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Biomedical subjects

M Cervinka

Publications and source records attributed to M Cervinka.

30 records · Page 2Linked to original sources
PubMed1984

Cinematographic study of the effects of cis-diammine-dichloroplatinum on mouse L cells.

Cells of mouse fibroblasts line L were grown one hour in the presence of cisplatin. Their fate was then followed by time-lapse microcinematography during six days. Up to the concentration 3.2 mumol 1(-1) there was little effect observed. Higher concentrations induced prolongation of mitosis and interphase, finally resulting in non-cycling cells with complete and persistent division arrest at 25 mumol 1(-1). After 72 hours following the treatment the cellular and nuclear volumes in non-cycling cells began to grow progressively. The mobility and the ruffling activity of the cell membrane were unaltered. Thus, energy generation, the function of the cytoskeleton, and synthetic processes seemed unchanged. The effect of cisplatin is cytostatic rather than cytotoxic.

Animals↗
PubMed1979

Fusion of L line daughter cells in the presence of Sendai virus.

Sendai virus induces the fusion of daughter cells in a population of murine fibroblasts (L cell line). Mitosis and the ensuing fusion of two daughter cells has been observed by means of time-lapse cinemicrography. The paper documents two types of cell fusion: a) two daughter cells become completely separated at the end of the mitosis, and fuse only after a certain period of time, or b) the daughter cells remain attached through a narrow bridge of cytoplasm which persists between the cells as a consequence of incomplete cytokinesis. Widening of the cytoplasmic bridge ultimately results in the fusion of cells. The interval between the termination of mitosis and the fusion ranged from 45 to 60 min. The biological significance of the resulting polyploid cells is discussed.

Animals↗
PubMed1977

Effect of intravenously infused noradrenaline on the cardiovascular system of cold-acclimated rats.

Total metabolism, body temperature and basic circulatory parameters (the heart rate, blood pressure, blood oxygen content and hind limb blood flow) were measured in anaesthetized cold-acclimated male laboratory rats exposed to the calorigenic action of noradrenaline. In addition, cardiac output, the oxygen extraction coefficient and peripheral vascular resistance were calculated from these data.

Adaptation, Physiological↗
PubMed1976

Substitution of calorigenic effects of noradrenaline and adrenaline and differences in their inhibition by propranolol.

The calorigenic effect of infused adrenaline and noradrenaline was measured in cold-acclimated rats. The slopes of the dose-response curves for the two catecholamines and the maxima of the curves were the same. The adrenaline dose-response curve showed a shift to the right, towards higher infusion doses, compared with the noradrenaline curve. Thermogenesis due to the two catecholamines was not additive throughout the whole range of doses used. In interaction with noradrenaline, propranolol caused a parallel shift of the dose-response curve to the right, whereas in interaction with adrenaline it depressed the maximum. The concept that the two catecholamines act via different regulation sites on a common thermogenetic effector is discussed.

Acclimatization↗
PubMedDate not supplied

Toxic effects of chromium acetate hydroxide on cells cultivated in vitro.

Many human activities, particularly industrial ones, result in an ever-growing production of toxic waste materials. The dynamics of the toxic effects of chromium acetate hydroxide, which is found in high concentrations in a waste sediment produced in the Czech Republic, were assessed by using a battery of in vitro tests carried out on two cell lines: L-929 (mouse fibroblasts) and Hep 2 (human laryngeal cells). Various markers of cell damage were assessed by phase-contrast, video and fluorescence microscopy, fluorometry, and DNA analysis. Chromium acetate hydroxide, over a concentration range of 1-0.02mol/l induced immediate cell death by fixation, whereas, at 0.002mol/l, the treated cells died in a much slower, more discrete manner. All the detected markers of cell damage, whether immediate or slow, clearly demonstrated that the cells died by necrosis. On the other hand, test concentration of 0.001mol/l appeared to constitute a threshold at which no pathological changes of Hep 2 cells were observed over 96 hours. We conclude that chromium acetate hydroxide has a high toxic potential in vitro, which should be considered when studying the toxicity of waste materials containing it.

Animals↗