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A Eiche

Publications and source records attributed to A Eiche.

14 recordsLinked to original sources
PubMed1990

Genotoxicity of p-aminophenol in somatic and germ line cells of Drosophila melanogaster.

p-Aminophenol (PAP; as a component of, e.g., hair dyes, photographic developers, as adsorbent in gas filters, as a metabolite of various fungicides, pesticides and drugs) has been tested for genotoxicity in Drosophila by means of the sex-linked recessive lethal test (SLRLT) and the somatic mutation and recombination test (SMART) of the wing. While the SLRLT was not significant, the SMART clearly indicated that the compound has genotoxic properties in this in vivo test in agreement with a majority of mammalian short-term tests in vitro and in vivo. The reducing agent dithiothreitol enhanced the genotoxic effects of PAP in the SMART; the reasons for this interaction remain to be elucidated.

Aminophenols↗
PubMed1987

Effect of pH shifts on the mutant frequency at the thymidine kinase locus in mouse lymphoma L5178Y TK+/- cells.

Evidence has been accumulating that conditions of nonphysiological pH may affect the results of in vitro genetic tests by mechanisms unrelated to the chemical being tested. Medium was pH-adjusted with HCl, NaOH or with organic buffers (Good's zwitterions). In the absence of S9 mix, no changes in mutant frequency were observed over a pH range of 6.4-9.2; a small, 1.9-fold increase was observed for a moderately toxic treatment (24% relative growth) at pH 6.3. However, in the presence of S9 mix, the mutant frequency increased sharply for pH values below 6.8. At pH 6.4, a 4-fold increase was induced, and pH 6.0 resulted in a 10-fold increase in mutant frequency. Basic pH shifts in the presence of S9 mix caused no changes in mutant frequency up to pH 8.0; treatment with pH 8.8 was highly toxic (5.3% relative growth) and caused a 3-fold increase in mutant frequency. Thirteen mutant clones induced at pH 6.0 with S9 mix were challenged with trifluorothymidine after their expansion in nonselective medium and all retained their resistance; another 14 clones were tested for thymidine utilization and all incorporated only 0.1-5.5% of the 14C-labeled thymidine used by the parental line. The induced mutants were primarily of the small-colony phenotype, which indicated clastogenic activity. This was confirmed with chromosome studies which showed a large increase in cells with aberrations consisting of chromatid breaks and complex rearrangements. The results show that the combination of weak acidity (pH 6-6.8) and S9 mix is mutagenic and clastogenic to L5178Y TK+/- cells.

Animals↗
PubMed1983

Genetic toxicity of dopamine.

The genetic toxicity of dopamine was studied in a battery of test systems including DNA single-strand break analysis in cultured human skin fibroblasts, the Salmonella/mammalian-microsome mutagenicity test, sister-chromatid exchange analysis in human lymphocytes, the mouse-lymphoma forward mutation assay, the sex-linked recessive lethal test in Drosophila melanogaster and the micronucleus test in mouse and rat. Dopamine at concentrations of 50-300 micrograms/ml induced DNA strand breaks in human fibroblasts. It also gave a positive response in the mouse-lymphoma forward mutation assay, where a dose-dependent increase in the frequency of mutant cells was observed in the presence of dopamine, 94-750 micrograms/ml. All other tests showed no response to dopamine. The dopamine-induced DNA strand breaks in human fibroblasts were inhibited by superoxide dismutase or dithiothreitol. Furthermore, dopamine caused nicking of circular Col El DNA and bound to calf thymus DNA in vitro. It is suggested that this genetic activity of dopamine in vitro relates to oxidation of dopamine and the generation of reactive oxygen radicals, semiquinones and quinones. It is unlikely that similar reactions would occur and cause genotoxic activity of dopamine in vivo.

Animals↗
PubMed1982

X-ray-induced recessive lethal mutations in adult and foetal female mice.

Tests of X-ray-induced recessive lethal mutations in adult and foetal mouse females were performed. The tests were based on family analysis which provided a possibility of making a distinction between pre-existing recessive lethal mutations and newly arisen (spontaneous + induced) ones. The way the tests were carried out provided material for the estimation of the frequency of spontaneous lethal mutations per genome. The two different estimates from this material, 0.72 and 0.91%, respectively, are similar and fall within the range previously suggested by Lüning [5]. The difference, though statistically nonsignificant, between data from irradiated mature and maturing oocytes in adult females and material from the unirradiated part, indicates a mutation rate of 13 x 10(-5) per rad per gamete according to one estimate and 8-12 x 10(-5) according to the other in comparison with 9 x 10(-5) from irradiated spermatogonia [6]. In the limited data obtained after foetal irradiation, there is no indication of oogonia and developing oocytes being more sensitive to irradiation than oocytes in adult females fertilized within 6 weeks of treatment.

Animals↗
PubMed1976

X-ray-induced recessive lethal mutations in the mouse.

A test of X-ray-induced recessive lethal mutations in mouse spermatogonia (500 rad) was carried out. The test was based on familial analysis, which allowed division on the P pairs into those with lethal heterozygous members and in others assumed to be lethal-free. The F1 males from the latter group, in back-crosses to their daughters, gave an excessive rate of intra-uterine death in comparison with lethal-free males. The excessive death is assumed to reflect the rate of new (induced + spontaneous) recessive lethals or rather lethal equivalents. Three ways of estimating the rate of new recessive lethal mutations gave a mean of 5.5% per genome. From the previous tests we can assume that 1% are spontaneous mutations. Thus the data indicate that the mutation rate per rad per gamete is 9 X 10(-5). This value is identical with a previous estimate. The results are discussed in relation to population tests performed in the early 60's. It is concluded that the lack of observable deterioration in the populations after several consecutive generations of exposure is in accord with the estimates in the present analysis which are more than an order of magnitude lower than assumed at the start of the population tests. It is also stressed that species with different DNA contents show similarities in point estimates of doubling dosages.

Animals↗
PubMed1975

Effects of low-dose X-irradiation and age of females on intra-uterine death in mice.

Pilot-tests were carried out on the effect of low X-ray doses (0, 2, 4, 8, 12, 16 and 32 rad) and age of females on intra-uterine death. The tests included the effects of various ages of females at exposure, of fractionated irradiation and pre-partal exposure. Females and males were taken from our inbred CBA strain. Virgin females, as well as females that had produced some litters, were used. From the results it is obvious that the age of the females at the time of mating had a considerable effect on the death rate (varying from about 8% in young females to 25-30% in old ones). The low-dose X-ray exposure does not seem to have had any detectable influence on the rate of intra-uterine death.

Animals↗