The Journal of Trace Elements in Experimental Medicine最新文献

{"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}

{"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}

{"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}

{"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}

{"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}

{"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}

{"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}

{"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}

{"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}

{"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}