Resistance of Mycobacterium chelonei-like organisms to formaldehyde.

Mycobacterium chelonei-like organisms have been isolated from patients in two outbreaks of peritonitis involving chronic peritoneal dialysis machines routinely disinfected with 2 to 3% formaldehyde. Susceptibility studies revealed that water-adapted M. chelonei-like organism strains could survive 2 h of exposure to 10% formaldehyde.     

Resistance of Thermus spp. to Potassium Tellurite

Two members of the genus Thermus were examined for their resistance to toxic inorganic compounds. They both proved to be fairly resistant to tellurite and selenite and to many other heavy metal salts. Cell extracts of Thermus thermophilus HB8 and of T. flavus AT-62 catalyze the reduction of K₂TeO₃ in a reaction which is dependent on NADH oxidation.     

Resistance of senescent keratinocytes to UV-induced apoptosis.

Irradiation with ultraviolet (UV) triggers programmed cell death (apoptosis) in keratinocytes. This process is believed to protect against skin carcinogenesis since the cells with damaged DNA are selectively removed, limiting the likelihood of the development of a malignant keratinocyte clone. The p53 protein is able to detect mutation-bearing DNA fragments and is thus indispensable for the UV-induced apoptosis in the epidermis. Since age is a risk factor for the development of skin tumors we investigated whether ultraviolet induces apoptosis and p53 activation in senescent keratinocytes. Cultured senescent keratinocytes were irradiated with broad-band ultraviolet, apoptosis was assessed using TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling) technique and the p53 activation pattern was determined with Western blotting and immunofluorescent staining with a panel of anti-p53 antibodies recognising different conformational forms of the protein (PAb 122, PAb 240, DO-7). In senescent keratinocytes arrested in the G1 phase of cell cycle, ultraviolet irradiation (100-2000 J/m2) caused accumulation and nuclear translocation of p53. However, in contrast to young cells where UV induces apoptotic cell death in G1, apoptosis was not detected in senescent cells. There were subtle differences in the p53 activation pattern between senescent keratinocytes and known patterns in young keratinocytes and other cell types. In senescent keratinocytes a constitutional nuclear expression of p53 (conformational form recognized by PAb 240) was present and the p53 induction in response to ultraviolet radiation was rapid. Suppression of apoptosis in senescent keratinocytes may be an important mechanism responsible for enhanced skin carcinogenesis in old age.     

Resistance of germfree rats to indomethacin-induced intestinal lesions.

Indomethacin given orally to conventional rats produced in three days a syndrome, often fatal, of intestinal lesions characterized by multiple ulcers and peritonitis. Male germfree rats were found to be resistant to this effect of indomethacin, while female germfree rats developed very mild lesions. Germfree rats became sensitive again to such lesions when monocontaminated with E. coli. In such animals, however, the lesions were less severe than in conventional animals, presumably because more than one microorganism is necessary for the full syndrome to develop. These results suggest that microorganisms are necessary for the development of indomethacin-induced intestinal lesions. Secondary bile acids, absent in germfree animals, may also be necessary. The prostaglandin deficiency caused by indomethacin appears to weaken the resistance of the intestinal mucosa to microorganisms and/or their toxins. The latter may then penetrate the mucosa, damage the cells and produce ulcers and perforations. Since several prostaglandins also protect against indomethacin-induced lesions, the hypothesis is advanced that certain prostaglandins may protect the mucosa ("cytoprotection") by preventing the spread of microorganisms and/or their toxin through the intestinal wall.     

Resistance of some common fungi to gamma irradiation.

Ten species of fungi representing the genera Alternaria, Aspergillus, Caldosporium, Curvularia, Fusarium, and Penicillium were examined for their relative resistance to gamma irradiation from a 137Cs source. Inactivation doses for dematiaceous fungi in agar medium ranged from 0.6 to greater than 1.7 megarads, whereas those for moniliaceous fungi were less than 0.3 megarad. D10 values (the dose required to reduce the inoculum by 1 log) for Curvularia geniculata (greater than 0.29 megarad) exceeded those for control spores of Bacillus pumilus (0.15 megarad).     

Cyanide Resistance in Achromobacter II. Mechanism of Cyanide Resistance.

Oka, Tetuo (University of Tokyo, Tokyo, Japan), and Kei Arima. Cyanide resistance in Achromobacter. II. Mechanism of cyanide resistance. J. Bacteriol. 90:744-747. 1965.-Photochemical data showed that the only oxidase found in the cyanide-sensitive cells of Achromobacter was cytochrome o, and that cyanide-resistant cells contained at least two oxidases. The oxidase responsible for cyanide resistance was a pigment the CO compound of which had its absorption band at a wavelength longer than 580 mmu. In addition, kinetic data suggested that there were two oxidases having different affinities for cyanide. From the data presented, resistance to cyanide in Achromobacter strain D was attributed to the induced formation of cytochrome a(2), which has a very low affinity for cyanide. Several characteristics of cytochrome a(2) as a cytochrome oxidase are summarized.     

Resistance of Thiobacillus novellus to mitomycin C and rifampicin.

Thiobacillus novellus is highly resistant to mitomycin C and rifampicin. This resistance is not due to insusceptibility of the target molecules to the drugs, since mitomycin C cross-links the DNA and rifampicin inhibits the DNA-dependent RNA polymerase of T. novellus in vitro.     

Resistance of ADP-ribosylated histones and HMG proteins to proteases.

Calf thymus histones (individually isolated or mixtures) and high mobility group proteins were ADP-ribosylated in vitro using [32P]NAD+ and immobilized purified poly(ADP-ribose) polymerase. The modified histones were then subjected to V8 protease or alpha-chymotrypsin digestion and the resulting peptides were separated by electrophoresis on acetic acid-urea-Triton gels. It was found that in vitro ADP-ribosylated histones were much more resistant to proteases than unmodified histones. A similar approach was applied to histones modified by the endogenous poly(ADP-ribose) polymerase in permeabilized NS-1 mouse myeloma cells in culture. In this case, the proteases could not discriminate between modified and unmodified histones and putative mono(ADP-ribosyl)ated peptides appeared in a digestion frame corresponding to that of bulk peptides. These differences are most probably due to the specificity or number of ADP-ribose groups added to the histones by the endogenous or exogenous poly(ADP-ribose) polymerase. Thus, depending on the size of poly(ADP-ribose) attached to nuclear proteins, these modified proteins might display different degrees of resistance to proteolysis.