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Biomedical subjects

J Koziorowska

Publications and source records attributed to J Koziorowska.

At least 55 records · Page 3Linked to original sources

The effect of crude preparations of vaccinia on mitosis and DNA synthesis of KB cells.

A morphologic study has been made on KB cells infected with various doses of vaccinia as to DNA synthesis and mitosis. Determination of mitotic indices revealed that the mitotic cell pool depended on the proportion of infected cells and the time after infection. By cytologic examination neither mitotic lesions were found nor an accumulation of mitotic cells at any one stage of mitosis was demonstrated. Radioautographs of infected cultures have shown that the frequency of cells labeled over nuclei was significantly increased as compared with control cultures. Following the greatest dose of virus (multiplicity of 20 PFU/cell) the ratio of cells synthesizing DNA to mitotic cells increased from 45:5 at 5 hr to 50:0 at 50 hr. Concommittant with the appearance of this disparity between the DNA-synthesizing cell pool and mitotic cell pool the nuclei of cells became "lightly" labeled. Following the lowest dose of virus (multiplicity of 0.0002 PFU/cell) the increase of the fraction of mitotic cells was proportional to the increase of the fraction of cells which were labeled over nuclei.

Cell Division↗

Effects of iron and copper ions on the inducibility of hydrogen peroxide in E. coli.

Inducing capacities of hydrogen peroxide in SOS chromotest were investigated in the absence and in the presence of iron and copper ions. Strain PQ37 of Escherichia coli and two strains with altered protection against oxidative damage (PQ300 and OG400) were employed. The latter two strains were more sensitive to the hydrogen peroxide inducing activity than strain PQ37. At the concentration of 150 nmol/ml and 300 nmol/ml, iron ions induced SOS response. At the concentration range from 30 nmol/ml to 300 nmol/ml iron enhanced the effects produced by H2O2. Results with copper were negative.

Colorimetry↗

Testing of cyclophosphamide and diethylstilbestrol for their ability to enhance virus survival in normal human cells.

A relatively simple assay for determining the capability of chemicals to induce the reactivation of UV-irradiated pseudorabies virus in human embryo cells is presented. Using this assay cyclophosphamide (CP) and diethylstilbestrol (DES) were tested in the presence and in the absence of exogenous metabolizing system. N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) was used for comparison. CP increased the survival of UV-irradiated pseudorabies virus exclusively in the presence of exogenous metabolizing system. In the cells pretreated with CP or MNNG the survival of the virus was dependent on time interval between host cell pretreatment and virus infection. No enhancement of virus survival was obtained in the cells pretreated with DES.

Animals↗

Effects of riboflavin on benzo(a)pyrene, 2-acetylaminofluorene and methyl methanesulfonate mutagenicity in vitro.

Riboflavin was shown to inhibit mutagenicity of benzo(a)pyrene and 2-acetylaminofluorene in the presence of S9 liver fractions deriving from B10.A mice as well as from DBA/2 mice and had no influence on mutagenicity of methyl methanesulfonate. The above findings confirm the supposition that antimutagenicity of riboflavin results from its interaction with enzymes responsible for metabolic activation of promutagens. The antimutagenic effects of riboflavin were more drastic in the presence of liver fractions from B10.A mice than in the presence of those from DBA/2 mice.

2-Acetylaminofluorene↗

Evaluation of the metabolizing capacity of S9 liver preparations from rats and mice using a test with Salmonella typhimurium TA100.

The S9 phenobarbital-induced preparations from Albino rats and 6 strains of inbred and outbred Pzh: SFISS mice were tested by an Ames test for their ability to metabolize the two promutagens 2-aminofluorene (2AF) and cyclophosphamide (CP), and to influence the mutagenic activity of the two directly acting mutagens methyl methanesulphonate (MMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). 2AF showed a mutagenic activity after incubation with all kinds of microsomal preparations. S9 from B10. mice (Ah+Ah+) was twice as active as that from D2.BN mice (Ah- Ah-). CP was mutagenic exclusively in the presence of S9 from Pzh: SFISS or B10. mice and from rats. Neither fraction deactivated significantly the mutagenicity of MMS. Microsomal preparations from Albino rats and outbred mice were most active in deactivating the mutagenicity of MNNG.

Animals↗

Protective action of ascorbic acid against mutagenicity of aminopyrine plus nitrite.

Mutagenicity of aminopyrine and of aminopyrine plus nitrite was tested by the micronucleus test in bone marrow of mice and by host mediated mutagenicity assay with mice as host animals and S. typhimurium strain G 46. In parallel the possibility of the protective action of ascorbic acid was studied. Aminopyrine at the dose of 90 mg/kg po when administered to mice together with potassium nitrite induced a significant increase in the frequency of micronuclei in polychromatic erythrocytes and proved to be mutagenic for a Salmonella strain. In both systems mutagenicity of the combination of aminopyrine at this dose plus nitrite was abolished completely by ascorbic acid (373 or 622 mg/kg po). Ascorbic acid neither induced a significant increase in the frequency of micronuclei nor was mutagenic for the strain G 46. A formulation of aminopyrine with ascorbic acid is proposed.

Aminopyrine↗

Comparative study of mutagenic, inductive and transforming activities of ledakrin.

Mutagenic activity of Ledakrin in microbial testing as well as its inductive effect on the release of free phages in lysogenic bacteria were compared with its transforming ability in human cell system. It has been found that Ledakrin is highy mutagenic both without metabolic activation and when activated in vivo. Ledakrin induces the release of free phages in E. coli K12(lambda +), but does not transform human fibroblasts in cell cuture in vitro.

Acridines↗

Neoplastic transformation in vitro.

Oncogenic transformation of cultured cells is considered to be analogous to the induction of tumors in animals. Two properties of transformed cells: the capacity to grow in soft agar and morphological alterations were used as a basis for quantitative studies on the transforming properties of chemicals. The majority of experiments on chemical carcinogenesis were so far performed on murine, hamster and rat cell systems. The most pertinent questions to be resolved now are connected with malignant transformation of human cells.

Animals↗

[Effect of lack of exogenous methionine on protein synthesis in normal and leukemic leukocytes cultured in vitro].

Experiments were performed on lymphocytes and leucocytes isolated from peripheral blood of healthy donors and on leucocytes from patients with acute myeloblastic and acute lymphoblastic leukaemia. The influence on protein synthesis of methionine depletion in the medium or replacement of methionine by homocysteine was measured in labelling experiments with tritiated valine. The rate of protein synthesis in lymphocytes and leucocytes from healthy donors cultivated in homocysteine--containing medium and stimulated with PHA did not differ significantly in the course of 5 days from the rate of protein synthesis in the basic medium. In leukaemic leucocytes cultivated in vitro in the time period of 34 h in the rate of protein synthesis in homocysteine--containing medium was similar to the rate of protein synthesis in the medium devoid of methionine.

Adult↗

Effect of excess methionine on methotrexate cell-killing action in vitro.

Methionine at the concentrations 10, 15 and 20 times higher than in complete Fischer's medium produced a transient impairment or a transient block in the growth of L 5178 Y cells in culture without influencing their viability. Autoradiographic data revealed that methionine-induced inhibition of DNA synthesis was followed by a partial synchronization of cells in the phase of DNA synthesis. Methionine at a high concentration (1.5 mg/ml) enhanced the cell-killing action of methotrexate under conditions of delayed drug addition and did not diminish it when added with the drug simultaneously.

Animals↗