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Biomedical subjects

M Sorsa

Publications and source records attributed to M Sorsa.

At least 127 records · Page 7Linked to original sources
PubMed1980

Increased sister chromatid exchange frequencies in lymphocytes of nurses handling cytostatic drugs.

In oncology units, personnel handling chemotherapeutic drugs may occasionally be exposed to small amounts of genotoxic agents. This exposure was obviously the cause of the increased frequencies of sister chromatid exchange (SCE) observed in nurses in daily contact with cytostatics (N = 20, mean SCEs/cell +/- SE 9.4 +/- 0.3) as compared to a group of office workers (N = 10, mean SCEs/cell 8.1 +/- 0.3). The oncology nurses also had a higher SCE frequency than other hospital nurses (N = 10, mean SCEs/cell 8.7 +/- 0.2), but this difference was not statistically significant. The SCEs of patients under chemotherapy were about five times higher (mean SCEs/cell 36.8 +/- 0.6) than those of healthy subjects.

Antineoplastic Agents↗
PubMed1979

Effects of styrene oxide on chromosome aberrations, sister chromatid exchange and hepatic drug biotransformation in chinese hamsters in vivo.

In vivo inhalation exposure to styrene oxide (25, 50, 75 and 100 ppm) for 2, 4 or 20 days (25 ppm only) had no effects on chromosomal aberration rates or sister chromatid exchange (SCE) frequencies (BrdU/labelling performed in vitro) in the bone marrow cells of Chinese hamsters. The only positive response in aberration frequency was obtained when styrene oxide was injected in lethal concentration (500 mg/kg body weight, i.p.) into the animal. One animal out of six showed slightly elevated SCE values after this high dose. The response of the hepatic drug metabolizing enzymes to styrene oxide exposure was found to be rather weak, which may be due to rather high activity of epoxide hydratase in Chinese hamsters as compared to e.g. mouse.

Animals↗
PubMed1978

Cytogenetic effects of styrene and styrene oxide.

Styrene and styrene oxide induce various cytogenetic effects, similar in both human lymphocytes in vitro and onion root-tip cells in vivo. Styrene appears to cause chromosome breakage in both systems, and in Allium it shows a strong c-mitotic effect. Styrene oxide, on the other hand, seems to destroy the tertiary folding of the chromatin. Cytotoxicity of styrene oxide is very high (complete mitotic inhibition occurs on 0.03% v/v) in human lymphocytes, whereas, in Allium, styrene is slightly more toxic than styrene oxide. Styrene glycol, a further metabolite of styrene oxide, does not cause mitotic inhibition.

Cells, Cultured↗
PubMed1978

Cytogenetic effects of styrene and styrene oxide on human lymphocytes and Allium cepa.

Styrene and styrene oxide induce cytogenetic effects already at very low concentrations (0.01% v/v or even less); the effects are similar in both in vitro human lymphocytes and in vivo onion root tip cells (Allium cepa L.). It is characteristic that styrene treatment is more potent in causing chromosome breakage in both systems. In Allium styrene induced inhibition of mitotic spindle action as revealed by a strong c-mitotic effect. Also the number of micronuclei and nuclear bridges increased in both test systems, especially after styrene oxide treatment. Furthermore, the metaphase chromosome morphology in the cells treated with styrene oxide was strongly affected. In both systems, chromosome destruction was observed, or else the chromosome material was decondensed and resulted in a characteristic fuzzy appearance of Allium chromosomes or a banded appearance of human lymphocyte chromosomes. A specific effect of styrene oxide on the chromosomal proteins is thus suggested. The data obtained from the autoradiographic studies with Allium support the idea that [7--3H] styrene oxide binds irreversibly to the cytoplasmic and nuclear macromolecules.

Autoradiography↗
PubMed1978

Chromosome aberrations in lymphocytes of workers exposed to styrene.

Workers exposed to styrene in the reinforced plastics industry show a significant increase of chromosome aberrations, mainly chromosome breaks, in peripheral blood lymphocytes. The high incidence of aberrant lymphocytes (mean 15.1 +/- 4.8%; referents 2.0 +/- 1.3 %) was retained when the same men were reexamined one year later (mean 16.2 +/- 2.9 %). However, the frequency of sister chromatid exchanges (SCE), a newly developed sensitive parameter for the detection of recombinational exchanges linked with DNA repair, was not significantly increased (mean 5.3 +/- 1.0 SCE/cell) in comparison to the referents (mean 4.4 +/- 0.6 SCE/cell). This finding suggests a specific role of styrene or its metabolites in inducing genetic lesions mainly manifesting themselves as chromosomal breaks.

Adult↗
PubMed1976

Mutangenicity and toxicity of amitrole. I. Drosophila tests.

Amitrole was highly toxic at early larval stages of Drosophila (LD50 is 40 ppm in medium). Toxicity of amitrole was also revealed by prolongation of development time even at 10 ppm. However, no mutagenic effects of amitrole were observed either in the sex chromosome non-disjunction test (females reared on medium containing amitrole at 10 ppm) or in the sex-linked recessive lethal test (males reared on medium containing amitrole at 10 ppm).

Amitrole↗
PubMed1976

Mutagenicity and toxicity of amitrole. II. Human lymphocyte culture tests.

Effects of amitrole (3-amino-1,2,4-triazole) on human leucocytes in culture were investigated. Amitrole interfered with lymphoblast transformation and inhibited cell growth in concentrations of 0.2% w/v and higher. Selected metaphases were examined for the presence of chromosome and chromatid aberrations. No clastogenic effects were observed.

Amitrole↗
PubMed1976

Mutagenicity and toxicity of amitrole. III. Microbial tests.

Amitrole (3-amino-1,2,4-triazole) inhibits bacterial growth both in Escherichia coli and Salmonella typhimurium at a concentration of 0.5% in minimal medium. Repression of growth already occurs at a concentration of 0.1% of amitrole in this medium. In complete medium the bacteria tolerate concentrations of amitrole as high as 1.7-2.4% before growth ceases. Mutagenicity was tested by differential growth comparisons on E. coli strains W 3110 thy pol A1, defective in DNA polymerase I, and its revertant pol A+. Known mutagens (MMS, NTG, mitomycin C) were used as positive controls. Analogous negative results were also obtained in a revertant test when several trp mutant strains of Salmonella were used.

Amitrole↗