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Biomedical subjects

M Nigli

Publications and source records attributed to M Nigli.

5 recordsLinked to original sources
PubMed1989

Relationship of embryotoxicity to genotoxicity of lead nitrate in mice.

Frequency of sister chromatid exchanges (SCEs), nucleolar organizing regions (NORs) and chromosomal aberrations were analysed, in maternal bone marrow and fetal liver and/or lung cells of ICR Swiss Webster mice, following maternal exposure to lead nitrate on gestational day 9. The number of implantations and morphological changes in day 18 fetuses, following the treatment, were also noted. Chemical analysis of lead in maternal and fetal tissues showed that it is readily transferred across the placenta. Lead caused a moderate, but statistically significant, increase in the frequency of SCEs in maternal bone marrow cells and significant reduction in NORs at the 2 highest dose levels (150 and 200 mg/kg b.w.). Lead treated animals showed several specific chromosomal aberrations, mostly deletions in maternal bone marrow and fetal cells. Aneuploidy was found to be frequently associated with the lowest dose levels of lead nitrate (100 mg/kg). Maternal treatment with lead nitrate also significantly increased embryonic resorptions and reduced placental weights. The results suggest that the embryotoxic effects of lead might be associated with the chromosomal changes.

Animals↗
PubMed1989

Embryotoxicity and in vivo cytogenetic changes following maternal exposure to cadmium chloride in mice.

Cadmium is a well-known teratogen in laboratory animals and a widespread environmental pollutant. The frequencies of sister chromatid exchanges (SCEs), nucleolar organizing regions (NORs) and chromosomal aberrations were analysed in maternal bone marrow and fetal liver and/or lung cells of mice, following maternal treatment with cadmium chloride, on gestational days 8 through 10. The embryotoxic effects and morphological changes on day 18 fetuses were also studied. Cadmium chloride is readily transferred across the placenta and significant levels were detected in both the placenta and fetus. No significant changes in the frequencies of SCEs or NORs in maternal and fetal cells were observed following exposure to cadmium chloride. Fetal tissues showed mitotic inhibition at the highest dose levels (8.4 and 11.4 mg/kg, b.w.). Maternal treatment with cadmium chloride increased embryonic resorptions and fetal lethality, as well as reduced placental weight; however, it did not produce significant chromosomal changes except at the highest dose level (11.4 mg/kg).

Abnormalities, Drug-Induced↗
PubMed1988

Structural gene encoding human factor XII is located at 5q33-qter.

The gene encoding human factor XII (F12) or Hageman factor has been mapped to 5q33-qter. This has been achieved by analyzing the results obtained from hybridizing a cloned fragment from the factor XII gene to a panel of human-hamster somatic cell hybrid DNAs and also by in situ hybridization to normal human metaphase cells. The previously reported results localizing F12 to 6p23 are discussed.

Animals↗
PubMed1987

DNA studies in a family with Duchenne muscular dystrophy and a deletion at Xp21.

We have performed Southern blot analysis on a large, four-generation kindred with Duchenne muscular dystrophy (DMD). Probes 754 (DXS 84), pERT87-1, pERT87-8, pERT87-15 (DXS164), and pXJ-1.1 did not hybridize to digested genomic DNA of affected males. Obligate-carrier mothers and unaffected brothers showed signals of a single X-chromosome copy intensity, and suspected noncarrier sisters demonstrated either a single band of two-copy intensity or informative polymorphisms. Uniform hybridization was seen with probes C7 (DXS28) and D2 (DXS43), which map distal to the DMD locus, and with OTC, which maps proximally. This deletion was present in six affected individuals and has been transmitted through 3 generations to date. On high-resolution chromosome analysis, a deletion within band Xp21 was consistently observed in one affected male studied and in one of the two X chromosomes in obligate carriers. This large molecular and cytogenetically visible deletion in affected DMD individuals without glycerol kinase deficiency, chronic granulomatous disease, retinitis pigmentosa (RP), or ornithine transcarbamylase deficiency is a very rare finding and should prove useful in specifically cloning additional probes within and flanking the DMD locus.

Adolescent↗