Disease relevance of disodium dioxido-dioxo-chromium

• The indicator system consists in sheep erythrocytes radiolabelled with sodium chromate (51Cr) and coated with protein A of Staphylococcus aureus (51Cr-labelled ES) [1].
• Effector cells were incubated with live herpes simplex virus-1, ultraviolet-inactivated herpes simplex virus-1, or media alone for 18 hours at 37 degrees C. K562 target cells were used in a sodium chromate release assay with an effector-to-target cell ratio of 100:1 [2].
• Ten patients with atopic dermatitis and ten healthy control subjects, matched for age, sex, and skin color, were studied for their peripheral blood natural cell-mediated cytotoxic activity against K-562 human leukemia cell line target cells, using the sodium chromate Cr 51 release assay [3].
• In a series of normal volunteers and patients with vasculitis a strict correlation has been found between this in vitro assay and the measure of splenic clearance of IgG-coated red blood cells (RBC), the classical approach for studying in vivo macrophage Fc-receptor function by using sodium chromate 51Cr as tag [4].
• Our study focused on examining the role of XRCC1 in sodium chromate-induced cytotoxicity and chromosomal aberrations in Chinese Hamster Ovary (CHO) cells [5].

High impact information on disodium dioxido-dioxo-chromium

• Furthermore, ESR studies suggested that tetraperoxochromate(V) is formed by the reaction of sodium chromate(VI) with hydrogen peroxide [6].
• Using a cyt c-specific monoclonal antibody, we observed a dose-dependent release of mitochondrial cyt c in cytosolic extracts of CHO cells exposed to apoptogenic doses of sodium chromate [7].
• As a model system, 2-(cyclohexylamino)ethanesulfonic acid (CHES) was used to buffer the indirect detection electrolyte of sodium chromate [8].
• Exposing cells to water soluble sodium chromate under conditions which produced similar time-dependent intracellular concentrations of chromium also produced a similar amount and spectrum of chromosome damage as lead chromate [9].
• Effect of vitamin E on survival, glutathione reductase and formation of chromium (V) in Chinese hamster V-79 cells treated with sodium chromate (VI) [10].

Biological context of disodium dioxido-dioxo-chromium

• Thirty micromolar sodium chromate (96% survival), which caused the least DNA damage, had no effect on GRP78 induction, general RNA synthesis, or mRNA synthesis [11].
• Studies with nonradioisotopic sodium chromate. I. Development of a technique for measuring red cell volume [12].
• HSAE cells exposed to lead chromate and sodium chromate underwent dose-dependent apoptosis [13].
• Chemotaxis was measured by radioactive counting of sodium chromate Cr 51 granulocytes migrating in modified Boyden chambers [14].
• Ten micromolar sodium chromate induced profound cell cycle delay and no metaphases were found [15].

Anatomical context of disodium dioxido-dioxo-chromium

• Treatment of chick embryo hepatocytes with 5 microM sodium chromate for 2 h caused the formation of DNA strand breaks, DNA interstrand cross-links, and DNA-protein cross-links [16].
• Cell-rich plasma from human peripheral blood was labeled with disodium chromate (51Cr) and diisopropylfluorophosphate (DF32P), and the uptake and distribution of the radionuclides by granulocytes, lymphocytes, monocytes, and erythrocytes were studied [17].
• The two lowest chromium doses used resulted in biologically relevant adduct levels (6 and 21 adducts per 1,000 DNA nucleotides) comparable with those measured in nuclear matrix DNA from cells treated with a 50% cytotoxic dose of sodium chromate in vivo [18].
• (51CR) sodium chromate incorporation ito the soluble protein fractin of the human erythrocyte: binding not associated with the hemoglobin monomeric subunit [19].
• In addition we investigated the effects of soluble hexavalent chromium, sodium chromate, in this cell line [15].

Associations of disodium dioxido-dioxo-chromium with other chemical compounds

• ESR studies using hydroxyl radical traps demonstrated that hydroxyl radical is generated both during the reaction of sodium chromate(VI) with hydrogen peroxide and the decomposition of potassium tetraperoxochromate(V), and that hydroxyl radical reacts significantly not only with mononucleotides but also with deoxyribose 5-phosphate [6].
• The carrier electrolyte consisted of 10 mM sodium chromate, 3 mM tetradecyltrimethyl-ammonium hydroxide (TTAOH), 2 mM sodium carbonate, and 1 mM sodium hydroxide, adjusted to a pH 11.0 +/- 0 [20].
• The effects of sodium chromate and carbon tetrachloride on the urinary excretion and tissue distribution of cadmium in cadmium-pretreated rats [21].
• The electrolyte consisted of 4.7 mM sodium chromate, 4.0 mM electroosmotic flow modifier (OFM) hydroxide, 10 mM 2-(N-cyclohexylamino)ethanesulfonic acid and 0.1 mM calcium gluconate (pH 9.1) [22].
• Anion-exchange high-performance liquid chromatographic determination of ascorbic acid and hexavalent chromium in rat lung preparations after treatment with sodium chromate in vitro and in vivo [23].

Gene context of disodium dioxido-dioxo-chromium

• In this study, the effects of sodium chromate on the expression of the 78-kDa glucose-regulated protein (GRP78) gene and on general transcription were investigated with respect to the DNA damage induced by this agent [11].
• In addition, by using western blotting, we found that p53 protein levels increased fourfold to sixfold after exposure to sodium chromate [24].
• Eight of 10 malignant effusions/media suppressed the induction of lymphokine-activated killer cell cytotoxicity, as measured in a 4-hour sodium chromate release assay [25].
• Rat beta 2-microglobulin has been isolated from the urine of rats pretreated with sodium chromate [26].
• Rat cystatin C was purified to apparent homogeneity from rat urine after induction of a tubular dysfunction with sodium chromate [27].

Analytical, diagnostic and therapeutic context of disodium dioxido-dioxo-chromium

• The nephrotoxicant sodium chromate by contrast had no influence on the CC16 content of BALF but markedly increased CC16 levels in both serum and urine as a result of impaired glomerular filtration and tubular reabsorption, respectively [28].
• Rabbit alpha 1-microglobulin was purified from the urine of sodium-chromate-treated animals by the use of gel chromatography on Sephadex G-100, affinity chromatography on concanavalin-A--Sepharose and ion-exchange chromatography on DEAE-Sephadex [29].
• Rat alpha 1-microglobulin was isolated from the urine of rats treated with sodium chromate, and was purified by the use of gel chromatography, affinity chromatography on concanavalin-A-Sepharose and ion-exchange chromatography [30].
• Morphological changes indicative of apoptosis, as well as internucleosomal DNA fragmentation, were detectable by 24 hr after treatment with lead chromate or soluble sodium chromate [31].
• The movements of plastic microspheres (7 to 10 mu in diameter) and autologous RBCs labeled with sodium chromate Cr 51 from the vitreous to the anterior chamber were studied in 24 rabbit eyes [32].

References