Neighbour restoration: a possible explanation for some "broken" survival curves of UV-irradiated Escherichia coli K12 cells.

Survival curves for UV irradiation of five non-filamenting strains of E. coli K12 decrease exponentially at moderate levels of radiation but are broken at high levels of radiation. That is, it appears a change in the slope of survival curves, featuring a tail. As this phenomenon was observed with strains bearing uvrA and recA mutations it must be independent of the products of these genes. Experiments with isolated surviving colonies and synchronized cultures eliminated genetic and phenotypic heterogeneity as reasons for the tails in the survival curves. UV survival increased 10- to 15-fold when UV-irradiated cells were plated either with cells unable to grow in the plating medium or with bacterial cell-free extracts. We suggest that factors related to the high cell densities used to obtain survival curves at high radiation levels (neighbour restoration) could be responsible for the survival increases, generating the tailed survival curves.

Genotoxic effect of a keto-aldehyde produced by thermal degradation of reducing sugars.

Reductone (HOCH2-CO-CHO), a keto-aldehyde formed, in alkaline pH, by thermal degradation of reducing sugars, blocks cellular respiration and macromolecular biosynthesis, inactivates far-UV (254 nm)-irradiated wild-type E. coli cells, and causes DNA strand breaks. So it may be supposed to be an inducer of SOS functions. Indeed, when Salmonella tester strains TA98, TA100 and TA102 were treated with reductone solutions, without metabolization, a mutagenic effect was detected for all of them. Besides, reductone induced lysogenic E. coli cells and cell filamentation, as measured by the Inductest and the SOS Chromotest. So reductone must be considered a genotoxic drug.

Near-ultraviolet illumination inhibits the liquid holding recovery in Escherichia coli B.

Liquid holding recovery (LHR) consists of an increase in the survival of UV-irradiated cells when they are held under non-nutrient conditions before plating. In this study we investigated in E. coli B cells the effect of the growth inhibition induced by near UV (365 nm) illumination (growth delay, GD) before irradiation with UV-254 nm on the amplitude of LHR and the induction of an SOS function (filamentation) during the liquid holding period. Our results demonstrated that pre-illumination with near-UV inhibits LHR and the induction of filamentation when the cells are incubated in nutrient medium. Moreover, this inhibition is due to GD, an effect caused by a photoproduct in the E. coli t-RNA, the 8-13 link.

Antioxidant capacity of cyclo-oxygenase and lipoxygenase inhibitors.

The present study analyzes the possible scavenger capacity of several anti-inflammatory drugs on growth of Escherichia coli K12, BW9 109, a strain hypersensitive to H2O2, in medium containing H2O2. Although all cyclo-oxygenase and/or lipoxygenase inhibitors protected the cells against H2O2, no correlation was found between their relative protective abilities and reported anti-inflammatory potencies.

Absence of mutagenicity of Potomorphe umbellata and Potomorphe peltata in the Salmonella/mammalian-microsome mutagenicity assay.

The development of short term tests for measuring the mutagenic activity of genotoxic chemicals has been helpful in increasing security. Natural products from the flora are largely used in popular medicine. Using the Salmonella/mammalian-microsome assay, we investigated the genetic toxicity of two plant species popularly used in malaria treatment, Pothomorphe umbellata and Pothomorphe peltata. The data show the absence of genetic toxicity for both plant species.

Effect of hydrogen peroxide on Escherichia coli radC.

High sensitivity to ionizing radiation is observed in Escherichia coli radC mutants. This is not seen for H2O2-treated cells but when the polA mutation is also present, cells are more sensitive than in the presence of the recA mutation. An increase in inactivation was observed for strains tested when cells are grown in minimal medium and starvation-induced resistance is observed in H2O2-treated cells.

Escherichia coli xthA mutant is not hypersensitive to ascorbic acid/copper treatment--an H2O2 generating reaction.

Ascorbate (vitamin C) in the presence of copper yields H2O2, which seems to be responsible for its toxic effects in bacteria. However, we found that the Escherichia coli xthA mutant strain, which is hypersensitive to H2O2, has almost the same sensitivity as the wild-type strain to ascorbate and copper treatment. Our results suggest that the DNA damage induced in E. coli by H2O2 generated in oxidized ascorbate solutions is different from that induced by direct H2O2 treatment.

Ascorbate-copper induced DNA lesions and repair in Escherichia coli K12 cells.

Multiple lines of evidence show that oxidation products of ascorbic acid (vitamin C) are capable of inducing a variety of genetic alterations in microbial and mammalian cells. We have studied the inactivation kinetics in repair proficient and deficient Escherichia coli K12 cells treated with oxidized solutions of ascorbic acid, in the presence of catalytic amounts of copper. Our results suggest that the repair pathways controlled by the recA and uvrA gene products (the latter in a recA strain) contribute to cell survival. However, the lack of beta-galactosidase induction, in the SOS chromotest, implies a role for the RecA protein other than SOS induction. Catalase and thiourea suppress the toxic effects of oxidized ascorbate solutions, confirming that H2O2 and hydroxyl radicals are intermediate agents in the damaging action. Single-strand breaks were detected in DNA from treated cells.

Damages induced in lambda phage DNA by enzyme-generated triplet acetone.

Exposure of lambda phage to triplet acetone, generated via the oxidation of isobutanal by peroxidase, leads to genome lesions. The majority of these lesions are detected as DNA single-strand breaks only under alkaline conditions, and so true breaks do not occur. Also, no sites sensitive to UV-endonuclease from Micrococcus luteus were found in DNA from treated phage. The participation of triplet acetone in the generation of such DNA damage is discussed.