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M Bignami

Publications and source records attributed to M Bignami.

47 records · Page 3Linked to original sources
PubMed1981

Microbial short-term assays with thiram in vitro.

The fungicide thiram was assayed in the following tests in vitro, with and without metabolic activation: (1) prophage lambda induction of Escherichia coli K12; (2) repair test in Salmonella typhimurium (strains TA1538 and TA1978); (3) induction of gene mutations in Aspergillus nidulans (methA1 suppressor induction). Thiram was positive in the repair test and in the A. nidulans forward-mutation test (4-6 fold increase) in the absence of metabolic activation. A slight increase was observed in prophage lambda induction with thiram in the presence of the metabolic activation system.

Aspergillus nidulans↗
PubMed1980

Mutagenicity of halogenated aliphatic hydrocarbons in Salmonella typhimurium, Streptomyces coelicolor and Aspergillus nidulans.

Eight structurally related halogenated aliphatic hydrocarbons mono-, di- and trichloroacetaldehyde (the last in the anhydrous and hydrate form), moni-, di- and trichloroethanol and allyl chloride, were tested for their ability to induce gene mutations in prokaryotic and eukaryotic microorganisms. The genetic systems employed were the Salmonella reversion test with strain TA1535 and TA100, with and without metabolic activation, a forward and a back-mutation system in S. coelicolor and two forward mutation systems in A. nidulans. Each compound was tested with the spot and plate incorporation assay techniques. Mono-, di- and trichloroacetaldehyde were mutagenic in all the microorganisms employed; all the halogenated ethanols were positive in A. nidulans, while in S. typhimurium and in S. coelicolor the only active forms were respectively the mono- and dichloroderivatives. Allyl chloride was active in S. typhimurium and S. coelicolor and negative in A. nidulans. The technical approach as well as the complex influence of different factors (toxicity, volatility and stability) on the genetic response of each of the compounds under test did not allow to obtain more than a qualitative relationship between mutagenic potency and chemical structure.

Animals↗
PubMed1979

Mutational studies with diquat and paraquat in vitro.

Diquat and paraquat were assayed in the following tests. (1) Ames test in Salmonella typhimurium (strains TA1535, TA1537, TA1538, TA98 and TA100) with and without rat-liver microsomal fractions. (2) Resistance to 8-azaguanine in Salmonella typhimurium (strain hisG46, TA92 and TA1535. (3) Repair test in Salmonella typhimurium (strains TA1538 and TA1978). (4) Gene mutations in Aspergillus nidulans: 8-AG resistance and methionine suppression (meth A1 locus). (5) Lethal recessive damage in Aspergillus nidulans. (6) Unscheduled DNA synthesis (UDS) in human epithelial-like cells (EUE). Diquat and paraquat were positive in S. typhimurium (in the repair test and the 8-AG resistance system), in A. nidulans (for gene mutations and lethal recessive damage induction) and in EUE cells (UDS induction).

Animals↗
PubMed1979

A new in vitro method for testing plant metabolism in mutagenicity studies.

A rapid method was proposed to detect whether a harmless agricultural chemical can be converted into a mutagenic one by plant metabolism. The method is based on the use of Nicotiana alata cell cultures. Results obtained with five pesticides (atrazine, dichlorvos, tetrachlorvinphos, Kelevan, and maleic hydrazide) suggest that the proposed method simulates the metabolism of the whole plant. This procedure was also successfully applied to the genetic system of Aspergillus nidulans. One pesticide, atrazine, induced mutations and somatic segregation only after metabolism during cocultivation with N. alata cells.

Atrazine↗
PubMed1977

Mutagenic and recombinogenic action of pesticides in Aspergillus nidulans.

Thirteen pesticides, aminotriazole, benomyl, captafol, captan, dalapon-Na, dichlorvos, dinobuton, dodine, ioxynil, mecoprop, neburon, picloram and tordon were tested for ability to induce (1) point mutations to 8-azaguanine resistance, (2) mitotic crossing-over, and (3) mitotic non-disjunction and haploidization in Aspergillus nidulans. Tests were performed at three different pHs, i.e. 4.5, 7, 8.2. Three of the pesticides, captan , captafol and dichlorvos induced point mutations; dichlorvos also induced a high frequency of mitotic crossing-over and non-disjunction; benomyl induced a very high frequency of non-disjunction whereas aminotriazole induced weakly both types of somatic segregation.

Aspergillus nidulans↗
PubMed1976

Localized mutagenesis in Streptomyces coelicolor A3 (2).

Nutritional mutants (co-mutants) were scored among nitrosoguanidine-induced revertants of four mutations in Streptomyces coelicolor A3 (2). All co-mutations were due to mutations in genes linked to the revertant locus. The co-mutant loci were located in a region of about 20 map units around the revertant locus (co-mutation region). Revertants for different loci showed co-mutation patterns different from each other and from that of random nitrosoguanidine-induced forward mutations. Mutations appeared to be completely abolished outside the co-mutation region (mutation restriction).

Cell Nucleus↗
PubMed1973

Comutation in Streptomyces.

Up to 6% of N-methyl-N'-nitro-N-nitrosoguanidine-induced back mutations in the hisA locus of Streptomyces coelicolor were forward mutations (comutations) in another closely linked his locus.

Alleles↗
PubMedDate not supplied

Split-dose exposure to N-methyl-N'-nitro-N-nitrosoguanidine in BALB/3T3 C1 a31-1-1 cells: evidence of DNA repair by alkaline elution without changes in cell survival, mutation and transformation rates.

Dose fractionation of a direct-acting chemical carcinogen, the alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), was studied for its concurrent effects on survival, DNA damage and repair, ouabain resistance (Ouar) mutations and neoplastic transformation, in the mouse embryo cell line BALB/3T3 C1A31-1-1. MNNG doses of 0.5, 1 and 2 micrograms/ml were added to the cells either as a single exposure or in two equal fractions separated by 1, 3 or 5 h intervals. No significant difference in cytotoxicity was found when single and split-dose treatments were compared. No recovery from sublethal damage was therefore found in this cell line by split-dose administration of MNNG, although such an effect was found when the same cell line was treated with single and split doses of X-rays. Repair of DNA damage as measured by alkaline elution was studied up to 24 h after a single MNNG exposure (0.5 micrograms/ml). DNA repair was rapid during the first 5 h after treatment and slow thereafter. DNA damage detected after split doses of MNNG at 1 and 5 h intervals was significantly lower than after a corresponding single dose. With both single and split doses, rejoining of single-strand breaks (ssb) was nearly complete after 24 h of repair time. Ouar mutation and neoplastic transformation frequencies were determined for single and split doses of MNNG with the second treatment being given during (1 h) or after (5 h) the period of rapid DNA repair. No significant differences in either effect were detected for dose splitting at any tested dose.

Animals↗