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Isotopes of chromium

About: Isotopes of chromium is a(n) research topic. Over the lifetime, 51 publication(s) have been published within this topic receiving 877 citation(s). The topic is also known as: Chromium Isotopes.
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Journal ArticleDOI
TL;DR: Chromium (CrCl3 · 6H2O), added in vitro to serum interfered with the subsequent color formation due to the addition of iron to siderophilin, and this interference occurred only at near saturation levels.
Abstract: 1. 1. Tracer and 1 μg/100 g body weight levels of 51Cr(III), given by stomach tube as hexaaquo chloride to rats, were at the highest level in the blood 1 h following administration. They subsequently decreased logarithmicly to 20% of the peak value after 24 h. 2. 2. Over 99% of the 51Cr in blood was associated with the non-cellular component. 3. 3. When given in vivo about 90% of the “carrier-free” 51Cr in the serum was found to be attached to the β-globulin fraction upon paper electrophoresis. 4. 4. Serum labelled in vitro with tracer amounts of 51Cr contained about 70% of the isotope in the β-globulin fraction. 5. 5. Starch-gel electrophoresis and subsequent autoradiography of serum labelled with trace amounts of 51Cr and/or 55Fe demonstrated that the 51Cr was located with the siderophilin in a patern similar to that of 55Fe. When siderophilin was precipated from 51Cr-labelled human serum, 80% of the isotopes was present in the precipitate. 6. 6. After application of excessive amounts of Cr(III) or Fe(II), a relative increase of the percentage of bound chromium at the expense of the β-globulin fraction was seen in all other serum protein fractions. 7. 7. Chromium (CrCl3 · 6H2O), added in vitro to serum interfered with the subsequent color formation due to the addition of iron to siderophilin. This interference occurred only at near saturation levels.

135 citations

Journal ArticleDOI
TL;DR: H2O2 exposure induces a dose‐dependent disturbance of intracellular calcium homeostatis and the rise in [Ca+++]i is mediated by exposure to H2 O2 in the early phase of the injury, and is not dependent on the continuing presence of the oxidant.
Abstract: The effects of exposure of cultured P388D1 cells to H2O2 on intracellular free calcium ([Ca++]i) was investigated utilizing the intracellular fluorescent calcium chelator "Quin 2." [Ca++]i rose from approximately 150 nM to greater than 2 microM over a time course that was strongly dependent on the concentration of H2O2 used (5 X 10(-5) to 5 X 10(-3) M). After exposure of P388D1 cells to 5 X 10(-3) M H2O2, Quin 2 was fully saturated between 15 and 30 min exposure. During this time, no apparent change in the rate of equilibration of 45Ca++ from the extracellular medium could be detected, whereas in cells preloaded with 45Ca, net 45Ca was lost from the cells at a greater rate than controls. Measurements of total cellular calcium by atomic absorption spectroscopy confirmed that there was a net loss of calcium from the cells during the first 30 min. At time points greater than 45 min after exposure to H2O2 the influx of extracellular 45Ca and net intracellular Ca++, Na+ and K+ rapidly increased. Half times for H2O2 catabolism by the cells varied from about 8 min at 5.0 X 10(-4) M H2O2 to 14.0 min at 5.0 X 10(-3) M. When the total [Ca++]i-buffering capacity of the Quin 2 pool was varied by increasing the loading of intracellular Quin 2 by 68-fold (1.1 X 10(2) - 7.6 X 10(3) amol per cell), the rate of rise of [Ca++]i was depressed by only 1.6-fold following exposure to 5 mM H2O2. During the rise of intracellular [Ca++]i, cell morphology was observed by both light and scanning electron microscopy and revealed that "surface blebs" appeared during this phase of injury. Both the rise in [Ca++]i and "blebbing" were observable before any loss in cell viability was detected by either loss of Trypan blue exclusion or loss of preloaded 51Cr from the cells. From these results we conclude the following, H2O2 exposure induces a dose-dependent disturbance of intracellular calcium homeostatis; the rise in [Ca++]i is mediated by exposure to H2O2 in the early phase of the injury, and is not dependent on the continuing presence of the oxidant; the rate of rise of [Ca++]i is largely independent of the quantity of calcium mobilized to the Quin 2 pool; during the early phase (less than 30 min) of rise of [Ca++]i, only intracellular calcium is involved in the response; these events occur concomitantly with gross morphological changes to the plasma membrane.(ABSTRACT TRUNCATED AT 400 WORDS)

123 citations

Journal ArticleDOI
Abstract: The interactions of chromium and proteins have been studied by various investigators. By tagging proteins with radioactive chromium, Grey and Stirling (1) demonstrated that plasma proteins bound tri valent chromium. Hexa valent chromium combined with hemoglobin only after reduction to the tri valent state. After undergoing reduction hexavalent chromium also interfered with nucleic acid determinations by combining with proteins (2). With an electrophoretic technic, no binding of hexavalent chromium to proteins could be detected; binding was postulated if the metal were converted to the trivalent form (3). Baetjer, Damron and Budacz (4) investigated the interactions of both tri- and hexavalent chromium with lung tissue. They found that only trivalent chromium was bound to the tissue; again hexavalent chromium had to undergo reduction to the trivalent state before it could combine with the lung tissue. Anderson (5) reported that skin, when treated with either tri- or hexavalent chromium bound considerable amounts to chromium. The blocking of certain functional groups in the skin had little effect on the amount of chromium bound. In these studies the oxidation state of the bound chromium was not determined; it was assumed that in the course of the reaction chromium remained in the original oxidation state.

54 citations

Journal ArticleDOI
TL;DR: SRIH had a profound effect on renal function in both IDD patients and NS, resulting in a reduction in RPF, GFR, and, as a consequence, Uvol.
Abstract: The acute effects of iv somatostatin (SRIH; 100 micrograms/h) on the urinary flow (Uvol), effective renal plasma flow (RPF), and glomerular filtration rate (GFR) were compared with those of a control infusion of 0.15 M NaCl in nine insulin-dependent diabetic (IDD) patients of less than 10 yr disease duration and six normal subjects (NS). RPF and GFR were measured using a standard primed constant isotope infusion of [125I]iodohippurate and [51Cr]chromium EDTA. Uvol, RPF, and GFR were measured during 20-min clearance periods. During the NaCl infusion mean Uvol, RPF, and GFR were 14.1 +/- 0.2 (+/- SEM), 708 +/- 4, and 150 +/- 1 mL/min in the IDD group and 12.7 +/- 0.4, 568 +/- 5, and 110 +/- 2 mL/min in the NS group, respectively. In the IDD patients Uvol, RPF, and GFR decreased from 16.6 +/- 1.8, 670 +/- 30, 146 +/- 4 mL/min pre-SRIH to 9.2 +/- 1 (P less than 0.001), 553 +/- 25 (P less than 0.001), and 130 +/- 5 (P less than 0.001) mL/min, respectively, at 120 min during the SRIH infusion. Similarly, in the NS group mean Uvol, RPF, and GFR were 14.2 +/- 0.6, 552 +/- 15, and 112 +/- 5 mL/min pre-SRIH and decreased to 7.4 +/- 0.6 (P less than 0.001), 422 +/- 7 (P less than 0.001), and 93 +/- 3 (P less than 0.001) mL/min, respectively, after 120 min of the SRIH infusion. SRIH, therefore, had a profound effect on renal function in both IDD patients and NS, resulting in a reduction in RPF, GFR, and, as a consequence, Uvol.

48 citations

Journal ArticleDOI
TL;DR: Results suggest that an injury of the lung epithelium could result from a HIV-specific CTL-induced immunologic conflict.
Abstract: HIV-related lymphocytic alveolitis is common in HIV-seropositive patients without lung infection or tumor. In some of them a fraction of alveolar lymphocytes are HIV-specific cytotoxic T-lymphocytes (CTL) bearing the CD8 and D44 cell surface markers and capable of killing HIV-infected alveolar macrophages. In order to evaluate the in vivo effect of these CTL on lung function, we measured the pulmonary clearance of aerosolized 99mTc-diethylene triamine penta-acetate (DTPA-CI) on 24 occasions in 22 patients with lymphocytic alveolitis. DTPA-CI has been selected as a highly sensitive test to detect injury of the lung epithelium. In 13 of the patients, we found a high DTPA-CI of 4.56 +/- 2.54%.min-1 (mean +/- SD), suggesting an increase of the epithelial permeability. The lymphocytic alveolitis was then characterized by a high cellularity, a high proportion of lymphocytes (59 +/- 18%), mainly composed of CD8+D44+ T-lymphocytes (149 +/- 109 cells/mm3), which spontaneously exhibited a cytolytic activity against the autologous alveolar macrophages in a standard 51Cr release assay. In the remaining 11 patients, DTPA-CI was normal (less than 1.78%.min-1), lymphocytic alveolitis being characterized by a low number or an absence of CD8+D44+ alveolar lymphocytes (9 +/- 13 cells/mm3) with no significant cytolytic activity. In the whole group, a significant correlation (r = 0.74, p = 0.0004) was found between the DTPA-CI and the number of CD8+D44+ lymphocytes and their cytotoxic activity against alveolar macrophages. Altogether, these results suggest that an injury of the lung epithelium could result from a HIV-specific CTL-induced immunologic conflict.

45 citations

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