Abstract

Organoselenium compounds have been pointed out as therapeutic agents. In contrast, the potential therapeutic aspects of tellurides have not yet been demonstrated. The present study evaluated the comparative toxicological effects of diphenyl diselenide (PhSe)2 and diphenyl ditelluride (PhTe)2 in mice after in vivo administration. Genotoxicity (as determined by comet assay) and mutagenicicity were used as end-points of toxicity. Subcutaneous administration of high doses of (PhSe)2 or (PhTe)2 (500 µmol/kg) caused distinct genotoxicity in mice. (PhSe)2 significantly decreased the DNA damage index after 48 and 96 h of its injection (p < 0.05). In contrast, (PhTe) caused a significant increase in DNA damage (p < 0.05) after 48 and 96 h of intoxication. (PhSe)2 did not cause mutagenicity but (PhTe)2 increased the micronuclei frequency, indicating its mutagenic potential. The present study demonstrated that acute in vivo exposure to ditelluride caused genotoxicity in mice, which may be associated with pro-oxidant effects of diphenyl ditelluride. In addition, the use of this compound and possibly other related tellurides must be carefully controlled.

Highlights

  • Selenium (Se) and Tellurium (Te) belongs to the chalcogen family, sharing similar electronic configuration and some chemical properties with sulfur (S) (Comasseto et al, 1997; Comasseto, 2010)

  • After 96 h, the group treated with (PhTe)2 presented diarrhea, low level of motor activity and a decrease in body weight; which is in accordance with previous finding from our laboratory (Maciel et al, 2000)

  • Comet assay After in vivo administration, diphenyl diselenide caused a significant decrease in DNA damage index (DI) both after 48 and 96 h

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Summary

Introduction

Selenium (Se) and Tellurium (Te) belongs to the chalcogen family, sharing similar electronic configuration and some chemical properties with sulfur (S) (Comasseto et al, 1997; Comasseto, 2010). The excess of selenium can be toxic due its ability to generate free radicals and catalyze thiol oxidation (Barbosa et al, 1998; Nogueira, Zen & Rocha, 2004; Rocha et al, 2012; Hassan & Rocha, 2012; Kade, Balogun & Rocha, 2013). The excess of free radical formation can damage mammalian tissues including thiol containing enzymes that are sensitive to pro-oxidant situations (Rocha et al, 2012; Rosa et al, 2007; Maciel et al, 2000). Diphenyl diselenide (PhSe), (Fig. 1) is a simple and stable organoselenium compound. How to cite this article Meinerz et al (2014), Differential genotoxicity of diphenyl diselenide (PhSe) and diphenyl ditelluride (PhTe).

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