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Biomedical subjects

W Siems

Publications and source records attributed to W Siems.

81 records · Page 5Linked to original sources
PubMed1983

[Oxidative damage of mice erythrocytes infected with Plasmodium berghei].

By using the model of infection with plasmodium berghei in white mice the attempt was made to explain the oxidative damages of red blood cells as a cause for haemolysis. In addition to a diminished new formation of erythrocytes there was an increased cell lysis under the impact of infection. Without any changes of the Met-Hb-percentage and of Heinz bodies an increase of GSH and GSSG could be measured. The conclusion was drawn that a damage of red blood cells caused by oxidation may occur by changing the relation of reduced tripeptides to oxidised ones.

Animals↗
PubMed1983

[Formate incubation of red blood cells from glucose-6-phosphate-dehydrogenase-deficient patients].

Attempts of incubating red blood cells of G6PD-defect carriers in 10 from 25 patients showed format in these blood samples is able under the elected conditions to suppress haemolysis, to reduce the numbers of Heinz's bodies and to enhance GSH-concentration. A more distinct efficiency could be observed in enzyme variants with instable temperatures and if kinetic properties had changed. Prevention of haemolysis is particularly suitable as a parameter because it will reflect all damages connected with an enhanced membrane permeability. The increase of GSH-concentration as an important equivalent of reduction in the metabolism of red blood cells may diminish the toxicity of damaging factors having an effect on oxidation. The number of Heinz's bodies is essential in those cases where oxidation products of haemoglobin are increasingly formed only under certain conditions of incubation. The findings allow a format therapy to be recommended for selected G6PD defects.

Anemia, Hemolytic↗
PubMed1983

[Effect of formate on mouse erythrocytes in vivo and in vitro].

The effect of formiat was tested in erythrocytes of mice damaged by oxidisation. Decrease of Heinz's bodies, stabilisation of reduced glutathion, and increase of enzyme activities by referring to an example of superoxidismutase could be identified as a positive effect. Possibilities of formiat reactions in the metabolism of red blood cells are discussed.

Animals↗
PubMed1983

Status of glutathione in the rat liver. Enhanced formation of oxygen radicals at low oxygen tension.

Rat livers were initially perfused and then stored at various temperatures up to 4 h. The intra- and extrahepatic status of glutathione, the accumulation of hydrogen peroxide in the preservation medium, the action of a OH-scavenger and of a xanthine oxidase-inhibitor were investigated as candidates for the assessment of oxidative alterations due to ischemia. Furthermore respiratory functions of mitochondria were measured. The increased efflux of GSSG from the liver tissue, the increase of the GSSGtot/GSHtot-ratio and the favourable effects of formate as OH-scavenger and of allopurinol as xanthine oxidase-inhibitor confirm the hypothesis about the oxidative damage under conditions of oxygen deficiency. The nucleotide degradation, especially the steps catalyzed by xanthine oxidase and uricase, is the main metabolic pathway for the generation of oxygen radicals under ischemic conditions.

Animals↗
PubMed1983

Balance of ATP consumption of reticulocytes.

The sum-total of ATP produced amounts to 135 mmoles X 1 reticulocytes-1 X hour-1. About 70% of the ATP consumption has been accounted for by specific processes. The main contributing processes are: the globin synthesis with about 28%; the Na+/K+-ATPase with 23%, and the ATP-dependent share of proteolysis with more than 15%. 30% of ATP consumption has not been accounted for. Cycloheximide (20 X 10(-6) M) leads to a dissociation between synthesis and degradation of proteins, which argues against any obligatory connection between these processes. About 90% of the lysine liberated from mitochondria by proteolysis were reutilized for the globin synthesis demonstrating the high nitrogen economy of reticulocytes. Each of the ATP consuming processes studied appears to control ATP production in an independent manner without competition with each other.

Adenosine Triphosphate↗
PubMed1982

Quantification of pathways of glucose utilization and balance of energy metabolism of rabbit reticulocytes.

In this work it is demonstrated that glucose constitutes the main substrate of energy metabolism of rabbit reticulocytes under aerobic conditions in the presence of 5 mM glucose. Amino acids and fatty acids are minor sources of energy. The shares of processes utilizing glucose in reticulocytes were estimated from tracer experiments. A new mathematical technique used permits the derivation of closed terms for the specific radioactivity of single positions of C atoms of the metabolites of the citrate cycle. By means of regression analysis, the undetermined flux rates in the citrate cycle were calculated. On the basis of the data an overall balance sheet of glucose utilization and of ATP generation is given. About 45% of the glucose of reticulocytes is catabolized via the citrate cycle, about the same percentage yields lactate. Only 2% of the glucose was oxidized in the oxidative pentose pathway whereas the remainder is used for the formation of serine and glycine required for hemoglobin synthesis. These results are related to knowledge about the main processes utilizing ATP in reticulocytes, i.e. the synthesis of hemoglobin and the energy-dependent proteolysis. Our approach to the investigation of metabolic relations in the reticulocytes can be applied to other tissues in which equilibria between large metabolite pools play a role.

Adenosine Triphosphate↗
PubMed1981

Balance of glucose utilization in rabbit reticulocytes.

The shares of glucose utilizing processes in red blood cells under aerobic conditions were estimated in tracer experiments and with mathematical methods. A complex method of these pathways in reticulocytes is given. Our approach to the solution of the problem in reticulocytes can be transferred to other tissues. The new mathematical technique used is suitable for derivation of closed terms for the specific radioactivity of single positions of C-atoms of the metabolites of citrate cycle. Therefore, by means of regressions analysis, the calculation of unknown concentrations and flux rates is possible.

Animals↗
PubMedDate not supplied

Metabolic rates of 4-hydroxynonenal in tubular and mesangial cells of the kidney.

The degradation of the lipid peroxidation product 4-hydroxynonenal (HNE) in primary cultures of kidney tubular and mesangial cells was determined. Using various initial concentrations of the aldehyde a decline of cellular viability was found. Mesangial cells were more susceptible to the toxic effects of HNE. In consumption studies of HNE the decline of the exogenously added aldehyde was comparable in both cell types after addition of 10 and 1 micromol HNE/l. After addition of 100 micromol/l aldehyde a drastically lower HNE degrading capacity was found in mesangial cells as compared to tubular cells. The loss in the HNE degrading capacity was accompanied by an increased formation of HNE-protein aggregates as demonstrated by immunoblots. Therefore, we concluded that the low ability of mesangial cells to degrade HNE may be a factor of the toxicity of free radicals on the kidney.

Aldehydes↗