Relative effectiveness of the 300–320 nm spectral region of sunlight for the production of primary lethal damage in E. coli cells

Cell inactivation by sunlight exposure has been studied in E. coli CSR 603 (uvrA recA phr), a K12 derivative which is deficient in all known repair systems. Under suitable conditions, unfiltered sunlight inactivates these cells to 10⁻³ survival within 30 sec. The effects of unfiltered sunlight have been compared with those of sunlight filtered through 1-cm layers of aqueous caffeine solutions ranging in concentration from 1 to 20 mg/ml. In the wavelength region of solar emission below 320 nm, which is most critical for DNA damage, the transmission of these liquid filters changes from 10 to 90% within 8-nm intervals. Thus our results permit minimum estimates for the fraction of lethal lesions produced by the solar spectrum below certain wavelengths. In an experiment analyzed in this manner more than 80% of primary lethal lesions are caused by wavelengths <312 nm, and more than 50% by wavelengths <306 nm, while the contribution of wavelengths >380 nm to primary lethal damage is below 1%.     

Altered potassium permeability in vitamin E-deficient rat erythrocytes

Erythrocytes of vitamin E-deficient rats were investigated as an in vivo model of oxidant stress and cellular aging. To measure possible membrane damage related to the enhanced oxidant stress, the permeability of the erythrocyte membrane to potassium was determined. Rates of non-hemolytic potassium loss were calculated from comparison of total potassium loss and hemolysis rates. The non-hemolytic potassium loss rates for erythrocytes of vitamin E-deficient rats were as much as 2.5-fold higher than controls. The abnormally high permeability of vitamin E-deficient rat erythrocytes indicates molecular damage at the membrane level, and may be significant to our understanding of the normal aging process in erythrocytes and other cells.     

Influence of clay particles (Illite) on substrate utilization by sulfate-reducing bacteria

The presence of calcium-or iron-saturated illite had a positive effect on the conversion of ethanol and acetate by non-starved cultures of Desulfobacter postgatei D.A41, but had no effect on non-starved cultures of Desulfobulbus propionicus Lindhorst and Sesulfovibrio baculatus H.L21. Starvation of these cultures at room temperature induced adhesion of cells of D. baculatus H.L21 to the surface of the clay particles. No adhesion of cells of D. propionicus Lindhorst and D. postgatei D.A41 was ever observed. However, for the three strains studied, the presence of clay particles had a positive effect on conservation of the oxidative capacity of the cultures during starvation.     

Evidence for photoenzymatically repairable, lethal "non-dimer" photoproducts, formed in E. coli cells by 365-nm radiation or by sunlight greater than 360 nm.

Three pairs of E. coli strains with different dark-repair potentials, viz. H/r30 and H/r30-R, H_s30 H_s30-R, CSR 603 and AB 2480, have been investigated for their survival after exposure to 254-nm and 365-nm radiation. Each pair consists of a non-photorepairable (phr^?) and a photorepairable (phr⁺) strain of otherwise identical or similar genotype. At 254 nm, the mean inactivation fluence (F_0.37) is for the dark-repair proficient phr^? strain (H/r30) 300–750 times greater than for the completely dark-repair deficient phr^tt- strain (CSR 603), but at 365 nm the F_0.37's differ by a factor of only 5–10. Comparison of survival curves of phr^? and phr⁺ strains indicates that, at all three levels of dark-repair potential, lethal damage resulting from 365-nm exposure is extensively photorepaired by the same wavelength. Qualitatively similar effects were observed with sunlight from which all wavelengths < 360 nm were filtered out. Furthermore, we have shown that fluences of 365-nm radiation used in our experiments do not damage the enzymatic dark-repair systems themselves. These results seem compatible with one another only if one assumes that photoenzymatic repair is capable of abolishing lethal DNA damage other than the common types of cyclobutane dipyrimidines occurring after 254-nm irradiation.     

Beitr?ge zur kenntnis des baues, der funktion und der entwicklung des akzessorischen kopulationsorgans von segestria bavarica c. l. koch

Ohne Zusammenfassung     

Bioconversion of para-substituted monophenolic compounds into corresponding catechols by alginate entrapped cells ofMucuna pruriens

Alginate-entrapped cells ofM. pruriens were able to convert a number of parasubstituted monophenolic compounds into the corresponding catechols. All catechols produced were released into the medium, which offered the opportunity to isolate these products via a relatively simple procedure. Prepurification was performed on a Sephadex G10 gel and catechols were concentrated on Affigel 601. The identity of all products was confirmed with combined liquid chromatography/mass spectrometry (LC/MS) or MS using the desorption chemical ionization technique, depending on the catechol. For the entrapped cells and for a cell homogenate prepared of the same cell line ofM. pruriens the substrate specificities were qualitatively identical when judged on initial rates of synthesis calculated on protein basis.     

On the lack of host-cell reactivation of UV-irradiated phage T5 II. Further characterization of the repair inhibition exerted by T5 infection

Experiments reported in the preceding paper [4] had shown that host-cell reactivation (HCR) of UV-irradiated phage T1 in excision-repair proficient Escherichia coli cells is inhibited by superinfection with phage T5. Theoretical considerations have led to predictions concerning the dependence of repair inhibition on the multiplicity of superinfecting T5 phage and on the UV fluence to which they were exposed. These predictions have been supported by experimental results described in this paper. The fluence dependence permitted calculation of the relative UV sensitivity of the gene function responsible for repair inhibition; it was found to be about 2.3% that of the plaque-forming ability of phage T5.The T5-inhibitable step in excision repair occurs early in the infective cycle of T1. Furthermore, experiments involving the presence of 400 μg/ml chloramphenicol showed that HCR inhibition of T1 is caused by a protein produced after the FST segment of T5 (i.e. the first 8% of the T5 genome) has entered the host cell. A previously described minor T1 recovery process, occuring in both excision-repair-proficient and -deficient host cells, is inhibited by T5 infection due to a different substance, which is most likely associated with the “second-step-transfer” region of T5 DNA (involving the remainder of the genome). Superinfection with T4ν₁ phage resulted in HCR inhibition of T1, resembling that observed after T5 superinfection. The discussion of these results suggests that inhibition of the bacterial excision repair system by T5 or T4 infection occurs at the level of UV-endonucleolytic incision, and that lack of HCR both in T-even phages and in T5 can be explained in the same manner.