Sodium dichromate

About: Sodium dichromate is a research topic. Over the lifetime, 421 publications have been published within this topic receiving 6202 citations. The topic is also known as: Disodium salt & sodium bichromate.

Chromium(VI)-induced DNA Lesions and Chromium Distribution in Rat Kidney, Liver, and Lung

Abstract: DNA lesions were detected in rat organ nuclei following an i.p. injection of sodium dichromate. Kidney, liver, and lung nuclei were examined for DNA interstrand cross-links, strand breaks, and DNA-protein cross-links using the alkaline elution technique. The time course for formation of cross-links in kidney nuclei revealed the presence of DNA interstrand and DNA-protein cross-links 1 hr after injection of sodium dichromate. By 40 hr in kidney, DNA interstrand cross-links had been repaired, but DNA-protein cross-links persisted. In liver nuclei, the time course for formation of cross-links after injection of dichromate showed a maximum in DNA-protein cross-linking at 4 hr and a maximum in DNA interstrand cross-linking at 2 hr. By 36 hr, in the liver, both types of lesions had been repaired. In lung nuclei, both DNA interstrand and DNA-protein cross-links were observed 1 hr after dichromate injection; however, by 36 hr, only DNA-protein cross-links persisted. No DNA lesions were detectable in kidney 1 hr after an i.p. injection of chromium(III) chloride. Chromium distribution in rat kidney, liver, and lung was measured and is discussed with respect to the observed DNA lesions. The lung and kidney may be more sensitive than liver to chromiuminduced DNA damage, an observation which correlates with the reported toxicity and carcinogenicity data for chromlum(VI) in both animals and humans.

Nanofiltration of concentrated aqueous salt solutions

Abstract: Nanofiltration processes using one or more conventional nanofiltration membrane modules under a positive applied pressure is used to selectively change the concentration of one solute, such as sodium chloride or sodium chlorate providing monovalent ions, from another solute such as sodium sulfate or sodium dichromate to provide multivalent ions in high salt aqueous concentrations. The process is particularly useful in favourably lowering the concentration of undesirable ions, particularly, of silica and dichromate ions in chloralkali and chlorate brine containing solutions and favourably raising the sodium sulphate level relative to sodium chloride in chloralkali liquor.

Metabolic deactivation of hexavalent chromium mutagenicity.

Abstract: Hexavalent chromium compounds (sodium dichromate, potassium chromate, chromic acid, basic zinc chromate and basic lead chromate) were found to be mutagenic for his − strains of S. typhimurium by inducing both frameshifts and base-pair substitutions. However, addition of either microsomal fractions from rat liver or of human erythrocyte lysates resulted in a complete loss of mutagenicity. As confirmed by chemical analysis, reversal of mutagenicity could be ascribed to reduction of the metal to the inactive trivalent form through a simple oxido-reductive reaction. In fact, reducing agents (ascorbic acid and sodium sulfite) and metabolites (GSH, DPNH and TPNH, either directly tested or obtained by mixing G6PD with S-9 mix) prevented hexavalent chromium mutagenicity, whereas an oxidizing agent (potassium permanganate) totally inhibited reversal of mutagenicity by liver and erythrocyte preparations. Enzymic conversion appeared to be involved in deactivation processes through a large production of TPNH via the hexose monophosphate oxidative pathway and other ancillary systems. On the other hand, microsomal preparations from rat lung displayed an extremely poor inactivating effect on chromium mutagenicity, and those from rat muscle, as well as human serum or plasma, were ineffective. These findings could bear relevance for the elective localization of chromium-induced tumors in human lung and could account for the results of animal carcinogenicity tests, which generally showed the development of tumors, but only at implant sites.

Influence of Dichromate Ions on Corrosion Processes on Pure Magnesium

Abstract: The corrosion behavior of Mg is of interest because of its growing use as an alloy in the transportation industry and also because it is a major component of some intermetallic phases in Al alloys, such as the deleterious S (Al 2 CoMg)-phase found in AA2024-T3. Pure Mg corrodes rapidly in a chloride-containing solution and even dissolves in water if the surface hydroxide is damaged by scratching the surface, for example. Uniform dissolution is drastically reduced in NaCl solutions (from 0.01 to 0.5 M) with the addition of very dilute concentrations of dichromate (10 -4 M). However, it is replaced by a strong localized attack in the form of fast filiform-like attack. On a large-grained sample with a defined defect structure, the attack can be seen to propagate at twin boundaries. Orientation imaging microscopy analysis found that corrosion was limited to planes near {0001} orientations with propagation being in prismatic directions. Auger electron spectroscopy analysis shows that interaction of chromate with the Mg hydroxide results in incorporation of reduced chromium ions in the hydroxide surface layer. Formation of a more resistant surface film could explain the very local nature of the corrosion in this case. The interaction between dichromate ions and Mg hydroxide can also explain the higher corrosion resistance of S-phase particles in chloride solutions containing dilute dichromate, although differences in the surface film formed compared to pure Mg are observed. Sputter-etching of the surface in order to assess the depth of the attack revealed that very hard or isolating corrosion products difficult to sputter are produced along the filiform path and that chromium compounds are not integrated in the corrosion products. Focused ion beam sectioning followed by scanning electron microscopy investigation of the sectioned area, demonstrates the presence of a continuous protective surface film. Adhesion between the Mg hydroxide and the metal is lost at the location of the corrosion filament, suggesting that the mechanism of propagation is similar to filiform corrosion under a coating. The depth of attack is a couple of micrometers with large cracks present within the corroded area that could induce severe surface damage.