Biomedical subjects

C Deininger

Publications and source records attributed to C Deininger.

21 records · Page 2Linked to original sources

PubMed1989

Induction of sfiA SOS function by peroxides using three different E. coli strains.

Five peroxides and two related compounds were tested for genotoxicity by the SOS Chromotest using 3 different E. coli strains (PQ37, PM21, GC4798). All tested hydroperoxides (hydrogen peroxide, tert-butylhydroperoxide, cumene hydroperoxide) were clearly positive in all strains. From a comparison of results obtained from the different strains it can be concluded that neither DNA lesions leading to the induction of excision repair nor covalent binding of radicals to DNA is responsible for the induction of sfiA-SOS function by hydroperoxides. Among the remaining compounds tested, only dibenzoylperoxide gave a clearly positive result in strain PQ37 whereas di-tert-butylperoxide and azobisisobutyronitrile showed only borderline activity. When using strains PM21 and GC4798, none of the latter compounds was positive. Paraquat was inactive in all strains.

DNA↗

PubMed1989

Induction of SOS repair by monofunctional methanesulphonates in various Escherichia coli strains. Structure-activity relationships in comparison with mutagenicity in Salmonella typhimurium.

Seventeen monofunctional alkylmethanesulphonates of widely varying structures were investigated in the SOS Chromotest using the Escherichia coli strains PM21, PQ37 and GC4798. As a measure of the SOS-inducing activity, the beta-galactosidase enzyme units (Up/mumol) were determined. Strains PM21 and PQ37 gave similar results in spite of the presence of different genetic markers. In general, the SN1 type secondary compounds (O-alkylation) induced higher SOS repair than the SN2 type primary compounds (N-alkylation). However, methylmethanesulphonate exerted the highest SOS induction of all tested strains, presumably due to its extremely high SN2 reactivity. In general, strain GC4798, which lacks 3-alkyladenine-DNA glycosylases I and II, was more sensitive towards monofunctional alkylating compounds and in particular towards the SN2 type compounds. A good correlation was found between the SOS repair response in the E. coli strains PM21 and PQ37 and the mutagenicity in Salmonella typhimurium TA100. There was, however, little correspondence when comparing the two measures used for the SOS-inducing activity in this work, the SOSIP (SOS-inducing potency) and the specific beta-galactosidase activity (Up/mumol). This effect was explained by the different toxicity corrections used for the calculation of the two measures. Whereas for the SOSIP value the single constitutive enzyme alkaline phosphatase is used, for the Up/mumol the absorbance at 600 nm, which indicates the growth delay (overall toxicity), is utilized. The influence of the toxicity corrections is discussed in more detail.

Alkylating Agents↗

PubMedDate not supplied

Identification and characterization of deoxyguanosine adducts of methyl vinyl ketone and ethyl vinyl ketone. Genotoxicity of the ketones in the SOS Chromotest.

The reaction of the alpha, beta-unsaturated ketones methyl vinyl ketone (MVK) and ethyl vinyl ketone (EVK) with nucleosides and 5'-mononucleotides was studied. The genotoxic activity of MVK and EVK in the SOS Chromotest was investigated. Three different types of adducts with deoxyguanosine were found and their structures elucidated: the cyclic 1,N2 adducts, the linear N7 adducts with one still-unreacted carbonyl function, and the cyclic 1,N2, linear N7, bis adducts. The spectroscopic and other relevant characterization data for the deoxyguanosine adducts and the corresponding guanine adducts are presented here together with details of the chromatographic methods used for isolation. The adducts described could also be isolated in the reactions of MVK and EVK with 2'-deoxyguanosine 5'-monophosphate. No adducts could be isolated either with nucleosides other than deoxyguanosine or with nucleotides other than 2'-deoxyguanosine 5'-monophosphate, indicating that the guanine moiety is the most reactive DNA constituent for MVK and EVK. MVK and EVK were clearly genotoxic in the SOS Chromotest according to the criteria of Quillardet and Hofnung. The formation of these adducts was proposed as the mechanism for the genotoxicity of MVK and EVK: all data available support the assumption that MVK and EVK represent a mutagenic and carcinogenic risk for mankind.

Butanones↗