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Biomedical subjects

G Prodi

Publications and source records attributed to G Prodi.

At least 73 records · Page 4Linked to original sources
PubMed1977

An in vitro study on the interaction between dimethylnitrosamine and nucleic acids via a microsomal system.

Radioactive alkylated bases, ribose or phosphate, were never found either in acid and alkaline hydrolysates of polyribonucleotides or in alkaline hydrolysates of DNA after incubation with 14C-dimethylnitrosamine (DMNA) in a microsomal system. Two radioactive compounds, which were co-chromatographed with methylamine and N-methylhydrazine, respectively, on column, paper, and thin-layer, were always detected. They differed from the compound derived from 7-methylguanosine after the alkali-mediated fission of the imidazole ring in its molecule. The in vitro system employed well represents the in vivo situation (7-methylguanine which is liberated from DNA after acid hydrolysis); however, it has given results which do not agree with the generally-accepted mechanism of DMNA alkylation at the N-7 position of guanine.

Animals↗
PubMed1976

Selective effect on T and B cell subpopulations in rat lymphoid organs after urethan treatment.

In vitro phytohemagglutinin (PHA) and concanavalin A (Con A) responsiveness of thymus and bone marrow cells, and E, EA, and EAC rosette-forming cells (E, EA, EAC) of these organs and spleen were studied in Fisher rats at various time intervals following a carcinogenic treatment with urethan (UR). Immediately after treatment, organ cellularities were drastically reduced with a progressive recovery as time passed. 1 day after treatment, the response of thymocytes to PHA showed a fourfold increase while organ cellularity dropped to 1%. This response fell below normal values after 7 days with an overshoot after days 14 and 21. UR-treated bone marrow cells showed a response to PHA below normal values after 1 and 7 days, a twofold increase after 3 days and an overshoot after 14 and 21 days. The responsiveness to Con A of both organs was affected by UR treatment to a much lesser extent, although following a pattern similar to that of PHA. E were never found, whether in normal nor in UR-treated animals. As far as the B-cell compartment is concerned, UR causes a progressive diminution of EAC, while the number of EA remains unaffected. The data are discussed in terms of selective effect on T- and B-cell subpopulations.

Animals↗
PubMed1975

Effect of urethan on the synthesis of nucleic acids in thymus, spleen, and bone marrow.

Urethan, in a single dose of 1 mg/g body weight, exerts a strong inhibitory effect on DNA synthesis in lymphoid organs and bone marrow of rat. The inhibition observed in spleen and thymus is longer lasting than that exerted on bone marrow or regenerating liver, demonstrating a marked sensitivity of lymphoid cells to the drug. This effect can explain the rapid reduction of weight and cell number in thymus and spleen under urethan treatment, in absence of any lymphocytolytic action. The different effect of urethan on the different subpopulations of lymphoid cells therefore appears to be due to their kinetics rather than to a specific sensitivity of some of them.

Animals↗
PubMed1975

Non-enzymatic and microsome-dependent binding of poly-cyclic hydrocarbons to DNA and polynucleotides.

The binding of tritium-labeled 7,12-dimethylbenz[a]anthracene (DMBA), benzo[a]pyrene (BP) and 3-methylcholanthrene (MCA) to DNA or polynucleotides in vitro was re-examined both in the presence and in the absence of rat liver or human placental microsomes. A high level of non-enzymatic binding was evident when thymus DNA was used as acceptor. This non-enzymatic binding made it difficult to determine the effect of microsomes, except in the case of BP when induced rat microsomes were used. Better results were obtained using polynucleotides: a definite microsome-dependent binding occurred between all the polynucleotides and all the hydrocarbons tested. No clear evidence of binding catalysed by microsomes from human placenta was found except in polynucleotide-BP interactions: further studies are required to completely evaluate the ability of such nucleic acid-microsomal system for testing in vitro possible oncogenic substances in animals and humans.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1975

The binding of dimethylnitrosamine to nucleic acids catalyzed by liver enzymic fractions.

The in vitro binding of a metabolite of dimethylnitrosamine (DMNA) to calf thymus DNA catalyzed by a microsomal system from rat liver is reported. The amount ob binding is unaffected by using microsomes induced by 3-methylcholanthrene and/or normal or induced pH 5 enzymes. The microsomal system is also effective in catalyzing covalent binding of the nitroso compound with synthetic polyribonucleotides.

Animals↗
PubMed1975

Identification of dimethylnitrosoamine metabolites in vitro.

The incubation of dimethylnitrosoamine (DMNA) in the presence of rat liver microsomes leads to production of formaldehyde, formic acid, methylamine, and N-methylhydrazine. When pH 5-enzymes are added to the medium there is also the formation of N-methylhydroxylamide and N,N-dimethylhydrazine. The last compound is the only metabolite produced, to a lesser extent, by the pH 5-enzymes. Thus, the denitrosated or non-denitrosated metabolites are produced either by an oxidative dealkylation and by a reduction of DMNA, catalysed by microsomal and cellular soluble enzymes.

Animals↗
PubMed1975

Degradation of dimethylnitrosoamine catalysed by physical and chemical agents.

Decomposition of dimethylnitrosoamine (DMNA) by chemical and physical agents was further investigated. Both photoirradiation with sunlight or ultraviolet ray and reductive reactions under acid conditions (likely occurring in the stomach) led to the formation of formaldehyde, formic acid, and N-methydrazine, in addition to denitrosated compounds such as methylamine, dimethylamine, and N-methylhydroxylamine. N-Methylhydrazine was the only compound which was not detected by photoirradiation under neutral conditions. The agreement between physiochemical and metabolic degradation products and the possible biological meaning are discussed together with the problem of environmental contamination by the nitroso compound.

Dimethylnitrosamine↗