Biomedical subjects
Publications and source records attributed to E Talafant.
Serum lipoproteins were stained by the addition of Sudan Black B solution. The normal lipoproteins and the excess of Sudan Black were removed with heparin and zinc acetate solution. The abnormal lipoprotein-X remained in the supernatant, the blue colour of which was measured. The empirically obtained constant was used for calculation, thus avoiding standardization.
Non-esterified cholesterol was determined enzymatically with the cholesterol oxidase-peroxidase reaction using phenol and 4-aminophenazone as chromogens. This assay as done in the supernatant containing the lipoprotein-X. Other serum lipoproteins were removed by precipitation with heparin and zinc acetate followed by centrifugation. No standardization was required, the lipoprotein-X concentration being calculated with the use of the constant.
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Turbidimetric determination of the cholestasis characterizing lipoprotein-X is based on the separation from the serum investigated of interfering lipoproteins by precipitation with the appropriate concentration of heparin and zinc acetate followed by centrifugation. In the supernatant the abnormal lipoprotein-X, which is not precipitated under these conditions, was determined by measuring the turbidity after addition of calcium chloride and heparin.
Two procedures for quantitative determination of the cholestasis-characterizing lipoprotein-X are described. Both procedures are based on ether-extract-ability of phospholipids which are relatively loosely bound in lipoprotein-X. The presence of cetyltrimethylammonium bromide at adequate concentration allowed complete ether extraction of phospholipids from lipoprotein-X even at low concentration, without affecting the phospholipids of normal lipoproteins. In one modification phospholipids were extracted into ether ion-paired with a bilirubin conjugate (e.g. Woodward's K conjugate) the concentration of which was then estimated in the ether extract. In the second modification phospholipids were directly determined in the ether extract. Calibration was done either with a lipoprotein-X concentrate or with a clear sonicated lecithin sol added to normal serum. The results obtained by both methods are in a good agreement with the results by agar gel electrophoresis.
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High serum gamma-glutamyl transpeptidase activity was found in cord blood of newborn boys. This activity decreased to lower values on the 4th and 7th days. In newborns treated for 3 days following the birth with a combination of phenobarbital and nicethamide an increase of gamma-glutamyl transpeptidase activity occurred from the 4th to the 7th days. The 7th day levels were significantly higher when compared with the controls. Simultaneous determination of urinary glucaric acid excretion confirmed the induction of hepatic microsomal enzymes in glucuronic acid pathway. This could also be demonstrated by a pronounced decrease of serum bilirubin levels in groups receiving the enzyme inducers whether phenobarbital was administered intramuscularly or orally as sodium salt solution.
The urinary excretion of glucaric and glucuronic acid was investigated in neonates receiving phenobarbital intramuscularly or orally. Whereas there was no significant difference from the control-subjects in glucuronic acid elimination, the increase in glucaric acid excretion was significantly higher in the intramuscularly treated neonates. Infants with orally administered phenobarbital showed only insignificantly greater glucaric acid elimination. The decrease of serum bilirubin levels was more pronounced in the intramuscularly treated than in the orally treated group. The determination of glucaric acid may be an important reflection of hepatic microsomal induction of the enzymes of the glucuronic acid pathway.
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