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S Parodi

Publications and source records attributed to S Parodi.

At least 163 records · Page 9Linked to original sources
PubMed1982

Decreased viscosity of rat-liver DNA treated by 3'-methyl-4-dimethylaminoazobenzene, detected with a new viscometric approach.

DNA damage induced in vivo by 3'-methyl-4-dimethylaminoazobenzene (3'CH3DAB) was investigated with 2 differently sensitive techniques: the alkaline elution assay and the viscometric measurement of DNA damage. 3'CH3DAB appeared to be falsely negative with the alkaline elution assay, whereas with the viscometric approach, which is about 30-50 times more sensitive, it appeared positive, and the DNA damage was dose-dependent.

Animals↗
PubMed1982

Comparison between sensitivity of a viscometric method and sensitivity of the alkaline elution assay for the determination of DNA damage induced by dimethylsulfate in vitro.

DNA damage induced by dimethylsulfate (DMS) was measured with a new oscillating crucible viscometer, having a U-shaped circular channel. Rat liver nuclei were treated in vitro. Viscosity was measured by lysing nuclei in an aklaline lysing solution (pH 12.5; 25 degrees C). Nuclei were lysed immediately in the viscometer and released DNA started to uncoil. In control samples the viscosity increased very slowly with time, reaching a maximum only after about 8 h. A progressively more rapid increase in viscosity was seen with increasing concentrations of DMS. The time of DNA disentanglement was sensitive to about 30 times less breaks than the alkaline elution assay.

Animals↗
PubMed1982

DNA damage in liver, kidney, bone marrow, and spleen of rats and mice treated with commercial and purified aniline as determined by alkaline elution assay and sister chromatid exchange induction.

Aniline of unknown purity has been reported to induce spleen hemangiosarcoma in rats. Aniline has been found to be negative in terms of mutagenicity in both bacteria and yeasts. We have found that both commercial (already rather pure) and repurified aniline are clearly positive to a similar extent in inducing DNA damage in vivo in liver and kidney of rats. Both the commercial and repurified product are also clearly positive in induction of sister chromatid exchanges in vivo in male Swiss mice bone marrow cells. Liver, kidney, and bone marrow DNA damage was absent in male Swiss mice.

Aniline Compounds↗
PubMed1981

[Specific effects of Cr ions on DNA: a comparison between the interaction of CrIII with purified DNA and with DNA from cultured cells].

Affinity between CrIII and purified calf thymus DNA were studied by equilibrium dialysis at different pHs. Chromium was dosed by atomic spectrometry. This affinity was compared with Chromium-DNA affinity after treatment of living mammalian cells with CrVI and its intracellular reduction. Preliminary results seem to suggest that affinity is similar in both cases and not especially high (K approximately 10(5) 1/mole).

Animals↗
PubMed1981

[Affinity between CrIII and purified DNA, studied by competition with an intercalating agent: ethidium bromide].

The affinity between CrIII and purified calf- thymus DNA was studied at neutral pH by competition with ethidium bromide. Competition results indicated an affinity between CrIII and DNA of the order of 10(5) 1/mole. These results are in good agreement with previous results CrIII - DNA affinity was studied by the independent method of equilibrium dialysis and chromium dosage by atomic spectrometry.

Animals↗
PubMed1981

[DNA damage after treatment in-vivo with several aromatic amines: 2,4-diaminotoluene, 4-aminobenzene (aniline) and paradimethylaminoazobenzene (butter yellow)].

Three aromatic amines, 2,4 diaminotoluene, aminobenzene and paradimethylaminoazobenzene were examined for their capability of damaging rat liver DNA. Compounds were tested by the "in vivo"/DNA alcaline elution assay. 2,4 diaminotoluene was very positive, aminobenzene weakly positive, paradimethylaminoazobenzene probably negative. All the compounds were tested at doses already clearly toxic.

Aniline Compounds↗
PubMed1981

DNA-damaging activity in vivo and bacterial mutagenicity of sixteen aromatic amines and azo-derivatives, as related quantitatively to their carcinogenicity.

Sixteen aromatic amines and azo-derivatives were studied. They were: benzidine; 2-acetylaminofluorene; 3'-methyl-p-dimethylaminobenzene; o-aminoazo-toluene; p-dimethylaminoazobenzene; 2,4-diamino-toluene; 4,4'-oxydianiline; 2,4-diaminoanisole; 4,4'-methylenedianiline; 2-naphthylamine; Auramine O; Rhodamine B; Ponceau MX; 1-naphthylamine; p-aminoazobenzene and aniline. The compounds were examined for their capability to induce alkaline DNA fragmentation in rat liver after treatment in vivo, for their mutagenicity in the Salmonella strains TA 98 and TA 100, for their acute toxicity and for their carcinogenicity in mice and rats. For each parameter a quantitative potency index was established, and the correlation existing amongst the different parameters investigated. Only mutagenicity in the strain TA 98 was slightly correlated with carcinogenic potency (r = 0.408). DNA fragmentation and toxicity were not correlated with carcinogenicity. A significant correlation was found between DNA fragmentation and toxicity (r = 0.539). No correlation was found between DNA fragmentation and mutagenicity. The lack of correlation between DNA fragmentation and carcinogenicity is in contrast with previous results obtained with a family of hydrazine derivatives (12) and a group of nitrosocompounds (22). For these two groups of chemicals correlation between DNA fragmentation and carcinogenicity existed, but not between carcinogenicity and mutagenicity in the Ames' test. It is suggested that short term tests can perform very differently for different classes of chemicals.

Amines↗
PubMed1981

DNA-damaging activity in vivo and bacterial mutagenicity of sixteen hydrazine derivatives as related quantitatively to their carcinogenicity.

Sixteen hydrazine derivatives (hydrazine, 1,1-dimethylhydrazine, 1,2-dimethylhydrazine, phenylhydrazine, procarbazine, isoniazid, isocarboxazid, nialamide, 2,4-dinitrophenylhydrazine, phenelzine, hydralazine, dihydralazine, carbamylhydrazine, mebanazine, iproniazid, and 1-carbamyl-2-phenylhydrazine) were tested for DNA-damaging activity by the alkaline elution technique and for mutagenic activity in the Salmonella-microsome (Ames) test. The first nine compounds listed (56%) were found to induce a significant DNA fragmentation in the liver and/or in the lung of i.p.-treated male Swiss mice. The DNA-damaging potency varied over an approximately 30-fold range. Thirteen of the first 14 compounds listed (81% of the total), isocarboxazid being inactive, were positive in the Ames test, with a broad range of activity towards the five bacterial strains of Salmonella typhimurium used (TA1535, TA100, TA1537. TA1538, and TA98) and of metabolic behavior in the presence of S-9 mix containing rat liver, mouse liver, or mouse lung postmitochondrial preparations from Aroclor-treated animals. The mutagenic potency varied over an almost 7000-fold range. For 11 of the 16 hydrazine derivatives tested, homogeneous carcinogenicity data (induction of pulmonary tumors in mice chronically treated p.o.) were available from literature. Elaboration of these data showed that carcinogenic potency varied over an approximately 1900-fold range. The five most potent carcinogens were all positive in the DNA damage test. Their carcinogenic potency varied over a 130-fold rage and their DNA-damaging potency varied over a 22-fold range. DNA-damaging potency seemed to vary on a more compressed scale, but regression analysis indicated the existence of a strong positive correlation between in vivo DNA-damaging and carcinogenic potencies, while a lack of correlation was found between mutagenic and carcinogenic potencies. There was no correlation between DNA-damaging and mutagenic potencies.

Animals↗
PubMed1980

Detection by alkaline elution of rat liver DNA damage induced by simultaneous subacute administration of nitrite and aminopyrine.

DNA fragmentation induced in the livers of rats by oral treatment with NaNO2 and aminopyrine was evaluated by the alkaline elution technique. Whereas simultaneous administration of the two compounds in a single dose produced only a minimal increase of the DNA elution rate, their intake with drinking water for 20 successive days caused DNA fragmentation comparable to that observed after a single ip injection of 10-20 mg/kg N-nitrosodimethylamine. Either NaNO2 or aminopyrine alone induced borderline DNA damaging effects, if any, in both rats receiving a single dose and those treated for 20 successive days.

Aminopyrine↗
PubMed1980

Alkaline elution assay as a potentially useful method for assessing DNA damage induced in vivo by diazoalkanes.

In order to evaluate directly in vivo the extent of correlation existing between mutagenic-carcinogenic activity of diazoalkanes and their DNA damaging activity, alkaline elution was used to study the induction of single-strand breaks in and repair of DNA from mice treated with N-diazoacetylglycine amide (DGA). A dose-dependent DNA fragmentation was present, 4 hr after ip injection of single doses of DGA, in liver, lung, kidney, spleen, thymus, and bone marrow. The differences among these organs in the amount of DNA damage were small, even if sometimes statistically significant. Elution profiles indicated that a progressive conversion of alkali-labile sites to single-strand breaks took place in the first 50 min of elution. Twenty-four hr after treatment with 1000 mg/kg, DNA damage was only slightly reduced in liver, lung and bone marrow. A detailed statistical analysis of the variability of experimental results is reported in order to give information about the reliability of the method, and to allow the possibility of calculating the number of separate experiments required to reach statistical significance for a given increase of DNA elution rate.

Alkalies↗
PubMed1979

[Induction of sister chromatid exchange (SCE) and incorporation of BUdR in mouse cells treated with methotrexate].

MTX (approx. DI 50) induced an approx. 140% increase in SCE over controls. Increasing the BUdR concentration from 10(-5) to 10(-4) M an approx. 135% increase in SCE over controls was also obtained. The quenching of the H33258 dye fluorescence, measured microspectrofluorimetrically, suggested an increased in corporation of BUdR in MTX treated cells, roughly compatible with almost a doubling of the SCE control level in absence of MTX. Thus, at least a large fraction of the MTX induced SCE increase appeared to be dependent from an enhanced BUdR incorporation.

Animals↗
PubMed1979

DNA damage and repair induced by diazoacetyl derivatives of amino acids with different mechanism of cytotoxicity. Correlations with mutagenicity and carcinogenicity.

Eight synthetic N-diazoacetyl amino acids, prepared by inserting a diazoacetyl group onto the alpha-nitrogen of a natural amino acid, and two natural diazoazetyl amino acids, azaserine (9-diazoacetyl-L-serine) and DON (6-diazo-5-oxo-L-norleucine), have been studied by autoradiography for their capacity to induce DNA repair synthesis in mouse cells cultivated "in vitro". Dose-dependent unscheduled DNA synthesis was present in cells treated with the eight N-diazoacetyl derivatives, and was absent in cells exposed to approximately equitoxic concentrations of azaserine and DON. Azaserine and DON, unlike N-diazoacetyl derivatives, did not alkylate gamma-(4-nitrobenzyl) pyridine at an appreciable extent. When DNA damage (single stranded breaks or weak points in alkali) was measured by the sensitive technique of alkaline elution, DGA was found about 4 times as potent as azaserine and about 12 times as DON on a molar basis, but about 800 and 17,000 times as potent as azaserine and DON respectively by extrapolating to equitoxic concentrations. Carcinogenicity and mutagenicity seem to follow mainly the capability of inducing DNA damage.

Alkylation↗