Gamma-ray induced inhibition of DNA synthesis in ataxia telangiectasia fibroblasts is a function of excision repair capacity

The extent of the deficiency in γ-ray induced DNA repair synthesis in an ataxia telangiectasia (AT) human fibroblast strain was found to show no oxygen enhancement, consistent with a defect in the repair of base damage. Repair deficiency, but not repair proficiency, in AT cells were accompanied by a lack of inhibition of DNA synthesis (replicon initiation) neither γ-rays or the radiomimetic drug bleomycin. Experiments with 4-nitroquinoline 1-oxide indicated that lack of inhibition was specific for radiogenic type damage. Thus excision repair, perhaps by DNA strand incision or chromatin modification, appears to halt replicon initiation in irradiated repair proficient cells whereas in repair defective AT strains this putatively important biological function is inoperative.     

Sendai virus stimulates chemiluminescence in mouse spleen cells.

Sendai virus stimulates chemiluminescence within a few seconds after it is added to a suspension of mouse spleen cells. Virus rendered non infectious by irradiation with ultraviolet light induces a similar burst of chemiluminescence. Heating or pronase treatment of the virus abrogate this reaction, as does sonication of the cells before the addition of the virus. The ability of the virus to stimulate chemiluminescence is correlated with its hemagglutination, neuraminidase, cell fusion and hemolytic properties. It is suggested that Sendai virus-induced chemiluminescence is initiated by the interaction of the virus envelope spike glycoproteins with the cell membrane.     

Algal oxidation of aromatic hydrocarbons: formation of 1-naphthol from naphthalene by Agmenellum quadruplicatum, strain PR-6.

Hydroxyurea induces repair replication in human lymphoblastoid NC37 BaEV cells during incubation with liver microsomes and NADPH. Catalase reduces hydroxyurea-induced repair by more than 95%, suggesting that hydrogen peroxide derived from hydroxyurea in the presence of the metabolic activation system is involved in the DNA damage.     

Enzymatic inactivation of human alpha-1-proteinase inhibitor by neutrophil myeloperoxidase.

Peanut agglutinin was acylated with a new heterobifunctional, cleavable photosensitive crosslinking reagent, N-[4-(p-azidophenylazo)benzoyl]-3-aminopropyl-N′-oxysuccinimide ester. The lectin derivative binds specifically and reversibly to neuraminidase-treated human erythrocyte ghosts and upon irradiation covalent attachment of over 35% of the bound lectin occurs. The affinity-crosslinked ghosts were solublized in deoxycholate, immunoprecipitated with anti-peanut agglutinin antiserum, and analyzed by sodium dodecylsulfate polyacrylamine gel electrophoresis. Bands containing both peanut agglutinin and membrane glycoproteins were detected with apparent molecular weights of 58 000, 85 000, 110 000 and 135 000. Upon subsequent cleavage with sodium dithionite, asialoglycophorin A (apparent M.W. 41 000 and 85 000) and a second glycoprotein (apparent M.W. 58 000 – 61 000) were tentatively identified as the receptors for peanut agglutinin in the intact membrane.     

Regulation of the binding of 7,12-dimethylbenz[a]-anthracene to DNA of cultured murine epidermal cells at metabolic level: competition of the binding by polycyclic aromatic hydrocarbons and by other precarcinogens.

The binding of labeled carcinogen [3H]DMBA to murine epidermal cells (MEC) DNA in culture has been studied. The influence of unlabeled noncarcinogenic and carcinogenic polycyclic aromatic hydrocarbons (PAH), several PAH metablites, and various directly and indirectly acting non-PAH carcinogens on the binding of [3H]DMBA to MEC DNA has been examined. All the carcinogenic PAH and some of non-carcinogenic PAH effectively inhibit the binding of [3H]DMBA to MEC DNA. The non-PAH chemical carcinogens requiring metabolic activation also reduce the binding of labeled DMBA to MEC DNA; however, a higher concentration of these compounds is required for 50% inhibition of binding than the concentrations of PAH for the same degree of inhibition of binding of [3H]DMBA to MEC DNA. The directly acting carcinogens do not significantly inhibit the binding of [3H]DMBA to DNA. The relationship between structures of PAH and their ability to inhibit the binding of [3H]DMBA to MEC DNA is also discussed. Thus, it appears that the binding of DMBA to cellular DNA is primarily controlled at a level of metabolism and to some extent at the level of binding of reactive metabolites to DNA.     

Radioimmune assay of tubulin applied to oligomers, synaptic membranes, and plants

A radioimmune assay for microtubule protein, tubulin, is described, in which unknown amounts of native or denatured tubulin can be quantitated by the ability to compete with pure [¹²⁵I]tubulin for rabbit antibodies produced against purified bovine brain tubulin. The assay is used to demonstrate that crude extracts of mouse brain contain negligible amounts of 30–36S tubulin oligomers under conditions where purified tubulin forms substantial amounts of such structures. Also, the particulate fraction of osmotically shocked and sonicated brain synaptosomes contains negligible tubulin antigenic activity. By contrast, soluble extracts of soybean, especially rapidly dividing regions of the plant, were found to contain significant amounts of cross-reacting material, providing further evidence for the conservative evolutionary nature of this ubiquitous and important protein.     

Inhibitory effect of hydroxyurea on [3-H]leucine incorporation in human peripheral lymphocytes.

Hydroxyurea (HU), generally considered to be a specific inhibiter of DNA synthesis, has an inhibitory effect on the incorporation of TCA-precipitable [3-H]leucine in peripheral lymphocytes. This action is not secondary to the inhibition of DNA synthesis since incorporation of [3-H]leucine is unaffected when DNA synthesis is inhibited by 5-fluorodeoxyuridine (FUdR); it does not appear to be directly related to inhibition of RNA synthesis; and it is not mediated at the level of translation since HU has no effect on protein synthesis in rabbit reticulocytes. The relevance of these findings to the use of HU as a DNA inhibitor is discussed.