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Biomedical subjects

P Rocchi

Publications and source records attributed to P Rocchi.

At least 37 records · Page 2Linked to original sources
PubMed1982

[Induction by dimethylnitrosamine of mutants resistant to diphtheria toxin in human cells].

Stable spontaneous mutants resistant to the protein synthesis inhibitor diphtheria toxin have been selected in human cell line EUE at a very low frequency (less than 8 x 10-6). We have assayed in this system the mutagenic activity of dimethylnitrosamine (DMNA): mutation increases by this compound have been used as an estimate of his mutagenic activity. Treatment of cells with this compound increased the frequency of diphtheria toxin resistant mutants only at the highest dose used (10-1 M).

Cell Line↗
PubMed1981

Induction of diphtheria toxin-resistant mutants in human cells by ultraviolet light.

Stable spontaneous mutants resistant to the protein synthesis inhibitor diphtheria toxin (DT) have been selected in human cell line EUE at a very low frequency (less than 8 x 10(-6)). U.v.-induced mutation has been quantitatively measured: treatment of cells with u.v. light increased the frequencies of diphtheria toxin resistant (DTr) mutants up to 1000-fold. The maximum recovery of DTr mutants was observed after a short expression period, for all u.v. doses tested, and was followed by a decrease in mutation frequency on subsequent passages.

Cell Line↗
PubMed1980

Effect of pesticides on scheduled and unscheduled DNA synthesis of rat thymocytes and human lymphocytes.

The action of seventeen pesticides (insecticides, fungicides and herbicides) has been studied with short-term in vitro system using rat thymocytes and/or human lymphocytes. The parameters studied were: a)the action of chemicals tested in scalar doses on DNA synthesis of rat thymocytes; b)damage exerted by pesticides on human lymphocyte DNA measured as unscheduled DNA sythesis; c)the interference of chemicals tested with human lymphocyte repair capability after damage exerted on cells by ultraviolet rays. The results obtained suggest that some of tested pesticides don't induce damages to human lymphocyte DNA, some others elicit low DNA repair if compared to the repair following a standard ultraviolet irradiation and some of them (6/17) exert a marked inhibition of cell repair processes after ultraviolet irradiation. Data are discussed on the basis of a possible role played by these substances as carcinogenic agents in the environment.

Animals↗
PubMed1980

Polycyclic hydrocarbons induction of diphtheria toxin-resistant mutants in human cells.

Stable spontaneous mutants resistant to diphtheria toxin are present in the human cell line (EUE) at a frequency of 0-8 x 10(-6). Mutation increases by a number of polycyclic hydrocarbons have been used as an estimate of their carcinogenic potency. Eight polycyclic hydrocarbons of decreasing carcinogenic potency were assayed: 7,12-dimethylbenz[a]anthracene, 3-methylcholanthrene, benzo[a]pyrene, benz[a]anthracene, dibenz[a,c]anthracene, dibenz[a,h]anthracene, chrysene, anthracene, and a well known mutagenic substance, ethyl methanesulfonate. In our system, which does not require an exogenous source for metabolic activation, the most potent hydrocarbons, 7,12-dimethylbenz[a]anthracene, 3-methylcholanthrene and benzo[a]pyrene revealed a strong mutagenic effect, whereas three non-carcinogenic hydrocarbons, anthracene, benz[a]anthracene and chrysene were not mutagenic. Our results indicate that there is a relationship between mutagenesis and carcinogenic potency for the tested polycyclic hydrocarbons. The maximum recovery of diphtheria toxin mutants was observed after an expression time of three weeks, corresponding to 10 cell generations.

Biotransformation↗
PubMed1977

Compared effects of N-hydroxyurethan, urethan and hydroxyurea on DNA synthesis. In vivo and in vitro studies.

The effect of N-hydroxyurethan (HUR) on DNA synthesis has been tested both in vivo on various tissues and in vitro on concanavalin A (ConA)-stimulated rat thymocytes and compared with the action of urethan and hydroxyurea. HUR suppresses scheduled DNA synthesis, except that of non-stimulated spleen cells in vitro. The inhibition is efficient and rapid and takes place immediately if the drug is administered at the peak of the S-phase. UR inhibits DNA synthesis in vitro only at much higher doses and with different time course. It is effective or slightly effective if it is administered at the peak of the S-phase. A conversion of urethan into HUR the latter depressing DNA synthesis could partly explain the differences observed. No toxicity was found after treatment with drugs at the concentration employed. Finally, the relationships between drug doses and cell responses have been particularly observed in vivo.

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↗