Author for correspondence: João Batista T. Rocha, Department of Chemistry, Center of Natural and Exact Sciences, Federal University of Santa Maria, 97105–900, Santa Maria, RS, Brazil (fax +55 55 220 8031, e-mail firstname.lastname@example.org).
Diphenyl Diselenide and Ascorbic Acid Changes Deposition of Selenium and Ascorbic Acid in Liver and Brain of Mice
Article first published online: 3 NOV 2003
Pharmacology & Toxicology
Volume 88, Issue 3, pages 119–125, March 2001
How to Cite
Jacques-Silva, M. C., Nogueira, C. W., Broch, L. C., Flores, É. M. M. and Rocha, J. B. T. (2001), Diphenyl Diselenide and Ascorbic Acid Changes Deposition of Selenium and Ascorbic Acid in Liver and Brain of Mice. Pharmacology & Toxicology, 88: 119–125. doi: 10.1034/j.1600-0773.2001.d01-92.x
- Issue published online: 3 NOV 2003
- Article first published online: 3 NOV 2003
- (Received June 21, 2000; Accepted October 11, 2000)
- Cited By
Abstract: Sodium selenite (Na2SeO3) is the selenium form used in the composition of dietary supplements, and diphenyl diselenide (PhSe)2 is an important intermediate in organic synthesis, which increases the risk of human exposure to this chemical in the workplace. These compounds have been reported to inhibit the cerebral and hepatic aminolevulinic acid dehydratase (ALA-D) in vitro, and now we show that ascorbic acid can reverse some alterations caused by in vivo selenium exposure, but not ALA-D inhibition. The effect of Na2SeO3 or (PhSe)2 and ascorbic acid on selenium distribution, total non-protein thiol, ascorbic acid content (liver and brain) and haemoglobin was also examined. Mice were exposed to 250 μmol/kg (PhSe)2, or 18.75 μmol/kg Na2SeO3 subcutaneously, and to ascorbic acid, twice a day, 1 mmol/kg intraperitonially, for 10 days. Hepatic ALA-D of mice treated with (PhSe)2 was inhibited about 58% and similar results were observed in the animals that received ascorbic acid supplementation (P<0.01, for (PhSe)2-treated and (PhSe)2+ascorbic acid-treated mice). The haemoglobin content decreased after treatment with (PhSe)2 (P<0.01). However, the haemoglobin content of the (PhSe)2+ascorbic acid group was significantly higher than in the (PhSe)2-treated mice (P<0.05), and similar to control (P>0.10). Ascorbic acid treatment decreased significantly the hepatic and cerebral deposition of Se in (PhSe)2-exposed mice (P<0.01). Hepatic non-protein thiol content was not changed by treatment with (PhSe)2, ascorbic acid or (PhSe)2+ascorbic acid. Hepatic content of ascorbic acid was twice that in mice that received (PhSe)2, independent of ascorbic acid treatment (P<0.001). The results of this study suggest that vitamin C may have a protective role in organodiselenide intoxication.