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.

Mechanistic insights from the NTP studies of chromium.

Abstract: Hexavalent chromium (Cr(VI)) is a contaminant of water and soil and is a human lung carcinogen. Trivalent chromium (Cr(III)), a proposed essential element, is ingested by humans in the diet and in dietary supplements such as chromium picolinate (CP). The National Toxicology Program (NTP) demonstrated that Cr(VI) is also carcinogenic in rodents when administered in drinking water as sodium dichromate dihydrate (SDD), inducing neoplasms of the oral cavity and small intestine in rats and mice, respectively. In contrast, there was no definitive evidence of toxicity or carcinogenicity following exposure to Cr(III) administered in feed as CP monohydrate (CPM). Cr(VI) readily enters cells via nonspecific anion channels, in contrast to Cr(III), which cannot easily pass through the cell membrane. Extracellular reduction of Cr(VI) to Cr(III), which occurs primarily in the stomach, is considered a mechanism of detoxification, while intracellular reduction is thought to be a mechanism of genotoxicity and carcinogenicity. Tissue distribution studies in additional groups of male rats and female mice demonstrated higher Cr concentrations in tissues following exposure to Cr(VI) compared to controls and Cr(III) exposure at a similar external dose, indicating that some of the Cr(VI) escaped gastric reduction and was distributed systemically. The multiple potential pathways of Cr-induced genotoxicity will be discussed.

Application of response surface methodology for the extraction of chromium (VI) by emulsion liquid membrane

Abstract: Response surface methodology (RSM) is used to optimize the process parameters for the extraction of chromium from aqueous solution of waste sodium dichromate recovered from the pharmaceutical industry wastewater using emulsion liquid membrane technique. The liquid membrane used was composed of kerosene oil as the solvent, SPAN-80 as the surfactant and potassium hydroxide as internal reagent and trioctylamine as carrier. The process parameters namely, feed concentration, pH, internal reagent concentration and surfactant concentration on the extraction of chromium were optimized using Box–Behnken design. The optimum conditions for the extraction of chromium (VI) were: feed concentration (224.04 ppm), pH (2.76), internal reagent concentration (0.71 N) and surfactant concentration (1.92%, w/w). At the optimized condition the maximum chromium extraction was found to be 92.50%.

Possible role of glutathione in chromium(VI) metabolism and toxicity in rats.

Abstract: The effect of Cr(VI) on liver, kidney, and lung glutathione (GSH) levels and the effect of GSH depletion on Cr(VI)-induced nephrotoxicity were studied in male Sprague-Dawley rats (150-200 g). GSH levels, measured as nonprotein sulfhydryls, were determined between 0.5 and 26 hr after intraperitoneal injection of the maximum non-toxic dose of sodium dichromate (10 mg/kg). While Cr(VI) at this dose did not significantly change hepatic, renal, or pulmonary GSH levels, there appeared to be an initial decrease of hepatic GSH followed by an increase to approximately 120% of control between 5 and 12.5 hr after Cr(VI) treatment. The increase in hepatic GSH levels was significant 5 hr after treatment with 20 mg/kg sodium dichromate, was manifested as an increase in both non-protein sulfhydryls and total glutathione, and was prevented by L-buthionine sulfoximine (BSO) pretreatment. In rats pretreated with 4.0 mmol/kg BSO to deplete GSH, subsequent treatment with Cr(VI) further reduced hepatic GSH levels 2 hr after Cr(VI) treatment and inhibited weight gain in the first 24 hr after treatment. Intraperitoneal injection of Cr(VI) did not inhibit hepatic glutathione reductase activity, even at toxic doses. Depletion of renal GSH to approximately 25% of control with BSO potentiated the acute nephrotoxicity of 30 mg/kg sodium dichromate as measured by serum urea nitrogen levels and relative kidney weight. However, GSH depletion with BSO did not appear to affect the incidence of glucosuria, haematuria, or lysozymuria over a range of Cr(VI) doses, nor did it affect renal uptake of Cr. Taken together, these data show that GSH protects against the acute nephrotoxicity of Cr(VI), although it is not clear whether GSH is directly involved in the intracellular metabolism of Cr(VI) at non-toxic doses.