Binding: Digital
Format: HTML
Label: Elsevier
Manufacturer: Elsevier
Publication Date: June 06, 2005
Publisher: Elsevier
Studio: Elsevier

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Product Description:
This digital document is a journal article from Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, published by Elsevier in 2005. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.

Description:
Stannous chloride was found genotoxic in microbial test systems of the yeast Saccharomyces cerevisiae, in one strain of Salmonella typhimurium and in the Mutoxitest of Escherichia coli. Five isogenic haploid yeast strains differing only in a particular repair-deficiency had the following ranking in Sn^2^+-sensitivity: rad52@D>rad6@D>rad2@D>rad4@D>RAD, indicating a higher relevance of recombinogenic repair mechanisms than nucleotide excision in repair of Sn^2^+-induced DNA damage. Sn^2^+-treated cells formed aggregates that lead to gross overestimation of toxicity when not undone before diluting and plating. Reliable inactivation assays at exposure doses of 25-75mM SnCl"2 were achieved by de-clumping with either EDTA- or phosphate buffer. Sn^2^+-induced reversion of the yeast his1-798, his1-208 and lys1-1 mutant alleles, in diploid and haploid cells, respectively, and putative frameshift mutagenesis (reversion of the hom3-10 allele) was observed. In diploid yeast, SnCl"2 induced intra-genic mitotic recombination while inter-genic (reciprocal) recombination was very weak and not significant. Yeast cells of exponentially growing cultures were killed to about the same extend at 0.1% of SnCl"2 than respective cells in stationary phase, suggesting a major involvement of physiological parameters of post-diauxic shift oxidative stress resistance in enhanced Sn^2^+-tolerance. Superoxide dismutases, but not catalase, protected against SnCl"2-induced reactive oxygen species as sod1@D had a three-fold higher sensitivity than the WT while the sod2@D mutant was only slightly more sensitive but conferred significant sensitivity increase in a sod1@D sod2@D double mutant. In the Salmonella reversion assay, SnCl"2 did not induce mutations in strains TA97, TA98 or TA100, while a positive response was seen in strain TA102. SnCl"2 induced a two-fold increase in mutation in the Mutoxitest strain IC203 (uvrA oxyR), but was less mutagenic in strain IC188 (uvrA). We propose that the mutagenicity of SnCl"2 in yeast and bacteria occurs via error-prone repair of DNA damage that is produced by reactive oxygen species.

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