PubMed · 9139129
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1995. Dry cleaning.. https://pubmed.ncbi.nlm.nih.gov/9139129/
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Chlorinated drinking waters produced from humus-rich waters often have a high content of halogenated organic by-products which increases the mutagenicity of drinking water. With in vitro chlorination experiments we studied the formation of chloroform (CHCl3) and mutagenicity of artificially recharged ground water samples. The water samples where obtained from an artificial ground water plant which infiltrates humus-rich lake water through an esker island. The chlorination experiments showed that bank filtration reduced strongly the formation of chloroform and mutagenicity of chlorinated water. Reduction in the amount of chloroform and mutagenicity in chlorinated waters was strongly associated with the decrease in the total content of organic carbon and with the decrease in molecular weight of organic matter during bank filtration.
The base pair substitution mutational profiles induced by the heterocyclic amine cooked food mutagens PhlP and IQ in Salmonella typhimurium strains TA100 and TA1535 were determined by colony hybridization analysis. Both PhlP and IQ induced predominantly GC-->TA transversions in strain TA100 (rfa,delta uvrB/pKM101) with a pronounced preference for the second codon position (CCC--> CAC; 72% of total). PhlP also reverted strain TA1535 (rfa, delta uvrB) efficiently at concentrations similar to those required for strain TA100. In contrast to the PhlP-induced mutational profile observed in strain TA100, in strain TA1535 PhlP induced exclusively GC-->AT transitions at the second codon position (CCC-->CTC; 96-99% of total). Base substitution mutagenesis induced by heterocyclic amines related to PhlP is generally SOS-dependent, requiring the presence of plasmid pKM101 in Salmonella hisG46 strains. Thus, the SOS dependent reversion of S. typhimurium strain TA100 probably reflects error-prone lesion bypass at the major PhlP- guanosine adduct at the C-8 position. The GC-->AT transition mutations induced by PhlP in strain TA1535 appear to be SOS-independent, however, suggesting that these mutations may arise from the formation of PhlP-DNA adducts other than the replication-blocking C8-dG lesion.
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