PubMed · 10171439
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
F L Kiechle, R Ingram-Main. 1993. Bedside testing, Part 2. Bedside testing: beyond glucose.. https://pubmed.ncbi.nlm.nih.gov/10171439/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
It has been reported that considerable differences exist between the relative molar absorptivity values of the geometrical and structural photoisomers of bilirubin. We have devised an accurate HPLC method for photoisomer quantification based on the following principle: the sum of both the integrated peak areas corrected by each factor for each photoisomer, and the integrated peak area of unchanged (ZZ)-bilirubin [(ZZ)-B] after an anaerobic photoirradiation, should be constant and equal to the integrated peak area of initial (ZZ)-bilirubin [(ZZ)-Bi] before photoirradiation. On this basis, the following equation can be used to determine each factor. [equation: see text] alpha, beta, gamma and delta represent the factors used to correct the integrated peak areas of individual bilirubin photoisomers, and they are arranged in the order of the formula. It was demonstrated that the relative 455 nm molar absorptivity values for (ZZ)-bilirubin and all its geometrical and structural photoisomers, i.e., (ZZ)-bilirubin, (ZE)-bilirubin (EZ)-bilirubin, (EZ)-cyclobilirubin (= lumirubin) and (EE)-cyclobilirubin in the HPLC eluent, are, respectively, 1.0, 0.81 (= alpha), 0.54 (= beta), 0.47 (= gamma) and 0.39 (= delta).
BACKGROUND: Negative interference of bilirubin with assessment of creatinine concentration is generally known from the biochemical aspect. The objective of the presented work was to find the bilirubin level and creatinine concentration where this phenomenon has actually a clinical impact. METHODS AND RESULTS: In 200 samples selected at random the bilirubin and creatinine levels were examined by the classical Jaffé method and a method where the effect of bilirubin is suppressed. After dividing the group into 8 sub-groups by bilirubin and creatinine concentrations it was revealed that the interference plays a statistically significant role (p < 0.01) already at total bilirubin concentrations above 70 mumol.l-1. In abnormal creatinine levels the interference is manifested only at bilirubin concentrations above 150 mumol.l-1 (p < 0.001). The degree of interference in the whole group is directly proportional to the bilirubin level (r = 0.5497, p < 0.001). CONCLUSIONS: At bilirubin levels above 70 to 150 mumol.l-1 its interference with assessment of the creatinine concentration can be so significant that it must be taken into account when evaluating the patient's renal function.
Human serum albumin (HSA) reduced the phospholipid hydroperoxide, 1-palmitoyl-2-(13-hydroperoxy-cis-9, trans-11-octadecadienoyl)-l-3-phosphatidylcholine (PLPC-OOH) to the corresponding hydroxy-derivative with a high apparent affinity (Km=9. 23+/-0.95 microM). Removal of bound lipid during purification increased this activity. At physiological concentration, HSA reduced the phospholipid hydroperoxide in the absence of a cofactor. However, in the presence of a cofactor (reductant), the rate of the reaction was increased. All of the major aminothiols in plasma could act as reductants, the best being the most abundant, cysteine (Km=600+/-80 microM). For every nanomole of PLPC-OOH reduced by HSA, 1.26 nmol of cystine was formed, indicating a reaction stoichiometry of 1 mol PLPC-OOH to 2 mol cysteine. We used chemical modification to determine which amino acid residues on HSA were responsible for the activity. Oxidation of thiol group(s) by N-ethylmaleimide led to a reduction in the rate of activity, whereas reduction of thiols by either dithiothreitol or the angiotensin-converting enzyme inhibitor, captopril, increased the activity. Both N-ethylmaleimide-modified HSA and dithiothreitol-treated HSA exhibited increased apparent affinities for PLPC-OOH. For a range of preparations of albumin with different modifications, the activity on PLPC-OOH was dependent on the amount of free thiol groups on the albumin (correlation coefficient=0.91). Patients with lowered albumin concentrations after septic shock showed lowered total plasma thiol concentrations and decreased phospholipid hydroperoxide cysteine peroxidase (PHCPx) activities. These results therefore show for the first time that HSA exhibits PHCPx activity, and that the majority of the activity depends on the presence of reduced thiol group(s) on the albumin.