.1002/jtra.10056","url":null,"abstract":"The essentiality of zinc for humans was recognized in 1963. It is now evident that nutritional deficiency of zinc in human populations throughout the developing world is common. The major factor responsible for this deficiency is the consumption of mainly cereal proteins rich in phytate. The clinical manifestations of zinc deficiency include growth retardation and male hypogonadism in the adolescents, rough skin, poor appetite, mental lethargy, delayed wound healing, cell-mediated immune dysfunctions, and abnormal neurosensory disorders. A conditioned deficiency of zinc has been observed in many diseased states. In this work I have summarized our current knowledge concerning the molecular mechanisms of zinc action on T helper cells. Our studies showed that in zinc-deficient HUT-78 cells, phosphorylated IκB and Iκk, ubiquitinated IκB, and binding of nuclear factor (NF)-κB to DNA were significantly decreased. Zinc increased the translocation of NF-κB from cytosol to nucleus. These data show that zinc plays an important role in the activation of NF-κB in HUT-78 cells. We showed a significant effect of zinc on gene expression of interleukin (IL)-2 and IL-2 receptors α and β. We also showed that a decrease in gene expression of IL-2 and its receptors in zinc-deficient HUT-78 cells may be the result of decreased activation of NF-κB in zinc-deficient cells. J. Trace Elem. Exp. Med. 16:139–163, 2003. © 2003 Wiley-Liss, Inc.","PeriodicalId":101243,"journal":{"name":"The Journal of Trace Elements in Experimental Medicine","volume":"16 4","pages":"139-163"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/jtra.10056","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72362801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Recent advances in cellular iron metabolism 细胞铁代谢研究进展
Pub Date : 2003-01-01 DOI: 10.1002/jtra.10035
Prem Ponka
Iron is essential for oxidation–reduction catalysis and bioenergetics, but unless appropriately shielded, iron plays a key role in the formation of toxic oxygen radicals that can attack all biological molecules. Hence, specialized molecules for the acquisition, transport, and storage (ferritin) of iron in a soluble nontoxic form have evolved. The delivery of iron to most cells occurs after the binding of transferrin to transferrin receptors on the cell membrane. The transferrin receptor complexes are then internalized by endocytosis, and iron is released from transferrin by a process involving endosomal acidification. Iron is then transported through the endosomal membrane by the Fe2+ transporter Nramp2/DMT1. Importantly, the identical transporter is involved in the absorption of inorganic iron in the duodenum, a process that is facilitated by the ferric reductase, Dcytb, which provides Fe2+ for Nramp2/DMT1. Organisms and cells have limited ability to excrete excess iron and only some specialized cells evolved active mechanisms to export iron. Iron release from these “donor cells” (primarily enterocytes and macrophages that recycle hemoglobin iron) is mediated by ferroportin 1. The ferroxidase activity of copper-containing proteins, hephaestin and ceruloplasmin, facilitates the movement of iron across the membranes of enterocytes and macrophages, respectively. Cells are also equipped with a regulatory system that controls iron levels in the labile pool. Levels of iron modulate the capacity of iron regulatory proteins to bind to the iron responsive elements present in the untranslated regions of mRNAs for several proteins involved in iron metabolism (e.g., ferritin, transferrin receptor, Nramp2); these associations, or lack of them, in turn control the expression of these proteins. Despite these homeostatic mechanisms, organisms often face the threat of either iron deficiency or iron overload. J. Trace Elem. Exp. Med. 16:201–217, 2003. © 2003 Wiley-Liss, Inc.
铁对氧化还原催化和生物能量学至关重要,但除非得到适当的保护,否则铁在形成可以攻击所有生物分子的有毒氧自由基方面发挥着关键作用。因此,以可溶性无毒形式获取、运输和储存铁的专门分子(铁蛋白)已经进化出来。铁向大多数细胞的递送发生在转铁蛋白与细胞膜上的转铁蛋白受体结合之后。转铁蛋白受体复合物随后通过内吞作用内化,铁通过内体酸化过程从转铁蛋白中释放。然后,铁通过Fe2+转运蛋白Nramp2/DMT1转运通过内涵体膜。重要的是,相同的转运蛋白参与十二指肠中无机铁的吸收,这一过程由铁还原酶Dcytb促进,Dcytb为Nramp2/DT1提供Fe2+。生物体和细胞排泄过量铁的能力有限,只有一些专门的细胞进化出输出铁的活性机制。这些“供体细胞”(主要是回收血红蛋白铁的肠细胞和巨噬细胞)的铁释放是由ferroportin 1介导的。含铜蛋白质铁蛋白和铜蓝蛋白的铁氧化酶活性分别促进铁穿过肠细胞和巨噬细胞膜的运动。细胞还配备了一个调节系统,控制不稳定池中的铁水平。铁水平调节铁调节蛋白与存在于mRNA的非翻译区中的铁反应元件结合的能力,用于参与铁代谢的几种蛋白质(例如,铁蛋白、转铁蛋白受体、Nramp2);这些结合,或缺乏这些结合,反过来又控制着这些蛋白质的表达。尽管有这些稳态机制,生物体经常面临缺铁或铁过载的威胁。J.Trace Elem。Exp.Med.16:201–2172003。©2003 Wiley-Liss,股份有限公司。
{"title":"Recent advances in cellular iron metabolism","authors":"Prem Ponka","doi":"10.1002/jtra.10035","DOIUrl":"https://doi.org/10.1002/jtra.10035","url":null,"abstract":"Iron is essential for oxidation–reduction catalysis and bioenergetics, but unless appropriately shielded, iron plays a key role in the formation of toxic oxygen radicals that can attack all biological molecules. Hence, specialized molecules for the acquisition, transport, and storage (ferritin) of iron in a soluble nontoxic form have evolved. The delivery of iron to most cells occurs after the binding of transferrin to transferrin receptors on the cell membrane. The transferrin receptor complexes are then internalized by endocytosis, and iron is released from transferrin by a process involving endosomal acidification. Iron is then transported through the endosomal membrane by the Fe2+ transporter Nramp2/DMT1. Importantly, the identical transporter is involved in the absorption of inorganic iron in the duodenum, a process that is facilitated by the ferric reductase, Dcytb, which provides Fe2+ for Nramp2/DMT1. Organisms and cells have limited ability to excrete excess iron and only some specialized cells evolved active mechanisms to export iron. Iron release from these “donor cells” (primarily enterocytes and macrophages that recycle hemoglobin iron) is mediated by ferroportin 1. The ferroxidase activity of copper-containing proteins, hephaestin and ceruloplasmin, facilitates the movement of iron across the membranes of enterocytes and macrophages, respectively. Cells are also equipped with a regulatory system that controls iron levels in the labile pool. Levels of iron modulate the capacity of iron regulatory proteins to bind to the iron responsive elements present in the untranslated regions of mRNAs for several proteins involved in iron metabolism (e.g., ferritin, transferrin receptor, Nramp2); these associations, or lack of them, in turn control the expression of these proteins. Despite these homeostatic mechanisms, organisms often face the threat of either iron deficiency or iron overload. J. Trace Elem. Exp. Med. 16:201–217, 2003. © 2003 Wiley-Liss, Inc.","PeriodicalId":101243,"journal":{"name":"The Journal of Trace Elements in Experimental Medicine","volume":"16 4","pages":"201-217"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/jtra.10035","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72362802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 15
期刊
The Journal of Trace Elements in Experimental Medicine
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1