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Biomedical subjects

O Smahel

Publications and source records attributed to O Smahel.

At least 19 recordsLinked to original sources
PubMed1979

[Binding of butocin to serum proteins (author's transl)].

The binding of N-[-5-(6-purinylthio)-valeryl]-glycin ethylester (butocin, PVG) to serum proteins and pure human albumin was studied using the method of equilibrium dialysis. Its binding to protein in sera diluted 1:1 of 10 patients with malignant disease averaged 48.4 +/- 7.07%. At the butocin concentration of 20 micrograms/ml an average of 36% of butocin were bound to pure albumin. Only a small portion was bound to globulin fractions. Measurements of the saturation curve showed butocin to be bound to albumin molecule by one binding centre with a microscopic association constant kappa = 1.7 . 10(3) mol/l.

Blood Proteins↗
PubMed1978

Pharmacokinetics of butocine.

The pharmacokinetics of Butocine (glycine, N-[1-oxo-5-(1H-purin-6-ylthio)pentyl], ethyl ester) was studied in 8 individuals with malignant tumor after a single oral dose of 500 mg. Butocine is quickly absorbed from the alimentary tract. Highest serum levels were found 45 minutes after administration. Its urinary excretion is very low (2.5 per cent in 15 hours), 1.7 per cent being eliminated 3 hours after administration. Its renal clearance is likwise very low, i.e. 1.5 ml/min compared with endogenous creatinine clearance of 81.2 ml/min.

Aged↗
PubMed1975

The effect of cyclophosphamide on compensatory hypertrophy and some renal functions in rats.

Administration of 20 mg/kg cyclophosphamide to unilaterally nephrectomized rats for a period of two weeks significantly increased the ratio of kidney weight to total body weight. This rise is, however, accountable more by the decrease of total body weight than by weight increase of the kidney. The RNA-DNA ratio in the hyperttrophic kidney after cyclophosphamide did not differ significantly from that found in the hyperttrophic kidneys of controls. The results obtained show that in our experimental lay-out cyclophosphamide did not inhibit significantly the compensatory renal hypettrophy. After cyclophosphamide, the hypertrophic kidney produced urine with lower concentrations of endogenous creatinine, all osmotically active substances and potassium than found in controls.

Animals↗