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[en] The effects of whole-body γ-irradiation of rats (8Gy) on erythrocyte enzymes and biochemical components involved in lipid peroxidation were studied. Decreased superoxide dismustase and glutathione reductase activities, and lowered concentrations of reduced glutathione, were found to be the main factors responsible for observed increase in lipid peroxidation in the erythrocytes of irradiated rats. This increased lipid peroxidation did not result in the greater tendency to hemolysis in hypotonic media; on the contrary, the mean osmotic fragility was decreased at days D + 1 and D + 3 after irradiation. The behavior of the erythrocyte polulations towards hemolysis in hypotonic media appeared to be most homogeneous at days D + 4 and D + 8 after irradiation, which correspond to maxima of malonic dialdehyde concentrations in erythrocytes. Such a synchrony of variations suggests that crosslinking of primary amino groups of proteins or phospholipids by malonic dialdehyde might produce a rigidification in erythrocyte membranes, possibly leading to a more homogeneous behavior of the erythrocyte populations towards hemolysis in hypotonic media
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ANIMALS, BIOLOGICAL EFFECTS, BIOLOGICAL MATERIALS, BLOOD, BLOOD CELLS, BODY FLUIDS, CHEMICAL REACTIONS, DECOMPOSITION, DRUGS, ELECTROMAGNETIC RADIATION, ENZYMES, EXTERNAL IRRADIATION, IONIZING RADIATIONS, IRRADIATION, MAMMALS, MATERIALS, ORGANIC COMPOUNDS, PEPTIDES, POLYPEPTIDES, PROTEINS, RADIATION EFFECTS, RADIATIONS, RADIOPROTECTIVE SUBSTANCES, RESPONSE MODIFYING FACTORS, RODENTS, VERTEBRATES
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[en] Proton NMR spectroscopy allows the detection in plasma of resonances arising from N-acetyl-glucosamine (NAG) and N-acetyl-neuraminic acid (NANA) which have been shown to be borne by acute phase glycoproteins. These resonances can be identified using 2 different protocols of spectrum acquisition detecting different physical states in the global pool of glycoproteins, ie mobile and less mobile moieties of glycosylated chains. In this study we demonstrate that NMR spectroscopy allows a precise monitoring of the variations of glycosylated residues in cancers, inflammatory processes and bone marrow transplantation. The most important findings are that: (i), the distribution of glycosylated residues varies with the origin of the cancerous tissue; (ii), the level of these residues is a function of tumor development; (iii), the concentrations in NAG and NANA are well correlated with the standard biological parameters of acute phase and leucocyte activation. Proton NMR spectroscopy of glycosylated residues in plasma may offer a new means of monitoring sialic acid in cancer and other pathological conditions
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AMINES, BARYONS, BIOLOGICAL MATERIALS, BLOOD, BODY, BODY FLUIDS, CARBOHYDRATES, CATIONS, CHARGED PARTICLES, DISEASES, ELEMENTARY PARTICLES, FERMIONS, HADRONS, HEMATOPOIETIC SYSTEM, HEXOSAMINES, HEXOSES, HYDROGEN IONS, HYDROGEN IONS 1 PLUS, IONS, MAGNETIC RESONANCE, MATERIALS, MONOSACCHARIDES, NUCLEONS, ORGANIC COMPOUNDS, ORGANS, PATHOLOGICAL CHANGES, POLYSACCHARIDES, PROTEINS, RESONANCE, SACCHARIDES, SPECTRA, TISSUES
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[en] Survival and mutagenesis of UV-irradiated, temperature-sensitive simian virus 40 mutants (SV40) have been studied after infection of human fibroblasts. Survival of the viral progeny obtained after 6,8 or 10 days at permissive temperature decreases as a function of the UV-dose delivered to the virus. In cells which have been pretreated with 10 Jm-2 of UV 24 hours before infection, progeny survival was increased as compared to survival in control cells. The reactivation factor varies from one to ten, depending on the number of lytic cycles carried out at permissive temperature. The level of mutation frequency, as measured by the reversion from a temperature sensitive growth phenotype towards a wild type phenotype, increases with the dose of UV-irradiation given to the virus. Moreover, the mutation frequency is increased in the viral progeny produced in UV-irradiated human cells. Similar experiments carried out with SV40-transformed human fibroblasts, which constitutively express SV40 T antigen, gave comparable results. These experiments show that, as in monkey cells, a new error-prone recovery pathway can be induced by pretreating human cells with UV-light before infection
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[en] A modified assay has been devised for the physiological reaction, indole-3-glycerol phosphate to Trp, of the enzyme tryptophan synthetase. The assay may be applied to crude bacterial extracts, and is based on the measurement of incorporation of radioactivity from [3H]Ser into Trp. Comparison with previous colorimetric assays indicates an improvement in sensitivity of about 30-fold, and advantages in terms of sample economy and simplified manipulation
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[en] In order to analyze the molecular mechanisms of mutagenesis in mammalian cells, we devised an analytical assay using Simian Virus 40 as biological probe. To study the possible correlations between the distribution of the lesions on the treated DNA and the distribution of mutations, we have located and quantified the lesions induced by ultraviolet light (254 nm) on a SV40 DNA fragment. At a fluence of 2,000J/m2, our results show that the formation frequency of thymine-thymine dimers (TT) is three to four times higher than the formation frequency of the other types of dimers (TC, CT, CC). On the other hand, the formation frequency of a dimer is influenced by the adjacent sequence. In particular, a pyrimidine in the 5' position of a thymine-thymine dimer enhances its formation frequency. At the dose used the formation frequency of the pyrimidine (6-4) pyrimidone photoproducts is twenty times less than the formation frequency of pyrimidine dimers. This paper shows the distribution of the major lesions induced by UV-light on a defined fragment of SV40 genome after UV irradiation. This work is necessary to get an insight in the molecular mechanisms of UV-mutagenesis
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[en] The effects of whole-body gamma irradiation (8.4 Gy) were studied on arachidonic acid (AA) metabolism in rat's blood platelets, from day D + 1 to day D + 10 after irradiation. AA conversion into thromboxane B2 (TxB2) increased at D + 1 and then gradually decreased to very low values from D + 7 to D + 10. This decrease in the conversion of exogenous AA into TxB2 was due to a lower AA incorporation into platelets and not to a decrease of cyclooxygenase and thromboxane-synthetase activities. AA incorporation into membrane phospholipids of blood platelets was much more decreased than AA incorporation into whole platelets; moreover, the lipid composition of the platelet membranes was markedly modified after irradiation, which must have resulted in structural and functional changes in these membranes; from these effects of whole-body gamma irradiation on platelets, the latter's membranes appeared as a major site of in vivo radiation damage in these cells
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ANIMALS, BIOLOGICAL EFFECTS, BIOLOGICAL MATERIALS, BLOOD, BLOOD CELLS, BODY FLUIDS, CARBOXYLIC ACIDS, CELL CONSTITUENTS, ELECTROMAGNETIC RADIATION, ESTERS, EXTERNAL IRRADIATION, IONIZING RADIATIONS, IRRADIATION, LIPIDS, MAMMALS, MATERIALS, MEMBRANES, MONOCARBOXYLIC ACIDS, ORGANIC ACIDS, ORGANIC COMPOUNDS, ORGANIC PHOSPHORUS COMPOUNDS, RADIATION EFFECTS, RADIATIONS, RODENTS, VERTEBRATES
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[en] The content of RECA protein, one of the SOS genes products, was determined in a bacterial extract by a two site-radioimmunometric assay. The variation of the RECA concentration after induction by physical or chemical treatments was used as a probe to analyse the SOS response. Relationships between either the number or the nature of DNA lesions and the level of the relative amplification of RECA have been established. The modulation of the recA gene expression is discussed
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[en] In the bacterium Escherichia coli DNA damaging treatments such as ultraviolet or ionizing radiation induce a set of functions called collectively the SOS response, reviewed here. The regulation of the SOS response involves a repressor, the LexA protein, and an inducer, the RecA protein. After DNA damage an effector molecule is produced -possibly single stranded DNA- which activates the RecA protein to a form capable of catalysing proteolytic cleavage of LexA. The repressors of certain temperate prophages are cleaved under the same conditions, resulting in lysogenic induction. SOS functions are involved in DNA repair and mutagenesis, in cell division inhibition, in recovery of normal physiological conditions after the DNA damage is repaired, and possibly in cell death when DNA damage is too extensive. The SOS response also includes several chromosomal genes of unknown function, a number of plasmid encoded genes (bacteriocins, mutagenesis), and lysogenic induction of certain prophages. DNA damaging treatments seem to induce DNA repair and mutagenic activities and proviral development in many species, including mammalian cells. In general, substances which are genotoxic to higher eukaryotes induce the SOS response in bacteria. This correlation is the basis of the numerous bacterial tests for genotoxicity and carcinogenicity
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[en] It has been shown that fructose metabolism in the human liver can be monitored quantitatively by means of 1H image-guided 31P MRS, implemented on a clinical MR imaging system equipped with surface coils and with appropriate data processing software. Temporal resolution of the 31P MRS measurements is of the order of 2 min
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[en] The RecA protein of Escherichia coli plays a central role in DNA repair mechanisms. When it is incubated with single-stranded DNA and a nucleoside triphosphate, the purified RecA protein acts both by promoting cleavage of the LexA protein, the repressor of the SOS genes, and by catalyzing strand exchange between a variety of DNA molecules. A model for the regulation of the activity of the RecA protein in a cell exposed to a DNA damaging treatment is proposed
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