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.

Binding of chromium to chromatin and DNA from liver and kidney of rats treated with sodium dichromate and chromium(III) chloride in vivo.

Abstract: The in vivo binding of chromium to whole chromatin, polynucleosomes, DNA, and cytoplasmic RNA-protein fraction from liver and kidney was examined after treatment of rats with sodium dichromate and chromium(III) chloride. Significant amounts of chromium were bound to DNA and the nonhistone proteins of chromatin and to cytoplasmic RNA-protein fraction. The binding of chromium to the nuclear and cytoplasmic nucleic acid fractions varied considerably, depending on the tissue and the oxidation state of the chromium administered. The level of chromium bound to whole chromatin was greater in the liver than in the kidney after treatment with either chromium compound. Chromium entered the liver and kidney tissues at a slower rate after chromium(III) treatment than after chromium(VI) treatment. At early times after chromium(VI) treatment, more chromium was bound to the liver and kidney chromatin and DNA than after chromium(III) treatment. A much smaller proportion of the chromium bound to chromatin was associated with the DNA after treatment with chromium(III) than after treatment with chromium(VI). However, 40 hr after injection, there was no significant difference in the level of chromium on the DNA from both the liver and kidney of chromium(VI)- and chromium(III)-treated animals. No DNA damage was detected in either liver or kidney nuclei after chromium(III) treatment, using the technique of alkaline elution. A possible correlation between chromium binding to chromatin and DNA damage is discussed.

Down-regulation of the DNA-repair endonuclease 8-oxo-guanine DNA glycosylase 1 (hOGG1) by sodium dichromate in cultured human A549 lung carcinoma cells.

Abstract: Hexavalent chromium is a genotoxic human pulmonary carcinogen that elevates DNA oxidation, apparently through the generation of reactive DNA-damaging intermediates including Cr(V), Cr(IV) and reactive oxygen species. We tested the hypothesis that elevation of DNA oxidation may also be through inhibition of the expression of the repair glycosylase for 8-oxo deoxyguanine (hOGG1) in cultured A549 human lung epithelial cells. Treatment with sodium dichromate (0-100 microM, 16 h) resulted in a concentration-dependent decrease in the levels of OGG1 mRNA as measured by both RT-PCR and RNase protection assay. Sodium dichromate at 25 microM and above gave a marked reduction of OGG1 mRNA expression which was not seen at 1 microM and below. No effect on the expression of the apurinic endonuclease hAPE or the house-keeping gene GAPDH was observed at any of the concentrations of sodium dichromate investigated. Treatment of cells with the pro-oxidant H(2)O(2) (0-200 microM) for 16 h had no detectable effect on the levels of OGG1 mRNA or protein expression suggesting that the effect of sodium dichromate is not mediated by H(2)O(2). Western blotting demonstrated that sodium dichromate (100 microM; 16 h and >25 microM; 28 h) markedly reduced levels of OGG1 protein in nuclear cell extracts. Additionally, treatment of cells with sodium dichromate (>25 microM, 28 h) resulted in a concentration-dependent decrease in the ability of nuclear extracts to nick a synthetic oligonucleotide containing 8-oxo deoxyguanine (8-oxo dG). We conclude that the elevation of 8-oxo dG levels observed in A549 cells treated with sodium dichromate may be, at least in part, due to a reduced capacity to repair endogenous and hexavalent chromium-induced 8-oxo dG.

Chromium (VI)-induced DNA damage in chick embryo liver and blood cells in vivo.

Abstract: Uptake of chromium (VI) and subsequent induction of DNA damage was examined in liver and blood cells of 14-day chick embryos after injection of sodium dichromate onto the inner shell membrane. Maximal loss of chromium from the inner shell membrane and distribution of chromium in liver, lung and blood was observed 2 h after injection. DNA strand breaks, interstrand cross-links and DNA--protein cross-links were measured using the alkaline elution technique. In chick embryo liver, chromium (VI) induced DNA cross-links in the absence of strand breaks. Maximal DNA cross-linking was detected in the liver 8 h after injection. Little or no DNA damage remained in the liver 10-24 h after injection. In contrast, chromium (VI) induced DNA strand breaks in the absence of cross-links in chick embryo blood cells. Maximal DNA strand breakage was observed in blood cells 8 h after injection. High levels of DNA strand breaks were present in blood cells even 24 h after treatment. These intra-embryonic tissue differences in chromium (VI)-induced DNA damage may be a result of the differences in glutathione, cytochrome P-450, other pathways of chromium (VI) metabolism or chromatin organization which exist in liver and blood cells.