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F Palitti

Publications and source records attributed to F Palitti.

At least 73 records · Page 4Linked to original sources
PubMed1988

Chromatographic and cytogenetic analysis of in vivo metabolites of fluoranthene.

Fluoranthene metabolites in rat serum were analysed by high-performance liquid chromatography (HPLC) with UV and fluorescence detection and compared with in vitro metabolites obtained by incubation with microsomal fraction of rat hepatocytes. In order to resolve very polar fluorescent compounds present in rat serum, a modification of HPLC existing methods for in vitro metabolites separation was necessary. Mutagenic 2,3-dihydrodiol was identified in both in vitro sample and rat serum: this result is in good accord with cytogenetic analysis on rats bone marrow cells, that shows a slight but significant increase of sister chromatide exchanges.

Animals↗
PubMed1988

Chromosomal damage induced by maleic hydrazide in mammalian cells in vitro and in vivo.

The induction of sister-chromatid exchanges (SCE) and chromosomal aberrations (Ch.Ab.) by the herbicide maleic hydrazide (MH) has been investigated in Chinese hamster ovary (CHO) cells grown in vitro and in bone marrow cells of mice treated in vivo. MH induces SCE and Ch.Ab. in CHO cells without metabolic activation; however, no induction of SCE was found in the in vivo experiments.

Animals↗
PubMed1988

Induction of sister-chromatid exchanges by procarcinogens in metabolically competent Chinese hamster epithelial liver cells.

An epithelial cell strain has been established from the livers of male Chinese hamsters (CHEL cells). These cells, which proliferate in culture and retain their metabolic enzymatic activities during several subcultures, were used in a sister-chromatid exchange assay to evaluate the effectiveness of polycyclic aromatic hydrocarbons (PAHs), aflatoxin B1 (AFB1) and cyclophosphamide (CP). The results obtained demonstrate that CHEL cells are metabolically competent to activate different classes of procarcinogens into biologically active metabolites. Moreover, they showed a selective capacity to discriminate chemical carcinogens from noncarcinogens. Thus, the CHEL cell system appears to be a promising alternative to the short-term tests that include cell-free rodent liver homogenate to evaluate new promutagens and/or procarcinogens.

Animals↗
PubMed1988

Frequencies of chromosomal aberrations induced in human blood lymphocytes by low doses of X-rays.

The dose-response for radiation-induced chromosome aberrations in human lymphocytes is usually fitted to the quadratic model. This assumes that the slope is essentially linear at low doses. Empirical observations of linearity at less than 200 mGy are, however, sparse. Some data have been published indicating a non-linear (threshold) response and these are reviewed. In particular one study with X-rays showed a plateau in response up to 50 mGy and with a significant dip below the control level at 4 mGy. The mechanism proposed to explain non-linearity is that low doses stimulate the enzymic repair capability of lymphocytes. Preliminary data are presented from a large experiment by six laboratories in which the low dose-response for X-rays has been re-examined. The plateau in the dose-response relationship, if it exists, does not extend to doses above approximately 10 mGy. No irradiated cells yielded aberration levels significantly below the control. Over the range 0-300 mGy the response can be fitted to a linear regression. There are, however, variations in sensitivity between cells from different donors. An unexpected finding was that some lymphocytes contained greater than 1 exchange aberrations. This may indicate a small subset of cells that are especially susceptible to the induction of aberrations by low doses.

Adult↗
PubMed1987

Inactivation of de novo DNA methyltransferase activity by high concentrations of double-stranded DNA.

The activity of eukaryotic DNA methyltransferase diminishes with time when the enzyme is incubated with high concentrations (200-300 micrograms/ml) of unmethylated double-stranded Micrococcus luteus DNA. Under similar conditions, single-stranded DNA induces only a limited decrease of enzyme activity. The inactivation process is apparently due to a slowly progressive interaction of the enzyme with double-stranded DNA that is independent of the presence of S-adenosyl-L-methionine. The inhibited enzyme cannot be reactivated either by high salt dissociation of the DNA-enzyme complex or by extensive digestion of the DNA. Among synthetic polydeoxyribonucleotides both poly(dG-dC).poly(dG-dC) and poly(dA-dT).poly(dA-dT), but not poly(dI-dC).poly(dI-dC), cause inactivation of DNA methyltransferase. This inactivation process may be of interest in regulating the 'de novo' activity of the enzyme.

DNA↗
PubMed1986

Substrate preferences of human placental DNA methyltransferase investigated with synthetic polydeoxynucleotides.

A DNA methyltransferase partly purified from human placenta has been tested on a variety of synthetic polydeoxynucleotides. The results showed that: the enzyme is most active as a 'maintenance' or 'hemi-' methylase but also has some de novo methylating activity; the presence or absence of A or T in the substrate strand has little influence on maintenance or de novo activity, while polymers containing C but not G in the same strand are poor de novo substrates and bind poorly to the enzyme; single-stranded polymers are about as good substrates as double-stranded ones, and the effects of nucleotide composition (particularly G and mC content) on enzyme activity with single strands are similar to those with double-stranded polymers; strands in which all the cytosines are methylated bind the enzyme well. A mechanism is suggested involving two different sites on the enzyme that recognize CG and mCG, and which rationalizes the activity of eukaryotic DNA methyltransferases towards single-stranded DNA.

DNA↗
PubMed1986

An in vitro and in vivo study on mutagenic activity of fluoranthene: comparison between cytogenetic studies and HPLC analysis.

The polycyclic aromatic hydrocarbon, fluoranthene (FT), has been shown to induce SCEs in vitro in CHO cells in the presence of metabolic activation. Negative results were obtained in vivo in mice. The HPLC analysis performed to investigate the presence of metabolites of FT both in the serum of treated mice and in culture medium of CHO cells confirmed some differences between in vitro and in vivo metabolism.

Animals↗
PubMed1986

Effect of post-treatments with caffeine during G2 on the frequencies of chromosome-type aberrations produced by X-rays in human lymphocytes during G0 and G1.

Human lymphocytes were irradiated with X-rays in G0 and G1, grown in the presence of 5-bromodeoxyuridine, and harvested at different times from 48 to 80 h after stimulation. Some cultures were exposed to 2.5-5 mM caffeine during the last 3 h before harvesting. The frequencies of chromosome-type aberrations were scored in first division (M1) metaphases. The post-treatment with caffeine increased the frequencies of mitoses and chromosome-type aberrations in irradiated cultures. The results suggest that cells carrying chromosome-type aberrations are delayed in G2 and that caffeine increases the frequencies of aberrations in dividing cells by removing this G2-block.

Caffeine↗
PubMed1985

Purification and characterization of mammalian DNA methyltransferases by use of monoclonal antibodies.

Previously, we have derived murine hybridomas producing monoclonal antibodies against DNA methyltransferase from human placenta (Kaul, S., Pfeifer, G. P., and Drahovsky, D. (1984) Eur. J. Cell Biol. 34, 330-335). One of these monoclonal antibodies, M2B10, which undergoes immune complex formation also with DNA methyltransferase from P815 mouse mastocytoma cells, was used for the immunoaffinity purification of mouse and human DNA methyltransferases. In sodium dodecyl sulfate-polyacrylamide gels and in immunoblotting studies, the immunoaffinity-purified mouse DNA methyltransferase revealed 5-6 polypeptides of molecular masses 150-190 kDa. The immunoaffinity-purified human placental DNA methyltransferase was characterized by a polypeptide of 158 kDa, presumably representing the native enzyme molecule and by polypeptides of 105-108 kDa and 50-68 kDa, probably generated by a limited proteolysis of the native enzyme molecule. The immunoaffinity-purified DNA methyltransferases preferred hemimethylated DNA substrates over unmethylated ones, and among all unmethylated substrates tested, poly[(dG-dC).(dG-dC)] had the highest methyl-accepting activity. DNA polymers of at least 90 base pairs in length were required for the binding reaction of the immunoaffinity-purified human DNA methyltransferase, and this initial binding was apparently independent of the nucleotide composition of the DNA polymer and of the presence of S-adenosyl-L-methionine.

Animals↗
PubMed1985

Hypomethylation of repair patches in HeLa cells.

In HeLa cells, under conditions where normal semiconservative synthesis is suppressed by hydroxyurea, the excision repair process after irradiation by UV results in a small amount of incorporation of nucleotides into nonreplicated DNA. By labelling the cytosine moieties of these repair patches, and measuring the ratio between cytosine and 5-methylcytosine, we have found that the level of methylation of cytosine in repair patches five hours after UV-irradiation of the cells is about half of that observed in normal semiconservatively synthesized DNA.

5-Methylcytosine↗
PubMed1984

Influence of caffeine and 3-aminobenzamide in G2 on the frequency of chromosomal aberrations induced by thiotepa, mitomycin C and N-methyl-N-nitro-N'-nitrosoguanidine in human lymphocytes.

The effects of post-treatments with caffeine in G2 on the frequency of chromosomal aberrations induced by thiotepa, mitomycin C and N-methyl-N-nitro-N'-nitrosoguanidine were studied in human lymphocytes. Caffeine was found to potentiate the frequency of chromatid aberrations induced by all 3 S-dependent agents tested; the most striking enhancement being obtained when caffeine was present during the last 1.5 h before harvesting. Post-treatments in G2 with 3-aminobenzamide had no influence on the aberration frequency induced by thiotepa and N-methyl-N-nitro-N'-nitrosoguanidine.

Benzamides↗
PubMed1984

Effect of caffeine on induced damage in cells of Xenopus laevis.

Xenopus laevis cells were treated with mitomycin C and subsequently treated with caffeine during either the S- or G2-phase of the cell cycle. The frequency of induced chromatid exchanges was especially increased by caffeine posttreatment during the S-phase. This increase took place at the expense of the frequency of isochromatid breaks, which was reduced, both when the caffeine posttreatment was given during the S- and G2-phase.

Animals↗
PubMed1984

Effect of L-ethionine on spontaneous and MMC-induced SCEs in G0 and G1 human lymphocytes under liquid-holding recovery conditions.

L-Ethionine is an ethyl analogue of the amino acid, methionine, well known as a carcinogen but not as a mutagen. Its activity is clearly related to its capacity to hypomethylate DNA and RNA. At a final concentration of 5 mM, L-ethionine completely inhibits DNA synthesis in PHA-stimulated human lymphocytes, probably acting on a methylation reaction critical for the initiation of the S phase. This block can be reversed. Utilizing this capacity of L-ethionine to block cell proliferation, we have studied the influence of G0 and G1 repair of premutational damage (PMD) (equivalent to liquid-holding recovery in bacteria) on spontaneous and MMC-induced SCEs in human lymphocytes. Our results clearly show that L-ethionine in our experimental conditions significantly increases the frequencies of spontaneous and MMC-induced SCEs. In view of the hypomethylating activity of the analogue, we hypothesize that this action at the replication fork level may increase the error-prone ligation of unrepaired lesions, thus influencing the frequency of occurrence of SCEs.

Antibiotics, Antineoplastic↗
PubMed1984

Biological monitoring of workers in the rubber industry. I. Chromosomal aberrations and sister-chromatid exchanges in lymphocytes of vulcanizers.

To evaluate the possible genetic consequences of the industrial exposure among the vulcanizers of a rubber plant we measured the in vivo levels of chromosomal aberrations and sister-chromatid exchanges in peripheral lymphocytes of 34 vulcanizers and in an adequate control population. The observed chromosomal aberration frequencies were 1.9 +/- 1.4 aberrations/100 cells in the exposed group and 2.1 +/- 1.5 aberrations/100 cells in the controls. No difference was found between the two groups for the mean value of sister-chromatid exchanges (5.2 +/- 1.3 in the exposed, 5.2 +/- 0.7 in the control group). Cigarette-smoking was clearly associated with increased sister-chromatid exchange frequencies both in the exposed and in the control groups, while chromosomal aberration frequencies were not correlated with smoking habits.

Chromosome Aberrations↗
PubMed1984

Enhancement of induced sister chromatid exchange and chromosomal aberrations by inhibitors of DNA repair processes.

The effect of post-treatment with inhibitors of DNA synthesis (hydroxyurea, aphidicolin) and repair (caffeine, 3-aminobenzamide) on the frequencies of chromosomal aberrations and sister chromatid exchange (SCE) induced by mitomycin C and decarbamoyl mitomycin C both in Chinese hamster cells and in human lymphocytes in vitro has been studied. The data show that in the case of Chinese hamster and human lymphocytes mitomycin C-treated cells there is an increased frequency of both chromosomal aberrations and SCE after a G2 post-treatment with the inhibitors, while no increase is observed for decarbamoyl mitomycin C-treated cells. Since SCE are DNA synthesis-dependent phenomenon, an increase in the frequency of SCE also in the G2 phase might suggest that after mitomycin C treatment there is a residual DNA synthesis still going on very late in the cell cycle.

Animals↗
PubMed1983

Formation of chromatid-type aberrations in G2 stage of the cell cycle.

CHO cells were treated in G1 stage of the cell cycle with chromosome-breaking agents that act in an S-dependent manner. The cells were challenged in G2 stage, before fixation, with various inhibitors of DNA synthesis or repair. Short-wave UV, mitomycin C, decarbomyl mitomycin and 4-nitroquinoline oxide (4NQO) were used as chromosome-breaking agents. The inhibitors of DNA repair or synthesis used were hydroxyurea, aphidicolin and caffeine. Permeabilization of cells followed by a treatment with Neurospora endonuclease (a treatment to convert DNA single-strand breaks into double-strand breaks) did not have any influence on the frequencies of chromatid aberrations induced by the chemicals used, whereas with the inhibitors the extent of potentiation varied depending on the mutagen and the inhibitor used.

Animals↗