The Journal of Trace Elements in Experimental Medicine最新文献

A copper balance study was performed during the successive 7 days when a patient with Wilson's disease went on a low-copper diet and was taking 1500 mg of trientine daily. The average copper intake was 944 μg/day, urine copper excretion was 503 μg/day, fecal copper excretion was 922 μg/day; therefore, trientine reduced body copper about 500 μg per day. We provide direct evidence that trientine maintains copper balance probably by enhancing both the urinary and fecal excretion, with a larger amount decoppered in the feces. J. Trace Elem. Exp. Med. 14:405–407, 2001. © 2001 Wiley-Liss, Inc.

Various molecular forms of chromium have been implicated in the regulation of glucose metabolism, and chromium deficiency can be associated with insulin resistance and impaired glucose tolerance. Protein-tyrosine phosphatases (PTPases), which negatively regulate signaling through the insulin receptor, are potential targets of chromium action, since this transition metal may inhibit catalysis at the thiol-dependent active sites of these enzymes. Treatment of cultured rat hepatoma cells with 0.1 mM CrCl₃ for 16 h increased the insulin-stimulated tyrosine phosphorylation of high M_r insulin receptor substrate (IRS) proteins by 49% to 7.3-fold over basal (n = 7; P= 0.03), without altering basal insulin receptor or IRS tyrosine phosphorylation or insulin-stimulated receptor autophosphorylation, suggesting a post-receptor effect of chromium on signal transduction. PTPase activity in cell extracts of CrCl₃-treated hepatoma cells before or after insulin stimulation was unchanged, indicating that if chromium acted via cellular PTPases, the effect was reversible and limited to the in vivo state. Chromium (Cr⁺³) ion and two organic derivatives, an oligopeptide chromium complex from bovine liver (Cr-pep), and a synthetic multinuclear complex of chromium with carboxylate ligands (Sm-Cr) were also tested for their direct in vitro inhibition of the enzymatic activity of LAR and PTP1B, two structurally variant PTPases that have been implicated in regulation of the insulin signaling pathway. PTP1B (rat and human) was strongly inhibited by CrCl₃ to 21–33% of control (n = 4–6; P< 0.001). In contrast, LAR activity was actually enhanced by CrCl₃ to 47% above the control value (n = 12; P< 0.001). The Cr-pep and Sm-Cr complexes had no effect on PTP1B and LAR activity at the tested concentrations using the pNPP assay. These data suggest that the metabolic effects of chromium may be mediated by inhibition of PTP1B, a PTPase that negatively modulates insulin signaling, consistent with other recent studies implicating PTP1B in the regulation of the dephosphorylation of post-insulin receptor substrate proteins. J. Trace Elem. Exp. Med. 14:393–404, 2001. © 2001 Wiley-Liss, Inc.

Chronic infection of iron-loaded coronary arteries by Chlamydia pneumoniae has been proposed as a heart disease risk factor. Another bacterial pathogen associated with increased risk for development of atherosclerosis is Coxiella burnetii. Like Chl. pneumoniae, C. burnetii is inhaled, multiplies in alveolar macrophages, subsequently becomes associated with arterial disease, and is enhanced by iron loading. J. Trace Elem. Exp. Med. 14:409–410, 2001. © 2001 Wiley-Liss, Inc.

Masculine infertility disorders are related to changes in trace element metabolism in the testis. In this study, toxic effects of thioacetamide in trace element (zinc, copper, selenium, and manganese) levels in the serum and testis of rats were studied at 1-, 4-, 8-, and 12-week posttreatment duration. A decrease in serum zinc, copper, and selenium was noticed whereas the level of these trace elements in the testis was increased. Manganese showed an increase in both serum and testis in response to thioacetamide treatment. Changes in trace element level showed structural damage in different organs such as the liver, kidney, and spleen. Further studies are needed to establish the effect of the changes in the level of trace elements in the structure and function of the testes of thioacetamide-treated rats. J. Trace Elem. Exp. Med. 14:383–392, 2001. © 2001 Wiley-Liss, Inc.

Lethal milk (lm) mutation in C57BL/6J inbred mice results in the reduction of zinc content in the milk and causes fatal neonatal zinc deficiency. Zinc injection to lm pups after birth helps them to overcome severe neonatal zinc deficiency and to maintain the normal body growth of lm pups. Thus, lm mutation displays a specific effect on the zinc content of the milk during lactation. The decrease in zinc content of the milk is not due to the low body zinc status in lactating lm dams. Also, oral zinc supplementation in lactating lm dams does not correct the low concentration of zinc in the milk. These findings suggest that lm mutation results in the defective cellular transport of zinc. The defective zinc transport might alter the expression of mammary genes because cellular zinc plays a critical role in diverse cellular functions. To investigate the effect of lm mutation on the expression of mammary genes, the differentially expressed cDNAs in lm mammary gland (MG) were explored using the mRNA differential display (DD) gel. One of the isolated cDNAs (M3) was expressed in the lm MG two times greater than that in the normal MG. The cloned partial M3 cDNA was shown to have the similarities to the unknown functional cDNAs in the yeast and human tissues. The M3 cDNA might have a common function in both lower and higher eukaryotes. The M3 mRNA is rich in the brain and the MG, but not in the liver and kidney. Hence, the M3 cDNA may have a certain function associated with the brain and the MG. More information regarding the cloned M3 cDNA might be provided by screening of the full length of M3 cDNA from cDNA library. J. Trace Elem. Exp. Med. 14:371–382, 2001. © 2001 Wiley-Liss, Inc.