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Genotoxicity of stannous chloride in yeast and bacteria
C Pungartnik1, C Viau, J Picada
1Dept. de Biofísica, Centro de Biotecnologia, UFRGS, Av. Bento Gonçalves 9500, 91507-970 Porto Alegre, RS, Brazil.
Abstract:
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 Sn2+ -sensitivity: rad52delta>rad6delta>rad2delta>rad4delta>RAD, indicating a higher relevance of recombinogenic repair mechanisms than nucleotide excision in repair of Sn2+ -induced DNA damage. Sn2+ -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 25-75 mM SnCl2 were achieved by de-clumping with either EDTA- or phosphate buffer. Sn2+ -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, SnCl2 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 SnCl2 than respective cells in stationary phase, suggesting a major involvement of physiological parameters of post-diauxic shift oxidative stress resistance in enhanced Sn2+ -tolerance. Superoxide dismutases, but not catalase, protected against SnCl2-induced reactive oxygen species as sod1delta had a three-fold higher sensitivity than the WT while the sod2delta mutant was only slightly more sensitive but conferred significant sensitivity increase in a sod1delta sod2delta double mutant. In the Salmonella reversion assay, SnCl2 did not induce mutations in strains TA97, TA98 or TA100, while a positive response was seen in strain TA102. SnCl2 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 SnCl2 in yeast and bacteria occurs via error-prone repair of DNA damage that is produced by reactive oxygen species.
Insights
Stannous chloride (SnCl2) is genotoxic in yeast and bacteria, primarily through reactive oxygen species and error-prone DNA repair. Yeast repair mechanisms involving recombination are more critical than nucleotide excision for DNA damage induced by SnCl2.
Area of Science:
- Genotoxicity testing
- Microbial mutagenesis assays
- DNA repair mechanisms
Background:
- Stannous chloride (SnCl2) is widely used, but its genotoxic potential requires thorough investigation.
- Understanding the mechanisms of SnCl2 genotoxicity is crucial for risk assessment.
Purpose of the Study:
- To evaluate the genotoxicity of stannous chloride (SnCl2) in microbial test systems.
- To elucidate the DNA repair pathways involved in SnCl2-induced genotoxicity.
- To investigate the role of reactive oxygen species (ROS) in SnCl2 mutagenicity.
Main Methods:
- Utilized Saccharomyces cerevisiae (yeast) strains with specific repair deficiencies (rad52delta, rad6delta, rad2delta, rad4delta).
- Employed Salmonella typhimurium reversion assays (strains TA97, TA98, TA100, TA102).
- Used the Mutoxitest of Escherichia coli (strains IC203 and IC188).
- Assessed the role of superoxide dismutases (SODs) and catalase in SnCl2-induced oxidative stress.
Main Results:
- SnCl2 demonstrated genotoxicity in yeast, Salmonella typhimurium strain TA102, and Escherichia coli Mutoxitest strain IC203.
- Yeast DNA repair involving recombination (rad52delta, rad6delta) was more critical than nucleotide excision (rad2delta, rad4delta) for SnCl2-induced DNA damage.
- SnCl2 induced intra-genic mitotic recombination in diploid yeast.
- Reactive oxygen species, particularly those targeted by superoxide dismutases, play a significant role in SnCl2 genotoxicity.
- Cell aggregation in SnCl2 solutions required specific buffer treatments (EDTA or phosphate) for accurate toxicity assessment.
Conclusions:
- SnCl2 is genotoxic in multiple microbial systems, acting via ROS-mediated DNA damage and subsequent error-prone repair.
- Recombinational DNA repair pathways are more important than nucleotide excision repair in mitigating SnCl2-induced DNA damage in yeast.
- Accurate genotoxicity testing requires addressing SnCl2-induced cell aggregation.
