Search PubMed⌕ Search

Biomedical subjects

A Montaldi

Publications and source records attributed to A Montaldi.

At least 37 records · Page 2Linked to original sources
PubMed1987

Solubilization by nitrilotriacetic acid (NTA) of genetically active Cr(VI) and Pb(II) from insoluble metal compounds.

The frequencies of sister chromatid exchanges (SCE) were significantly increased in cultured Chinese hamster cells by insoluble salts of Cr(VI) (PbCrO4) and Pb(II) (PbSO4). A further significant increase of this effect was produced when diluted suspensions of PbCrO4 (1-4 mg/l) and PbSO4 (10-40 mg/l) were preincubated with nitrilotriacetic acid (NTA) concentrations (0.25-1 mg/l) such as those that are possibly found in highly contaminated environmental situations. NTA enhanced the induction of SCE by PbCrO4 and PbSO4 even in the presence, in the preincubation solution and in the medium used to treat the cells, of Na+ and K+ concentrations largely exceeding (e.g., 10(2)-10(6) times) those of the genotoxic metals.

Acetates↗
PubMed1987

Differential effects of cordycepin on the induction of sister-chromatid exchange and chromatid breaks in BALB/Mo mouse lymphocytes treated with mitomycin C.

BALB/Mo mice lymphocytes, carrying endogenous Moloney murine leukaemia virus (M-MuLV), show significantly higher in vitro baseline frequencies of sister chromatid exchange (SCE) than lymphocytes from control (M-MuLV free) BALB/c mice. In vitro treatment of lymphocytes with cordycepin (10 micrograms/ml), an antiviral substance, lowers the level of SCE in BALB/Mo cells to the same value of BALB/c cells. The drug also reduces the higher sensitivity of BALB/Mo compared to BALB/c lymphocytes to the induction of SCE by mitomycin C (MMC) administered either in vitro (3 x 10(-8), 10(-7) M) or in vivo (0.3, 3 mg/kg). BALB/Mo lymphocytes treated in vivo with a high dose of MMC (10 mg/kg) show reduced susceptibility to the induction of SCE but increased frequencies of chromatid breaks and micronuclei. In this situation, cordycepin increases the level of SCE in BALB/Mo lymphocytes to exactly the level seen in BALB/c cells, but it does not affect the frequency of chromosomal aberrations. Since cordycepin is known to inhibit poly(A) synthesis, thus blocking RNA maturation, it is suggested that M-MuLV proviral integration is not the sole factor responsible for the altered susceptibility of BALB/Mo lymphocytes to SCE induction, but that it is most likely viral gene expression that is needed for this effect to occur. On the contrary, the high susceptibility of BALB/Mo lymphocytes to the induction of chromatid aberrations by a high dose of MMC administered in vivo seems to be independent of viral maturation.

Animals↗
PubMed1985

Increased mutagenicity of chromium compounds by nitrilotriacetic acid.

Nitrilotriacetic acid trisodium salt (NTA), which is a substitute for polyphosphates in household laundry detergents, and N-nitrosoiminodiacetic acid (NIDA), a derivative of NTA produced by metabolism of soil microorganisms, were tested for in vitro mutagenicity in bacteria and yeasts. No gene reversions in five strains of Salmonella typhimurium (TA 1535, TA1537, TA1538, TA98, and TA100), no forward gene mutations in Schizosaccharomyces pombe P1, and no mitotic gene conversions at two loci in Saccharomyces cerevisiae D4 were induced by NTA (up to 870 micrograms/plate or 40 micrograms/ml) and NIDA (up to 2,000 micrograms/plate or 1,000 micrograms/ml), independently of the presence of rat liver metabolic activation. The influence of NTA on the mutagenic and clastogenic activity of several chromium compounds was examined in the Salmonella/microsome assay and in the sister chromatid exchange (SCE) assay in mammalian cell cultures (Chinese hamster ovary [CHO] line). NTA does not affect the genetic inactivity of water-soluble Cr(III) (Cr2[SO4]3) and the direct mutagenicity of soluble Cr(VI) (Na2CrO4,K2Cr2O7) compounds. The very insoluble Cr(VI) compounds PbCrO4 and PbCrO4 X PbO are instead clearly mutagenic in the Salmonella/microsome assay (TA100 strain) only in the presence of NTA or NaOH. The mutagenicity of lead chromates is correlated with the amounts of Cr(VI) solubilized by NTA or alkali, as detected by the colorimetric reaction with diphenylcarbazide and atomic absorption spectrophotometry. In the SCE assay, the insoluble lead chromates are directly clastogenic owing to prolonged treatment conditions and cellular endocytosis. The chromosome-damaging activity of PbCrO4 is significantly increased by NTA but not by NaOH.

Acetates↗
PubMed1985

Interaction of nitrilotriacetic acid with heavy metals in the induction of sister chromatid exchanges in cultured mammalian cells.

The ability of nitrilotriacetic acid trisodium salt (NTA) to induce sister chromatid exchanges (SCE) and to influence the induction of SCE by heavy metal compounds was evaluated with mammalian cell cultures. In accordance with the generally negative results obtained by other investigators on the mutagenic effects of NTA, no increase of SCE frequency was observed in Chinese hamster cells (CHO line) or in primary cultures of mouse (BALB/c and BALB/Mo strains) lymphocytes, after treatment with NTA at subtoxic concentrations (2 X 10(-3) M and 10(-3) M, respectively). The induction of SCE by salts of heavy metals (Cd, Hg, Ni, Pb) was evaluated with CHO cells. Soluble (CdCl2, HgCl2, NiCl2, Pb [CH3COO]2) and insoluble (CdCO3, HgCl, NiCO3, PbSO4) compounds were tested, and, with the exception of Pb(CH3COO)2, all were found to increase the frequency of SCE. NTA apparently did not affect the ability of the soluble metal compounds to induce SCE, but it significantly increased the frequency of SCE induced by treatment with all the insoluble salts.

Acetates↗
PubMed1985

Effects of nitrilotriacetic acid on the induction of gene mutations and sister-chromatid exchanges by insoluble chromium compounds.

The influence of nitrilotriacetic acid trisodium salt (NTA) on the mutagenic and clastogenic activity of several water-insoluble or poorly soluble chromium compounds was determined by means of the Salmonella/microsome assay (plate test on TA100 strain) and the sister-chromatid exchange (SCE) test in mammalian cell cultures (CHO line). NTA in itself did not induce gene mutations nor did it increase the frequency of SCE. Cr(VI) compounds (Pb, Ba, Zn, Sr and Ca chromates) and an industrial Cr(VI) pigment, chromium orange (containing PbCrO4 PbO), were inactive or scarcely active mutagens in the Salmonella/microsome test when dissolved in water, but they were increasingly mutagenic when solubilized by 0.5 N NaOH or NTA (10 or 100 mg/ml). Also, the mutagenic activity of Cr(VI), contaminating an industrial Cr(III) pigment (chromite), was slightly enhanced by NTA. Mutagenicity of chromates was correlated with the amounts of Cr(VI) solubilized by NTA or alkali, as determined by the colorimetric reaction with diphenylcarbazide and atomic absorption spectrophotometry, and was decreased by incubation with microsomes, due to reduction of Cr(VI) to the genetically inactive Cr(III) form. In the SCE assay, the insoluble or poorly soluble Ba, Zn, Sr and Ca chromates and the insoluble Cr(VI) pigments zinc yellow (containing ZnCrO4 Zn(OH2], chromium yellow and molybdenum orange (both containing PbCrO4) were directly clastogenic due to cellular endocytosis taking place in prolonged treatments, and NTA significantly increased their chromosome-damaging activity.

Acetates↗
PubMed1985

Cordycepin reduces the sensitivity of BALB/Mo mouse lymphocytes to the induction of sister chromatid exchanges.

Lymphocytes from the spleen of BALB/Mo mice, which carry endogenous Moloney murine leukemia virus (M-MuLV), show in vitro frequencies of sister chromatid exchanges (SCEs) significantly higher than lymphocytes from control (M-MuLV free) BALB/c mice. In vitro treatment of lymphocytes with the antiviral antibiotic cordycepin (10 micrograms/ml) lowers the level of SCEs in BALB/Mo cells to the same value of BALB/c cells. M-MuLV yield is also markedly reduced in BALB/Mo lymphocytes cultured in the presence of cordycepin. The drug also abolishes the increased sensitivity of BALB/Mo lymphocytes to the induction of SCEs by mitomycin C (MMC) either in vitro (3 X 10(-8)/10(-7)M) or in vivo (0.3/3 mg/kg). Since cordycepin is known to inhibit poly(A)synthesis thus blocking RNA maturation, it is suggested that M-MuLV proviral integration is not per se the sole factor responsible for the more pronounced susceptibility of BALB/Mo lymphocytes to SCE induction, but most likely viral gene expression and amplification are needed for this effect to occur.

Animals↗
PubMed1985

Genetic effects of chromium tannins.

Seventeen tannins used in the hide and leather industry, most of which contain mainly Cr(III) sulphates, were tested for the ability to directly induce gene mutations in Salmonella typhimurium (TA 100 strain) and chromosomal effects (sister chromatid exchanges, SCE) in cultured hamster cells (CHO line). Total chromium [Cr(III) + Cr(VI)] content and contaminating Cr(VI) were determined spectrophotometrically by reaction with diphenylcarbazide. None of the tested compounds induced gene mutations, whereas eight tannins were able to increase significantly the frequency of SCE. A contamination with Cr(VI) was detected in four compounds (from 30 up to 100 parts of Cr(VI) per 10(6) parts of compound), insufficient to be revealed by the Salmonella assay but sufficient to account for the observed SCE increase. On the other hand, the increase of SCE induced by the other four tannins could not be explained by the level of Cr(VI) contamination, and can be ascribed to other impurities present in those industrial compounds. These four tannins did not induce gene mutations in the S. typhimurium assay even when strain TA 98 was used in addition to TA 100, independently of microsomal activation. By prolonging the time of the SCE assay from 30 to 48 h in order to facilitate Cr(III) endocytosis, a significant increase of the SCE frequency was induced by an analytical-grade Cr(III) reagent (chromium chloride), absolutely uncontaminated by Cr(VI), as well as by three Cr(III) tannins, otherwise inactive in the SCE assay.

Animals↗
PubMed1984

Induction of sister-chromatid exchanges in human lymphocytes exposed in vitro and in vivo to therapeutic ultrasound.

The induction of sister-chromatid exchanges (SCEs), chromosomal aberrations and cell-cycle delay was determined in human lymphocytes after treatment in vitro and in vivo with therapeutic ultrasound (u.s.). In vitro treatments (1 W/cm2; 0.860 MHz; for 40-160 sec) were performed on unstimulated lymphocytes from 9 donors: a statistically significant, dose-dependent increase in SCE frequency was produced, whereas no induction of chromosomal aberrations nor alteration of the distribution of 1st, 2nd and 3rd division metaphases were observed. The same increase in the frequency of SCEs was detected by treating in vitro stimulated lymphocytes with u.s. The effects of in vivo exposure to u.s. were detected on lymphocytes from 10 patients before, during and after u.s. therapy (0.6-1.0 W/cm2; 0.860 MHz; from 8 to 20 applications lasting 5-6 min each). SCE frequency was statistically significantly increased in all patients at mid-therapy, without a further increase during the second half of therapeutic cycle, and was restored to pretreatment level 3 months after the end of u.s. therapy. No increase in chromosomal aberrations was noticed during and after u.s. therapy, whereas erratic delays of the cell cycle were observed, not clearly related to u.s. application or SCE levels. A linear relationship was found between SCE frequency and age in 21 healthy donors.

Cell Cycle↗
PubMed1984

Trivalent chromium is neither cytotoxic nor mutagenic in permeabilized hamster fibroblasts.

BHK cells became reversibly permeable by a 30-min incubation in hypertonic medium. During permeabilization they were exposed to water-soluble Cr(VI) (K2Cr2O7) and Cr(III) (CrCl3). Thymidine uptake in the intracellular nucleotide pool, DNA replication, DNA damage and repair and sister-chromatid exchanges (SCE) were examined to detect the cytotoxic and genetic effects of Cr compounds. Cr(III) remained inactive also in permeabilized cells. An apparent induction of DNA damage by Cr(III), suggested by the Painter's test, was considered unreliable. Cr(VI) cytotoxic and genetic activity was enhanced in permeabilized cells, as demonstrated by increased inhibition of DNA replication and higher frequency of SCE.

Animals↗
PubMed1984

Short- and long-term studies on chemical carcinogenesis in BALB/Mo mice.

To study the interactions between chemical carcinogens and oncogenic retroviruses, BALB/Mo mice which carry the Moloney murine leukemia virus (M-MuLV) as an endogenous virus, and conventional (M-MuLV-free) BALB/c mice, as well as their Bc1 (M-MuLV+ or M-MuLV-) hybrids were injected neonatally with a single dose of urethane. BALB/Mo and V+ Bc1 mice showed accelerated lymphoma development; similar results were obtained in BALB/Mo mice receiving one or two doses of urethane transplacentally. Lung adenomas developed with shorter latency and higher incidence in BALB/Mo mice given urethane at birth; however, significant differences in the incidence of lung adenomas in BALB/Mo mice were found only in two experiments. Additional short-term experiments were carried out to investigate the mechanism of the higher susceptibility to sister chromatid exchange induction observed in BALB/Mo lymphocytes. It was found that BALB/Mo spleen lymphocytes incubated with cordycepin, an antiviral antibiotic, with or without mitomycin C treatment, showed reduction in both M-MuLV synthesis and sister chromatid exchange frequency, and the latter values were similar to those seen in control cultures. These data suggest that the integration of M-MuLV proviral DNA into the host genome is per se not sufficient to increase the susceptibility to carcinogenic stimuli, but that other events, such as viral gene expression and amplification, are most likely required for the chemical-viral synergistic effect to occur.

Adenoma↗
PubMed1983

Sister chromatid exchanges and chromosomal aberrations induced by mitomycin C in mouse lymphocytes carrying a leukemogenic virus.

The induction of chromosomal damage (sister chromatid exchanges (SCEs), chromosomal aberrations, and micronuclei) in T lymphocytes from mouse spleen was analyzed after treatment in vivo with different concentrations of mitomycin C (MMC). Lymphocytes were derived from BALB/Mo mice, which carry an endogenous type C retrovirus (Moloney murine leukemia virus, M-MuLV), and from BALB/c mice (controls, M-MuLV-free). Chromosomal damage was determined in vitro on lymphocytes stimulated with concanavalin A (Con A) and incubated for two generation cycles with bromodeoxyuridine (BUdR). The baseline frequency of SCEs was significantly higher in untreated BALB/Mo than in BALB/c lymphocytes. The frequencies of SCEs were significantly increased by increasing doses of MMC in both BALB/c and BALB/Mo T lymphocytes. Treatment with a low dose of MMC (0.3 mg/kg) produced an additive effect on SCE frequency in BALB/Mo lymphocytes, which was gradually suppressed by increasing the MMC concentration (3-5 mg/kg). Indeed, the levels of SCEs became significantly lower in BALB/Mo than in BALB/c lymphocytes at the highest MMC concentration tested (10 mg/kg), indicating that a negative synergistic effect was eventually produced. Chromosomal aberrations (breaks and total aberrations) were significantly increased by the highest MMC doses (5-10 mg/kg) and were more frequent in BALB/Mo than in BALB/c lymphocytes at 10 mg/kg MMC. The frequencies of micronuclei were increased by all MMC doses and were significantly higher in BALB/Mo than in BALB/c lymphocytes at 10 mg/kg MMC. These results are referred to interferences of M-MuLV and MMC with the function of enzymes, such as DNA topoisomerases, involved in the mechanism of SCE production.

Animals↗
PubMed1982

Cytotoxic, mutagenic and clastogenic effects of industrial chromium compounds.

Ten Cr(III) compounds, used in the leather tanning industry, and a Cr(III) compound, containing chromite and used as a pigment, were tested for cytotoxicity (inhibition of growth and survival of cultured hamster cells), mutagenicity (point mutations in S. typhimurium) and clastogenic activity (chromosomal aberrations and sister chromatid exchanges in hamster cells). Reference Cr compounds were potassium dichromate as Cr(VI), and chromium chloride and two different preparations of chromium nitrate as Cr(III). A contamination with Cr(VI) was detected in some of the Cr(III) tannins, chromite and one chromium nitrate. Cr(III) compounds were cytotoxic at concentrations of Cr(III) 100-500 times higher than Cr(VI), but contaminated Cr(III) compounds showed a significant cytotoxicity. Reference Cr(VI) but not Cr(III) was mutagenic: of the contaminated compounds only chromite and chromium nitrate, which contained higher levels of Cr(VI), were found to be mutagenic. The frequency of sister chromatid exchanges was significantly increased only by Cr(VI) and the more contaminated Cr(III) compounds. However, an increase of chromosomal aberrations was produced also by reference Cr(III) salts and the weakly contaminated industrial Cr(III) compounds. These results confirm the view that the active mutagenic agent in intact cell systems is Cr(VI), but indicate that industrial Cr(III) compounds cannot be considered genetically inert, as they can be contaminated by Cr(VI) and induce chromosomal aberrations.

Animals↗
PubMedDate not supplied

Reinforced HEAV'D therapy for adult acute lymphoblastic leukemia: improved results and revised prognostic criteria.

Thirty-six adults with acute lymphoblastic leukemia (ALL) were treated with adriamycin, vincristine, prednisolone, and asparaginase for remission induction, followed by vincristine-adriamycin-cyclophosphamide consolidation courses, cranial irradiation, a short ara-C plus VM-26 pulse, and vincristine plus cyclophosphamide rotating weekly with ara-C plus VM-26 for three months (reinforced HEAV'D). Thirty-one patients achieved a complete remission (86 per cent). Compared with historical results from a prior study, age > 30 years, absolute blast count > 15 x 10(9)/l, and CD10-negative immunophenotype were not associated with higher relapse rate and shorter survival, suggesting a positive effect from intensification therapy with ara-C and VM-26 in these poor prognostic categories. However, patients with an abnormal karyotypic pattern or a positive molecular study for BCR-ABL rearrangement detecting t(9;22) had a far greater likelihood of treatment failure (probability of remission at 3 years 0.10) than those with normal karyotype or negative molecular study (probability 0.70), and those not studied or with insufficient methaphases (probability 0.50) (p < 0.05 by log-rank test). These results underline the prognostic importance of chromosomal abnormalities and the usefulness of ara-C and VM-26 in the management of adult ALL.

Adolescent↗
PubMedDate not supplied

Genetic effects of chromium compounds.

Seven different test systems were utilized to investigate the genetic activity of chromium compounds: infidelity of DNA replication in vitro by DNA pol alpha from calf thymus, damage of DNA detected by alkaline elution in treated mammalian cells or in DNA purified and treated in vitro, DNA repair synthesis in mammalian cells in vitro detected by autoradiography or scintillation counting after labelling with [3H]dThd, gene mutations in the Salmonella typhimurium Ames test, gene mutations (6TG resistance) in cultured hamster cells, sister-chromatid exchanges in different rodent cell cultures, and transformation to anchorage-independent growth of hamster cells in vitro (soft-agar assay). Potassium dichromate and chromium chloride were used as water-soluble Cr(VI) and Cr(III) salts. Several reference mutagens (EMS, MMS, MMC, 4NQO) were included in the single tests as positive controls. Cr(VI) was active in all the tested systems, except in the induction of DNA damage and DNA repair synthesis in cultured cells. Cr(III), on the other hand, was absolutely inactive unless a direct interaction with purified DNA was permitted by the test conditions. The relevance of data from the various tests to the understanding of the mechanisms of the genotoxic activity of chromium is discussed. Effects other than the direct interaction of Cr(III) with DNA are inferred, which can cause infidelity of the DNA polymerase functions.

Animals↗
PubMedDate not supplied

Transient acute monoblastic leukemia with reciprocal (8;16)(p11;p13) translocation.

The translocation of t(8;16)(p11;p13) has been demonstrated in the blasts of a phenotypically normal newborn baby with acute monoblastic leukemia. No antileukemic therapy was administered and spontaneous, complete remission was observed at 2 months of age. The patient remains well 18 months after the diagnosis and continues to have a normal hemogram.

Chromosomes, Human, Pair 16↗
PubMedDate not supplied

Unusual leukemic presentation of rhabdomyosarcoma: report of two cases with immunological, ultrastructural and cytogenetical studies.

BACKGROUND: Bone marrow infiltration occurs rarely at presentation of rhabdomyosarcoma (RMS) or other childhood solid tumors. This possibility leads to misdiagnosis of leukemia and incorrect therapies might be administered. METHODS: We report two patients presenting with diffuse bone marrows involvement by neoplastic cells. Initial studies were not consistent with a diagnosis of leukemia and the cases were further studied extensively by indirect immunofluorescence, immunocytochemistry, electron microscopy and cytogenetics. RESULTS: In both cases blast cells were large, poorly differentiated, with immunological reactivity to the anti-desmin antibody. Ultrastructural findings of muscular features and chromosomal translocation t(2;13) (q37;q14) further confirmed the diagnosis of rhabdomyosarcoma of the alveolar subtype. This was then confirmed histologically in one patient. CONCLUSION: This study stresses the utility of analyzing cases of morphologically undifferentiated marrow blast cells by various techniques, as well as investigating for different types of both hematological and solid neoplasms.

Adolescent↗