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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | de Oliveira, Iuri Marques Degrandi, Tiago Hoerbe Jorge, Patrícia Mendes Saffi, Jenifer Rosa, Renato Moreira Guecheva, Temenouga Nikolova Henriques, João Antonio Pêgas |
| Description | Country affiliation: Brazil Author Affiliation: de Oliveira IM ( Departamento de Biofísica, Instituto de Biociências, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil.); Degrandi TH ( Departamento de Biofísica, Instituto de Biociências, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil.); Jorge PM ( Departamento de Biofísica, Instituto de Biociências, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil.); Saffi J ( Departamento de Ciências Básicas da Saúde, Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA), Porto Alegre, RS, Brazil.); Rosa RM ( Laboratório de Genética Toxicológica, Universidade Luterana do Brasil (ULBRA), Canoas, RS, Brazil.); Guecheva TN ( Departamento de Biofísica, Instituto de Biociências, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil. Electronic address: tgesheva@gmail.com.); Henriques JA ( Departamento de Biofísica, Instituto de Biociências, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil) |
| Abstract | The organoselenium compound, dicholesteroyl diselenide (DCDS) is a structural analogue of diphenyl diselenide (DPDS) and may be considered as a promising antioxidant drug in vivo. Nevertheless, little is known about the toxicological properties of DCDS. In the present study we evaluated the cytotoxic, genotoxic and mutagenic properties of DCDS in Chinese hamster lung fibroblasts (V79) and in strains of the yeast Saccharomyces cerevisiae, proficient and deficient in several DNA-repair pathways. The results with V79 cells show that DCDS induced cytotoxicity, GSH depletion and elevation of lipid peroxidation at lower concentrations than did DPDS. DCDS also generated single- and double-strand DNA breaks in V79 cells, both in the presence and in the absence of metabolic activation, as revealed by alkaline and neutral comet assays. Moreover, the induction of oxidative DNA base-damage was demonstrated by means of a modified comet assay with formamidopyrimidine-DNA glycosylase and endonuclease III. Treatment with DCDS also induced micronucleus formation in V79 cells as well as point and frame-shift mutations in a haploid wild-type strain of S. cerevisiae. Yeast mutants defective in base excision-repair proteins were the most sensitive to DCDS. Pre-incubation with N-acetylcysteine reduced DCDS's oxidative, genotoxic and mutagenic effects in yeast and in V79 cells. Our findings indicate that the presence of cholesteroyl substituents in DCDS results in elevation of its cytotoxic and genotoxic potential compared with that of DPDS in yeast and in V79 cells. However, due to dose-dependent contrasting behaviour of organoselenium compounds and differences in their toxicity in in vitro and in vivo systems, further studies are needed in order to establish the non-toxic concentration range for treatment in mammals. |
| File Format | HTM / HTML |
| ISSN | 13835718 |
| e-ISSN | 18793592 |
| Journal | Mutation Research/Genetic Toxicology and Environmental Mutagenesis |
| Volume Number | 763 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2014-03-15 |
| Publisher Place | Netherlands |
| Access Restriction | Open |
| Subject Keyword | Research Support, Non-u.s. Gov't Frameshift Mutation Cricetulus Oxidative Stress Toxicity Biological Markers Dna Damage Organoselenium Compounds Micronucleus Tests Dose-response Relationship, Drug Genetics Cell Line Cricetinae Discipline Genetics Cell Survival Discipline Biochemistry Drug Effects Comet Assay Cholesterol Chemically Induced Saccharomyces Cerevisiae Micronuclei, Chromosome-defective Animals Mutagens Lipid Peroxidation Toxicity Tests Analogs & Derivatives |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Health, Toxicology and Mutagenesis |
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