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PubMed1980

Inducibility of somatic colour and white spots in the mammalian spot test.

F1 embryos of the C57BL/6JHan x T-Stock were exposed to utero to 5, 10, 15 and 45 mg/kg b.w. of cyclophosphamide (CP) s.c. on the 10th day of pregnancy. 3-5 weeks post-partum the offspring were examined for the appearance of recessive coat-colour mosaics and white midventral spots (WMVS). The frequencies of the coloured spots were 0.93 and 2.59% at 5- and 10-mg/kg doses of CP, resp. These frequencies were dose-dependent, but the difference between the doses was not significant. No coloured spots were obtained with CP at 15 and 45 mg/kg. The frequencies of WMVS were much higher than those of coloured spots (1.40, 6.03 and 51.16%, resp.). The differences were highly significant. The reduction in the number of offspring compared with the raio of the offspring/female of the control (control = 100%) were 16.16, 22.72, 72.48 and 100% at the different doses of CP (5, 10, 15 and 45 mg/kg b.w.).

Animals↗
PubMed1987

Radiation-induced forward and reverse specific locus mutations and dominant cataract mutations in treated strain BALB/c and DBA/2 male mice.

Strain BALB/c and DBA/2 mice were chosen to investigate the effects of genetic background on the radiation-induced mutation rate since they exhibit differences in their radiation sensitivity. Males were exposed to 3 + 3-Gy X-irradiation and mated to untreated specific locus Test-stock females. Offspring resulting from treated spermatogonia were screened for induced specific locus forward and reverse mutations and dominant cataract mutations. Since BALB/c mice are homozygous brown and albino, specific locus forward mutations could be screened at 5 of the 7 specific loci (a, d, se, p, s), while reverse mutations could be screened at the b and c loci. Strain DBA/2 is homozygous non-agouti, brown and dilute. Therefore, specific locus forward mutations could be screened at 4 loci (c, se, p, s) and reverse mutations were screened at the a, b and d loci. Results indicate no effect of genetic background on the sensitivity to mutation induction of specific locus forward mutations, while for the dominant cataract alleles strain DBA/2 exhibited a higher mutation rate than either strain BALB/c or similarly treated (101/El X C3H/El)F1 mice. If, by confirmation, these differences should be demonstrated to be real, it is interesting that strain DBA/2 should exhibit a greater sensitivity to radiation-induced dominant mutations. First, strain DBA/2 was chosen as radiation resistant or repair competent. The observation that DBA/2 exhibited a higher sensitivity to radiation-induced mutation may indicate a role for repair, albeit misrepair, in the mutation process. Second, that the effect of genotype was only observed for the mutation rate to dominant cataract alleles may reflect a difference in the spectrum of DNA alterations which result in dominant or recessive alleles. A dominant allele is more likely misinformation, such that as heterozygote it interferes with the wild-type allele. By comparison, a recessive allele may result from any DNA alteration leading to the loss of a functional gene product. One reverse mutation at each of the a and d loci was recovered in the present experiments. The similarities of the present results for radiation-induced reverse mutations with the extensive data on the spontaneous reverse mutation rates are interesting. Reverse mutations were recovered only at the a and d loci. Further, the reverse mutations recovered at the a locus were to alternate alleles (at, Aw or Asy) while true reverse mutations were apparently recovered at the d locus.

Abnormalities, Radiation-Induced↗
PubMed1989

The acute effect on levels of catecholamines and metabolites in brain, of a single dose of MPTP in 8 strains of mice.

The neurotoxic agent MPTP produces profound and sustained changes in the biochemistry of the brain in mice after a single dose of 20 mg/kg. Acute neurochemical changes have been examined in detail in 8 strains of mice. Coloured mice were more intoxicated than white mice when treated with MPTP: white mice were little affected behaviourally by a dose that could kill a sensitive coloured strain. Although changes in levels of dopamine were a good indication of the effect of treatment--particularly in the dopaminergic areas, the best discriminator between strains was changes in the levels of adrenaline and noradrenaline. Changes in levels of dopamine, which generally decreased in coloured mice, were not good indicators of toxicity. The changes in levels of adrenaline and noradrenaline discriminated better between strains: they were usually decreased in coloured mice but could substantially increase in white strains, particularly in certain areas of the brain. This study showed that there is a very considerable genetic component to the acute toxicity of MPTP within a single species. Even very closely related mice reacted quite differently to the effect. Also, it showed that white mice, in particular those from the commonly used BALB/c strain, are a poor model for any study of the toxicity of MPTP.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1977

Effects of single albino gene substitutions on the performance of mice in a compound avoidance-discrimination task.

Congenic C57BL/6J mice of the +/+, +/c and c/c genotypes were tested for motoric activity, active avoidance and visual discrimination performance in a variant of the Thompson-Bryant box. The three genotypes were observed to be identical in terms of motor activity, but differed greatly with regard to both avoidance and discrimination performance. On the avoidance portion of the task the c gene appeared to act in an additive fashion, with the +/+ mice being superior to the +/c mice, which were in turn superior to the c/c animals. Visual discrimination performance, however, indicated that the + allele operated in a dominant manner; here c/c mice were found to be inferior in performance when compared to either +/+ or +/c animals while no differences were observed between the two pigmented genotypes. Therefore, under the conditions of the present experiment, the albino gene shows incomplete dominance for active avoidance behavior and recessiveness for visual discrimination performance.

Animals↗
PubMed1991

Lead in children's hair, as related to exposure in Tarragona Province, Spain.

Concentrations of lead were determined in the hair of 478 school children living in an industrial and an agricultural area of Tarragona Province, Spain. The influence of age, sex, hair colour and family occupation on the children's hair lead concentration was also evaluated. Girls had more lead in their hair than boys (10.54 vs 6.55 micrograms g-1), and the lead levels decreased with age. Lead concentrations in hair with respect to hair colour decreased in the order red, blond, brown, black. Family occupation was one of the most significant factors influencing the lead content of children's hair. Although the average lead content was higher in the industrial area (9.38 micrograms g-1) than in the agricultural area (7.80 micrograms g-1), this difference was not statistically significant.

Adolescent↗
PubMed1996

Neonatal MSG reduces hypothalamic DA, beta-endorphin, and delays weight gain in genetically obese (A viable yellow/alpha) mice.

Neonatal treatment with monosodium glutamate (MSG) decreases proopiomelanocortin (POMC) peptides and results in obesity. The yellow mouse is a model of obesity induced by the viable yellow (Avy) gene at the agouti locus on Chromosome 2, which results in overproduction of a POMC receptor antagonist. Thus we hypothesized that MSG, when imposed on the genetically susceptible model, would alter the development of obesity. Both yellow obese (Avy) and black lean (alpha/alpha) males were injected on Postnatal Days 1, 3, 5, 7, and 9 with 2.0 mg/g body weight MSG or saline SC. Their food intake, growth parameters, and neurochemical status were examined. Paradoxically, MSG interacted with the yellow phenotype to delay the rapid rate of weight gain characteristic of this model (p < 0.05). Food intake was decreased (p < 0.05) in both phenotypes treated with MSG, as was hypothalamic content of dopamine (p < 0.05) and of the POMC peptide, beta-endorphin (p < 0.001). The yellow obese phenotype was more sensitive than the black lean phenotype to the neurochemical effect of early postnatal MSG administration. Recent reports suggest the agouti locus protein is an antagonist of the receptor for another POMC peptide, melanocyte-stimulating hormone (MSH). Therefore, the balance of functional activity between various POMC peptides appears to be an important factor in the development of both acquired and genetic obesity.

Animals↗
PubMed1985

The mouse spot test. Evaluation of its performance in identifying chemical mutagens and carcinogens.

The published results on 60 chemicals and X-rays investigated in the mouse spot test were compared with data on the same chemicals tested in the bacterial mutation assay (Ames test) and lifetime rodent bioassays. The performance of the spot test as an in vivo complementary assay to the in vitro bacterial mutagenesis test reveals that of 60 agents, 38 were positive in both systems, 6 were positive only in the spot test, 10 were positive only in the bacterial test and 6 were negative in both assays. The spot test was also considered as a predictor of carcinogenesis; 45 chemicals were carcinogenic of which 35 were detected as positive by the spot test and 3 out of 6 non-carcinogens were correctly identified as negative. If the results are regarded in sequence, i.e. that a positive result in a bacterial mutagenicity test reveals potential that may or may not be realized in vivo, then 48 chemicals were mutagenic in the bacterial mutation assay of which 38 were active in the spot test and 31 were confirmed as carcinogens in bioassays. 12 chemicals were non-mutagenic to bacteria of which 6 gave positive responses in the spot test and 5 were confirmed as carcinogens. These results provide strong evidence that the mouse coat spot test is an effective complementary test to the bacterial mutagenesis assay for the detection of genotoxic chemicals and as a confirmatory test for the identification of carcinogens. The main deficiency at present is the paucity of data from the testing of non-carcinogens. With further development and improvement of the test it is probable that the predictive performance of the assay in identifying carcinogens should improve, since many of the false negative responses may be due to inadequate testing.

Animals↗
PubMed1986

Investigation of the potential for mitotic recombination in the mouse.

A variation of the mouse spot test is described that is designed to distinguish between spots of altered coat colour that arise by reciprocal mitotic recombination and those caused by somatic mutation or non-disjunction. Mouse fetuses that were heterozygous for two, linked coat colour genes were irradiated (1.5 Gy X-rays) in utero at 10.25-10.50 days post coitum (p.c.) or left untreated. Subsequently, the coats were classified for the presence of spots of altered colour. The irradiated embryos were heterozygous for the linked genes pink-eyed dilution (p) and albino (c) and were produced by both the repulsion and coupling crosses. Half of the reciprocal recombination events between the centromere and the proximal marker (p), in heterozygotes with p and c in repulsion, should produce twin spots. No such twin spots would be expected from a similar event in the coupling heterozygotes. The coats of 238 irradiated and 208 untreated repulsion heterozygotes plus 107 irradiated and 314 untreated coupling heterozygotes were classified for spots. One irradiated, repulsion heterozygote had a diffuse twin spot that was only recognisable by microscopic examination of the hairs. We conclude that if the treatment described induces mitotic recombination in the mouse, it does so with low efficiency.

Animals↗
PubMed1991

Mutagenic activity of 2-amino-N6-hydroxyadenine in the mouse spot test.

The base analogue 2-amino-N6-hydroxyadenine (AHA) was mutagenic in the spot test in (T x HT)F1 mouse embryos. Females were injected with single doses of 20 or 40 mg AHA per kg body weight on the 9th day of pregnancy. To rank the mutagenic potency of different compounds, the frequencies of genetically relevant spots induced by 1 mg/kg body weight were calculated. The observed somatic mutation frequency for 1 mg/kg AHA was lower (1.95 x 10(-3)) spots of genetic relevance) than that of mitomycin C (16 x 10(-3)), ethylnitrosourea (6.8 x 10(-3)) and cyclophosphamide (6.4 x 10(-3)) and therefore AHA was not classified as a very potent mutagen in this test system. The doubling dose to induce genetically relevant spots was calculated to be 20 mg/kg b.w. Based on these data, AHA is suggested to be a candidate to induce recessive specific-locus mutations in germ cells of mice.

Adenine↗
PubMed1989

Mouse mutants provide new insights into the role of extracellular matrix in cell migration and differentiation.

Migratory cell populations in the developing embryo disperse, localize and eventually differentiate in environments rich in extracellular matrix material. The extracellular matrix provides both a substratum for migration and a source of differentiative cues for the developing cells. Mutations in mice and other animals that alter embryonic interstitial environments are now providing information about the role of the extracellular matrix in these early developmental processes.

Animals↗