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Biomedical subjects

K Gasiorowski

Publications and source records attributed to K Gasiorowski.

30 records · Page 2Linked to original sources
PubMed1989

Genotoxicity of air pollution in a non-ferrous metal foundry in three bacterial tests and a micronucleus test--a comparative study.

Acetone extracts of dusts and fumes collected at workplaces in a non-ferrous metal foundry exhibited genotoxic activity in all of the tests used. Of the compared tests, the Ames method is the most useful for preliminary screening detection of the genotoxic agents that are present in acetone extracts of dusts and fumes emitted at workplaces in a non-ferrous metal foundry.

Air Pollutants, Occupational↗
PubMed1989

Some aspects of the copper(II)-DNA interaction.

The Cu(II) ion interaction with calf-thymus DNA was studied by means of differential pulse polarography and sweep voltammetry as well as chromatography and viscosimetry. Most of the complexes formed at high ionic strength (0.2 M) and lower Cu(II) concentrations are of a nondenaturing nature. Their formation has but a minor effect on unwinding process of the DNA double helix. The excess of Cu(II) (P = 5) leads, however, to distinct denaturation of the DNA structure. Metal ions have little effect on the denaturation induced by the polarographic reduction of DNA on the mercury electrode. This conclusion is consistent with the character of the polarographic process and with the fact that Cu(II) ions are not very effective in the interaction with AT pairs. Cupric ions have no renaturing ability towards thermally denatured DNA at 0.2 M ionic strength but distinct renaturation was observed at low ionic strength (0.05 M).

Chromatography, Liquid↗
PubMed1987

The influence of subcutaneously administered lead(II) acetate on the concentrations of copper, iron, and zinc in the blood, kidney, liver, and spleen of rats.

The concentrations of copper, iron, lead, and zinc in the blood, kidney, liver and spleen were determined before and after subcutaneous administration of lead(II) acetate (100 mg Pb kg-1 body weight) to male albino Wistar rats. The control rats had the following concentrations (microgram g-1 dry weight) of Cu, Fe, Pb and Zn: blood, 4.5, 3200, 2.1, 182; kidney, 36, 585, 120, 92; liver, 11.1, 720, 14.3, 124; spleen, 4.5, 420, 7.0, 76. After administration of lead, rats were sacrificed after 12, 24, 48, 72 and 96 h. The Pb concentration in the blood remained constant for the first 24 h at the level of the control group (2.1 micrograms g-1) and had decreased to half that level at 96 h. The lead concentrations peaked in the organs at 110-142% of those in the control group and had decreased at 96 h to levels considerably below those in the control group. The concentrations of Cu, Fe and Zn increased in the three organs to values 117-161% found for the control group. At 96 h the concentrations of Cu, Fe and Zn in the spleen had returned to levels of the control group; the concentrations in the liver were 112-153%, and in the blood 89-93% of those of the control group. In the kidney the iron (110%) and the zinc (126%) concentrations at 96 h were higher than the control values, whereas the copper concentration was the same as the control value. The concentrations in the blood were least affected. The most drastic changes were observed in the liver.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Cytophotometric and cytogenetic characteristics of primary hepatomas induced in Wistar rats by aflatoxin B1.

Karyograms of the primary hepatomas induced in Wistar rats by aflatoxin b1 exhibited hypodiploid chromosome sets, and destruction of the chromosomes. Cytophotometric investigations showed a decrease of DNA content in the neoplastic cells, even to about 40% of DNA content in the normal hepatocytes in rats. In the neoplastic destruction of the chromatin material in these hepatomas breaks and deletion of the chromatids predominate.

Aflatoxin B1↗
PubMedDate not supplied

[Neurotrophic growth factors in Alzheimer's disease].

In recent years disturbances in releasing neurotrophic growth factors have been viewed as one of the causes of the development of Alzheimer's disease. It is assumed that abnormalities concerning neurotrophic growth factors (e.g. disturbances in releasing them and (or a wrong response of nerve cells to released growth factors) may be co-responsible for the development of abnormal functions of recent memory or concentration. It is assumed that their role in neurodegenerative processes consists primarily of increasing the survival rate of nerve cells and exerting an effect on the transmitting functions of CNS neurons. Attempts made at present to use growth factors in A.D. with a view to increasing the survival rate of degenerating nerve cells and improving the transmitting functions of neurons will be continued in future in pace with the advancement of our knowledge of their mechanisms.

Acetylcholine↗