The toxic effect of strained hydrocarbon 2,2'—bis (bicyclo[2.2.1]heptane) (BBH) was studied using whole-cell bacterial lux-biosensors based on Escherichia coli cells in which luciferase genes are transcriptionally fused with stress-inducible promoters. It was shown that BBH has the genotoxic effect causing bacterial SOS response however no alkylating effect has been revealed. In addition to DNA damage, there is an oxidative effect causing the response of OxyR/S and SoxR/S regulons. The most sensitive to BBH lux-biosensor was E . coli pSoxS-lux which reacts to the appearance of superoxide anion radicals in the cell. It is assumed that the oxidation of BBH leads to the generation of reactive oxygen species, which provide the main contribution to the genotoxicity of this substance.

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Here we present the study of the genotoxic effect of a 2,2’-bis(bicyclo[2.2.1]heptane) (BBH), which is promising as a fuel component for liquid rocket engines. The use of Escherichia coli lux-biosensors showed that in addition to DNA damage causing SOS-response, there is also an oxidative effect on cells. The greatest toxicity is determined by the mechanism of formation of superoxide anion radical and is detected by the lux biosensor E. coli pSoxS-lux, in which the genes of bacterial luciferases are transcriptionally crosslinked with the promoter of the soxS gene. It is assumed that the oxidation of BBH leads to the formation of reactive oxygen species, which should give the main contribution to the toxicity of this substance.

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Dicyclopropanated 5-vinyl-2-norbornene (dcpVNB) is a strained polycyclic hydrocarbon compound with a high energy content, which makes it promising for the development of propellant components based on it. In this work, the genotoxic properties of dcpVNB were studied using whole-cell lux-biosensors based on Escherichia coli and Bacillus subtilis. It was shown that the addition of dcpVNB to bacterial cells leads to the appearance of DNA damage inducing the SOS response and Dps expression with slight activation of the OxyR-mediated response to oxidative stress. The highest toxic effect of dcpVNB is detected by the following lux-biosensors: E. coli pColD-lux, E. coli pDps, B. subtilis pNK-DinC, and B. subtilis pNK-MrgA, in which the genes of bacterial luciferases are transcriptionally fused to the corresponding promoters: Pcda, Pdps, PdinC, and PmrgA. It was shown that lux-biosensors based on B. subtilis, and E. coli are almost equally sensitive to dcpVNB, which indicates the same permeability to this compound of cell wall of Gram-positive and Gram-negative bacteria. The activation of Pdps after dcpVNB addition maintains even in oxyR mutant E. coli strains, which means that the Pdps induction is only partially determined by the OxyR/S regulon. Comparison of specific stress effects caused by dcpVNB and 2-ethyl(bicyclo[2.2.1]heptane) (EBH), characterized by the absence of cyclopropanated groups, shows that structural changes in hydrocarbons could significantly change the mode of toxicity.