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Biomedical subjects

F Schneider

Publications and source records attributed to F Schneider.

At least 289 records · Page 16Linked to original sources
PubMed1985

Uridine, but not cytidine can sustain growth of Ehrlich ascites tumor cells in glucose-deprived medium with altered proliferation kinetics.

Cell cycle kinetics and energy metabolism of Ehrlich ascites tumor cells grown in glucose-deprived medium supplemented with uridine, were investigated in order to extend our knowledge about the significance of the metabolic conversion of glucose for cell cycle progression of these cells. Viability (dye exclusion test) of uridine supplemented cells was not affected, although growth was reduced to 50 to 60% of the controls. Uridine did not significantly impair growth of controls in standard medium up to 20 mM. Studies on cell cycle progression using flow cytometry (BrdU-H33258 technique) revealed an accumulation of cells in G2M phase, which can be explained by a delay in the passage of G2M-compartment of about 12 +/- 2 h. After a 24 h culture period, 60% of the cell populations were found in G2M (30% in control cultures). This fraction increased to about 70% in the following passage. Protein and DNA synthesis corresponded to the proliferation rate. Oxygen uptake was increased by about 50%, glutamine consumption by 30%, lactate production was reduced to below 10% of the controls. The ATP/ADP concentration ratio was found in a physiological range of 4 to 6. It was calculated that cells grown in standard medium produced 60% of ATP via oxidative pathways and 40% via glycolysis; however, in glucose-free, uridine-supplemented medium the values are more than 90% and less than 10%. No significant differences in total ATP production were observed. Growth of the cells in glucose-deprived medium could not be sustained by cytidine. All our data substantiate the present concept that glycolytic ATP-production is not essential for maintenance of viability and growth of these cells.

Animals↗
PubMed1984

A comparative study on proliferation, macromolecular synthesis and energy metabolism of in vitro-grown Ehrlich ascites tumor cells in the presence of glucosone, galactosone and methylglyoxal.

Proliferation of in vitro grown Ehrlich ascites tumor cells is completely inhibited by 0.2-0.4 mM methylglyoxal and 1-2 mM glucosone or galactosone without severely affecting viability (dye exclusion test); no phase-specific arrest of cell growth is observed. Incorporation of [14C] thymidine into the acid-insoluble fraction of the cells decreases within a few minutes to less than 50% of that in controls in the presence of 0.4 mM methylglyoxal, and 2 mM glucosone or galactosone causes a comparable inhibition of DNA synthesis after 2 h or 4 h, respectively. The action of 0.4 mM methylglyoxal inhibits incorporation of [14C] leucine within a few minutes by more than 70%, while 2 mM glucosone and galactosone are significantly less effective (50%-60% inhibition after 12 h). While methylglyoxal and galactosone do not severely affect lactate production of the cells, 2 mM glucosone reduces glycolysis by 60%-70%; ATP/ADP ratios did not fall below 3.5 in the presence of the inhibitors (controls 4-6). It is suggested that the reaction potentialities of the oxaldehyde function of the inhibitors play an important role in their growth-inhibitory activity, besides exerting a specific effect on hexokinase (glucosone) and UTP-trapping activity.

Adenosine Diphosphate↗
PubMed1984

A collaborative evaluation of a rapid automated bacterial identification system: the Autobac IDX.

A collaborative evaluation of the Autobac IDX, a rapid, semi-automated bacterial identification system, was performed in three independent laboratories in three European countries. The system utilises growth inhibition by a series of chemical compounds. Subsequent analysis of the resultant data by quadratic discriminant function automatically results in a bacterial identification. Three sets of 30 strains were examined repeatedly in each of the participating laboratories. The reproducibilities obtained ranged from 85.6% to 96.6%, with an overall average of 91.8%. The accuracy of the system was also determined by examining 1076 isolates from the three participating laboratories. An overall accuracy of 90.3% was calculated by comparing the Autobac result with a reference method. When the results were weighted to represent clinical frequency, the accuracy was 93.6%.

Bacteria↗
PubMed1984

Proliferation, macromolecular synthesis and energy metabolism of in vitro grown Ehrlich ascites tumor cells after inhibition of ATP-ADP translocation by atractyloside.

In the presence of 3 mM atractyloside, growth of in vitro cultured Ehrlich ascites tumor cells is inhibited by 70% within 24 h. Viability of the cells is not severely affected (dye exclusion test). Incorporation of 2-[14C]-thymidine and U-[14C]-leucine into acid insoluble precipitate were reduced by 80% or 20% respectively as compared to controls. Flow cytometric analysis of cell cycle progression revealed a retardation rather than an arrest of cell growth by atractyloside. Morphological changes of the cells primarily concern mitochondria which are spherical shaped with translucent matrix rid of cristae. After transfer of atractyloside treated cells to normal medium, proliferation and macromolecular synthesis normalized within 3 to 6 h. At 3 mM of atractyloside, glucose consumption of the cells increased by 25%, lactate production by 30%. Lactate/glucose ratio was 1.9 after 24 h. Oxygen uptake was reduced by 35% after 12 h. The [ATP]/[ADP] ratio of the whole cells runs through a maximum between 12 and 18 h. The ratio never falls below 5.0. The ATP/ADP concentration ratio in the mitochondrial and extramitochondrial compartment were increased as compared to controls. delta G of ATP hydrolysis of the intact cells was in a normal range (-50 kJ), energy charge was 0.86 (controls 0.88). Transport of amino acids, uptake of glucose and activity of Na+, K+-ATPase of the plasma membrane were not impaired by 3 mM atractyloside.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1982

Further characterization of the growth inhibitory effect of rotenone on in vitro cultured Ehrlich ascites tumour cells.

As an approach for a better understanding of the mode of action of rotenone on mammalian cells we have studied the proliferation properties, metabolism and basic cell composition of Ehrlich ascites tumour cells cultured in vitro in the presence of 2.5 microM rotenone and after removal of the inhibitor. Experiments on asynchronous cells showed a rapid cessation of cell division accompanied by increased glycolytic rate, reduced oxygen consumption, moderate increase in DNA content and a fair increase in protein and RNA content of the cultures. DNA histograms obtained by flow-cytometry revealed an accumulation of cells in the G2 and M phase of the cell cycle. Electron micrographs taken after a 24 h treatment of cells illustrated the formation of giant mitochondria and fragmented nuclei. In order to elucidate the dual effect of rotenone- inhibition of mitochondrial energy metabolism and of mitotic processes- the influence on cells of rotenone at different stages of the cell cycle was tested using Ehrlich ascites tumour cells enriched in G1, S and G2 by centrifugal elutriation. DNA histograms and [3H]thymidine labelling index curves of cells from the different fractions cultured in the presence of 2,5 microM rotenone indicated that in addition to the observed accumulation in G2 and mitotic arrest of cells, the cell cycle progression is delayed in G1 phase. This may be explained by an effect of the inhibitor on the respiratory chain. S phase cells seemed to continue the cycle for several hours at a rate comparable to that of controls. Recultivation experiments on rotenone-treated asynchronous cells in inhibitor-free medium confirmed that some cells reinitiate DNA synthesis without preceeding cell division. Thus it must be concluded that cells at all stages of the cycle are affected by rotenone, but the impairment of cellular metabolism becomes manifest and lethal as soon as the acute block at mitosis is abolished and cells reenter the cycle.

Animals↗
PubMed1982

Uridylate trapping, induction of UTP deficiency, and stimulation of pyrimidine synthesis de novo by D-galactosone.

d-Galactosone (d-lyxo-2-hexosulose) is phosphorylated and metabolized to the uridine diphosphate derivative in AS-30D hepatoma cells and rat liver. These reactions were catalysed in vitro by galactokinase and hexose-1-phosphate uridylyltransferase. Nucleotide analyses by high-performance liquid chromatography and enzymic assays revealed that this galactose analogue interferes with cellular pyrimidine nucleotide metabolism leading to a deficiency of UTP. [(14)C]Uridine labelling of hepatoma cells indicated a division of [(14)C]uridylate from UTP into UDP-galactosone; the latter was formed at a rate of more than 1.7mmolxh(-1)x(kg AS-30D or liver wet wt.)(-1). As a consequence of UTP deficiency, d-galactosone (1mmol/1 or 1mmol/kg body wt.) strongly enhanced the rate of pyrimidine synthesis de novo as evidenced by incorporation of (14)CO(2) into uridylate and by an expansion of the uridylate pool. This resulted in a doubling of the total acid-soluble uridylate pool within 70min in the hepatoma cells and within 110min in rat liver. Combined treatment of hepatoma cells with d-galactosone and N-(phosphonoacetyl)-l-aspartate, an inhibitor of aspartate carbamoyltransferase, prevented the expansion of the uridylate pool and led to a synergistic reduction of UTP to 10% of the content in control cells. Hepatic UTP deficiency was selective with respect to other nucleotide 5'-triphosphates but was associated with reduced contents of UDP-glucose, UDP-glucuronate, and UDP-N-acetylhexosamines. Isolation of the UDP derivative of d-galactosone revealed an extremely alkali-labile UDP-sugar, probably an isomerization product of UDP-galactosone, that was degraded by elimination of UDP with a half-life of 45min at pH7.5 and 37 degrees C. The instability of UDP-galactosone may contribute in vivo to limit the time period of severe uridine phosphate deficiency in addition to the compensatory role of pyrimidine synthesis de novo. During the initial time period, however, d-galactosone is effective as a powerful uridylate-trapping sugar analogue.

Animals↗
PubMed1982

[Exercise-induced malignant hyperthermia in a patient with familial ichthyosis vulgaris. Muscular carnitine deficiency as contributing factor (author's transl)].

A young soldier with familial ichthyosis vulgaris developed malignant hyperthermia after an intensive exercise. Ichythyosis was considered as a predisposing factor, but the finding of a low muscular carnitine level raises the problem of a relationship between exercised-induced malignant hyperthermia and lipid metabolism disorders.

Adult↗
PubMed1982

Growth characteristics of anaerobically treated Ehrlich ascites tumor cells after reaeration as studied by combination of flow cytometry and centrifugal elutriation.

Centrifugal elutriation was applied to separate into the cell compartments asynchronous Ehrlich ascites cells grown under different culture conditions. The cytokinetic properties of the recultivated fractions were studied by flow cytometry. The present experiments prove that G1-cohorts grown 12 h under exclusion of oxygen accumulate in the late G1-compartment. The cytokinetic properties of these cells are not changed. In contrast the cytokinetic properties of anaerobically treated S-phase cells are changed; most of S-cells leave the cell cycle after they have attained the DNA content of G2-cells and continue to synthesize DNA without preceeding division. Cells with a DNA content up to the fourfold of normal values are found.

Anaerobiosis↗