Effect of dietary zinc source and method of oral administration on performance and tissue trace mineral concentration of broiler chicks. (9/924)

Two experiments were conducted with chicks to examine the effect of high dietary levels of soluble sources of Zn on tissue Zn, Cu, and Fe concentrations as influenced by two methods of oral Zn administration from 14 to 21 d of age. Treatments included the basal diet (62 ppm Zn), basal diet supplemented with 1,000 ppm Zn from Zn sulfate, acetate, or chloride fed continuously, or basal diet plus crop intubation with a single oral dose of water (control) or 1,000 ppm Zn dietary equivalent from the sources based on feed intake from the previous day. In Exp. 2, crop-intubated doses were administered daily from 14 to 21 d of age. In Exp. 1, chicks given Zn by gavage decreased (P < .0001) feed intake at 24 h after oral dose compared with chicks fed either the control or high-Zn diets. After the gavage dosing stopped, feed intake was similar among treatments. Bone Zn was increased (P < .0001) by Zn source and was greater at 24 than at 168 h after dosing by gavage. In chicks given a single gavage dose of Zn, liver and kidney Zn measured at 24 h after oral dosing was greater (P < .0001) than at 168 h. In birds given a single oral dose of Zn, time x Zn source interactions were observed in pancreas (P < .0001), mucosal cells (P < .01), and remaining intestinal tract segments (P < .001). In Exp. 2, greater bone, pancreas, kidney (P < .0001), and liver (P < .001) Zn accumulations were observed in chicks given daily gavage doses of Zn compared with those fed Zn in diets. Zinc from the four sources was absorbed and stored in tissues to a similar extent.  (+info)

Aluminum, iron, lead, cadmium, copper, zinc, chromium, magnesium, strontium, and calcium content in bone of end-stage renal failure patients. (10/924)

BACKGROUND: Little is known about trace metal alterations in the bones of dialysis patients or whether particular types of renal osteodystrophy are associated with either increased or decreased skeletal concentrations of trace elements. Because these patients are at risk for alterations of trace elements as well as for morbidity from skeletal disorders, we measured trace elements in bone of patients with end-stage renal disease. METHODS: We analyzed bone biopsies of 100 end-stage renal failure patients enrolled in a hemodialysis program. The trace metal contents of bone biopsies with histological features of either osteomalacia, adynamic bone disease, mixed lesion, normal histology, or hyperparathyroidism were compared with each other and with the trace metal contents of bone of subjects with normal renal function. Trace metals were measured by atomic absorption spectrometry. RESULTS: The concentrations of aluminum, chromium, and cadmium were increased in bone of end-stage renal failure patients. Comparing the trace metal/calcium ratio, significantly higher values were found for the bone chromium/calcium, aluminum/calcium, zinc/calcium, magnesium/calcium, and strontium/calcium ratios. Among types of renal osteodystrophy, increased bone aluminum, lead, and strontium concentrations and strontium/calcium and aluminum/calcium ratios were found in dialysis patients with osteomalacia vs the other types of renal osteodystrophy considered as one group. Moreover, the concentrations of several trace elements in bone were significantly correlated with each other. Bone aluminum was correlated with the time on dialysis, whereas bone iron, aluminum, magnesium, and strontium tended to be associated with patient age. Bone trace metal concentrations did not depend on vitamin D intake nor on the patients' gender. CONCLUSIONS: The concentration of several trace elements in bone of end-stage renal failure patients is disturbed, and some of the trace metals under study might share pathways of absorption, distribution, and accumulation. The clinical significance of the increased/decreased concentrations of several trace elements other than aluminum in bone of dialysis patients deserves further investigation.  (+info)

Effects of omitting vitamin and trace mineral premixes and(or) reducing inorganic phosphorus additions on growth performance, carcass characteristics, and muscle quality in finishing pigs. (11/924)

Three experiments were conducted to determine the effects of omitting vitamin and trace mineral premixes and(or) reducing inorganic phosphorus additions to finishing diets on growth performance, carcass characteristics, and muscle quality in pigs. In Exp. 1, a corn-soybean meal-based diet (.70% lysine, .65% Ca, and .55% P) was used as the control. Pigs (n = 128; average initial BW of 85.7 kg) were fed the control diet or the control diet without 1) the vitamin premix, 2) the trace mineral premix, or 3) both premixes. Omitting the premixes had no effect on ADG (P>.39); gain/feed (P>.17); carcass backfat thickness (P>.42); and marbling, color, and firmness of the longissimus muscle (P>.11). In Exp. 2, pigs (n = 128; average initial BW of 86.2 kg) were fed the control diet (.65% Ca and .53% P) used in Exp. 1 and the control diet without 1/3 (.56% Ca and .46% P), 2/3 (.51% Ca and .40% P), or all (.47% Ca and .31% P) of the added monocalcium phosphate (MCP). Omitting up to 2/3 of the MCP increased ADG (quadratic effect, P<.02) and had no effect on meat quality (P>.12), but backfat thickness increased slightly (quadratic effect, P<.02). In Exp. 3, pigs (n = 160; average initial BW of 86.6 kg) were fed the control diet used in Exp. 1 or the control without 1) the vitamin and trace mineral premixes, 2) 2/3 of the MCP, or 3) the premixes and 2/3 of the MCP. Treatment had no effects on ADG (P>.23), gain/feed (P>.94), stomach lesions (P>.37), or serum gamma globulins (P>.08). In conclusion, vitamin and trace mineral premixes and up to 2/3 of the supplemental MCP can be omitted during late finishing (i.e., approximately the final 30 d) to reduce nutrient excesses that increase cost of feeding and nutrients excreted in waste material.  (+info)

Experimental spinal cord injury: spatiotemporal characterization of elemental concentrations and water contents in axons and neuroglia. (12/924)

To examine the role of axonal ion deregulation in acute spinal cord injury (SCI), white matter strips from guinea pig spinal cord were incubated in vitro and were subjected to graded focal compression injury. At several postinjury times, spinal segments were removed from incubation and rapidly frozen. X-ray microanalysis was used to measure percent water and dry weight elemental concentrations (mmol/kg) of Na, P, Cl, K, Ca, and Mg in selected morphological compartments of myelinated axons and neuroglia from spinal cord cryosections. As an index of axon function, compound action potentials (CAP) were measured before compression and at several times thereafter. Axons and mitochondria in epicenter of severely compressed spinal segments exhibited early (5 min) increases in mean Na and decreases in K and Mg concentrations. These elemental changes were correlated to a significant reduction in CAP amplitude. At later postcompression times (15 and 60 min), elemental changes progressed and were accompanied by alterations in compartmental water content and increases in mean Ca. Swollen axons were evident at all postinjury times and were characterized by marked element and water deregulation. Neuroglia and myelin in severely injured epicenter also exhibited significant disruptions. In shoulder areas (adjacent to epicenter) of severely injured spinal strips, axons and mitochondria exhibited modest increases in mean Na in conjunction with decreases in K, Mg, and water content. Following moderate compression injury to spinal strips, epicenter axons exhibited early (10 min postinjury) element and water deregulation that eventually recovered to near control values (60 min postinjury). Na(+) channel blockade by tetrodotoxin (TTX, 1 microM) perfusion initiated 5 min after severe crush diminished both K loss and the accumulation of Na, Cl, and Ca in epicenter axons and neuroglia, whereas in shoulder regions TTX perfusion completely prevented subcellular elemental deregulation. TTX perfusion also reduced Na entry in swollen axons but did not affect K loss or Ca gain. Thus graded compression injury of spinal cord produced subcellular elemental deregulation in axons and neuroglia that correlated with the onset of impaired electrophysiological function and neuropathological alterations. This suggests that the mechanism of acute SCI-induced structural and functional deficits are mediated by disruption of subcellular ion distribution. The ability of TTX to reduce elemental deregulation in compression-injured axons and neuroglia implicates a significant pathophysiological role for Na(+) influx in SCI and suggests Na(+) channel blockade as a pharmacotherapeutic strategy.  (+info)

Trace element levels in drinking water and the incidence of colorectal cancer. (13/924)

We determined the levels of 15 elements in drinking water from 34 water treatment plants in Aomori Prefecture and studied how element levels relate to colorectal cancer incidence by district. Colorectal cancer incidence was calculated from the data of Aomori Colorectal Cancer Registry. Multiple regression analysis was performed by using age-adjusted incidences of rectal cancer and colon cancer by gender as object variables and each element level as an explanatory variable. The standardized partial regression coefficient was significant in gold (p < 0.01), magnesium (p < 0.01), selenium (p < 0.01) and tin (p < 0.05) for age-adjusted rectal cancer incidence in men as objective variable; in gold (p < 0.05), calcium (p < 0.01) and phosphorus (p < 0.01) with age-adjusted colon cancer incidence in men as the objective variable; and in sodium (p < 0.05), phosphorus (p < 0.05), tin (p < 0.05) and strontium (p < 0.01) with age-adjusted colon cancer incidence in women as the objective variable. These results confirm the need to further study trace elements in drinking water and food, and relationship to colorectal carcinogenesis.  (+info)

Human leukaemic cells. Determination of trace elements in nucleic acids and histones by neutron-activation analyses. (14/924)

Trace metals were measured by neutron-activation analyses in purified nucleic acids and histone(s) of lymphocytes from patients with acute lymphocytic leukaemia or infectious mononucleosis and from normal donor DNA isolated from lymphocytes of a patient with infectious mononucleosis and a normal donor showed a high a high content of Cr2+, Sb2+, Fe2+, and Zn2+, whereas DNA of lymphoblasts from a patient with acute lymphocytic leukaemia had a lower content of these trace metals, but the Co2+ content was 20-fold higher than in DNA or normal donor lymphocytic cells. Total histones from leukaemic cells had higher contents of most of the trace metals except for Zn2+, which was present in lesser concentration than in histones from normal donor lymphocytic cells. Lysine-rich (F1) histones showed lower contents of Cr2+, Sb2+ and Co2+, whereas arginine-rich (F3) histones had significantly higher contents of these trace metals. These observations may be of interest in that F3 histones more effectively inhibit RNA synthesis in human lymphocytic cells than do other species of histones.  (+info)

Changes in whole blood and serum components of grivet monkeys with experimental respiratory Francisella tularensis infection. (15/924)

Grivet monkeys infected with virulent Francisella tularensis Strain Schu S4 showed significant early changes in serum levels of trace metals, triglycerides and activities of alkaline phosphatase, lactate dehydrogenase and alpha-hydroxybutyrate dehydrogenase. Free amino acid levels decreased slightly and there was a marked increase in the phenylalanine: tyrosine ratio. Serum lysozyme activity and seromucoid levels also increased. Kanamycin therapy produced remission of overt signs but the changes in blood constituents were less readily affected. Immunization with the live vaccine strain of F. tularensis induced transient responses similar to those resulting from Schut S4 infection. Immunized monkeys subsequently challenged with the virulent Schu S4 strain showed no clinical signs or marked changes in blood constituents.  (+info)

Direct observation of trapping and release of nitric oxide by glutathione and cysteine with electron paramagnetic resonance spectroscopy. (16/924)

While the biosynthesis of nitric oxide (NO) is well established, one of the key issues that remains to be solved is whether NO participates in the biological responses right after generation through biosynthesis or there is a "secret passage" via which NO itself is trapped, transported, and released to exert its functions. It has been shown that NO reacts with thiol-containing biomolecules (RSH), like cysteine (Cys), glutathione (GSH), etc., to form S-nitrosothiols (RSNOs), which then release nitrogen compounds, including NO. The direct observation of trapping of NO and its release by RSNO has not been well documented, as most of the detection techniques measure the content of NO as well as nitrite and nitrate. Here we use spin-trapping electron paramagnetic resonance (EPR) technique to measure NO content directly in the reaction time course of samples of GSH and Cys ( approximately mM) mixed with NO ( approximately microM) in the presence of metal ion chelator, which pertains to physiological conditions. We demonstrate that NO is readily trapped by these thiols in less than 10 min and approximately 70-90% is released afterward. These data imply that approximately 10-30% of the reaction product of NO does not exist in the free radical form. The NO release versus time curves are slightly pH dependent in the presence of metal ion chelator. Because GSH and Cys exist in high molar concentrations in blood and in mammalian cells, the trapping and release passage of NO by these thiols may provide a mechanism for temporal and spatial sequestration of NO to overcome its concentration gradient-dependent diffusion, so as to exert its multiple biological effects by reacting with various targets through regeneration.  (+info)