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Biomedical subjects

B J Bolann

Publications and source records attributed to B J Bolann.

17 recordsLinked to original sources
PubMed2000

Tetradecylthioacetic acid and tetradecylselenoacetic acid inhibit lipid peroxidation and interact with superoxide radical.

Reactive oxygen species are thought to induce cellular damage and to play a pathological role in several human diseases. Tetradecylthioacetic acid (TTA) was previously reported to prevent the oxidative modification of low-density lipoprotein (LDL) particles and to act as an antioxidant. In this study we present a new fatty acid analogue, namely tetradecylselenoacetic acid (TSA), in which the sulfur atom of TTA is replaced by a selenium atom. TSA was more potent than TTA in increasing the lag time before the onset of LDL oxidation and this effect was dose dependent. TTA and TSA were shown to reduce the iron-ascorbate-induced microsomal lipid peroxidation, TSA being more efficient than TTA. TTA and TSA, in the presence of iron, interacted with the superoxide radical as assessed by direct and indirect testing methods. TSA like TTA failed to scavenge 1.1-diphenyl-2-picrylhydrazyl radicals. TSA bound copper ions as shown by the wavelength spectra measurement. These results suggest that TTA and TSA exert their antioxidant capacity by interaction with copper or iron ions in radical scavenging, TSA being more potent than TTA. Nevertheless, a chelating effect resulting in chemically inactive metal ions cannot be excluded.

Animals↗
PubMed2000

Validation of inductively coupled plasma atomic emission spectrometry technique (ICP-AES) for multi-element analysis of trace elements in human serum.

The use of inductively coupled plasma atomic emission spectrometry (ICP-AES) for the simultaneous determination of Al, B, Ba, Be, Cd, Co, Cr, Cu, Fe, Li, Mn, Ni, Pb, Se, Sr and Zn in human serum in a clinical laboratory was validated. Samples were digested and then analysed using yttrium as an internal standard and a serum-matched calibration standard. The criteria used to assess the analytical performance of the ICP-AES were detection and quantification limits, linearity, sensitivity, recovery, interference from alkali and acid, trueness and precision. Detection limits were 0.002-0.003 micromol/L for Mn, Sr, Ba, and Cd; 0.014-0.07 micromol/L for Co, Zn, Fe, Be, Li, Pb, Cu, Ni, and Cr; and 0.2-0.9 micromol/L for B, Se, and Al. Trueness, as controlled by analysis of bovine serum certified reference material, was acceptable for Co, Cu, Se and Zn, while Fe was 5.1% and Mn 6.2% below the lowest limit of the certified material interval. We conclude that ICP-AES can be used for multi-element analysis of B, Ba, Cu, Fe, Li, Se, Sr and Zn in serum. Serum levels of Al, Be and Co were below the detection limits while serum levels of Cd, Cr, Ni and Pb were below the quantification limits of the ICP-AES. These trace metals cannot be analysed as routine by the ICP-AES. However, in cases of intoxication with elevated serum concentrations mean recovery of 100+/-10% was obtained at an addition of 2.22 micromol/L for Al, 0.11 micromol/L for Be, 0.03 micromol/L for Co, 0.39 micromol/L for Cr, 0.14 micromol/L for Ni, and 0.12 micromol/L for Pb.

Calibration↗
PubMed2000

Trace element reference values in serum determined by inductively coupled plasma atomic emission spectrometry.

Serum reference values for Ba, B, Cd, Cu, Fe, Mn, Li, Se, Sr, and Zn in 141 healthy Norwegians were determined. The trace element concentrations were determined by the inductively coupled plasma atomic emission spectrometry technique that we have recently validated. The reference intervals were established according to the recommendations of the International Federation of Clinical Chemistry and Laboratory Medicine. Also coverage intervals with coverage uncertainties were calculated according to the International Union of Pure and Applied Chemistry. The population studied consisted of 69 men and 72 women of the ages 21-87 years. The effects of gender, age, smoking, and oral contraceptives on serum levels of trace elements were investigated. Median concentrations of the different trace elements in (micromol/l) were as follows: Ba (0.44), B (1.50), Cd (0.004), Cu (17.1), Fe (21.4), Li (0.06), Mn (0.003), Se (1.26), Sr (0.17), and Zn (13.3). An increase in serum Ba and Sr was detected with age. These metals and Se were also significantly higher in women over 50 years of age in comparison to younger women. Women had higher serum Cu than men and those on oral contraceptives had higher serum Cu and Fe. Serum B tended to increase with age, while it was significantly reduced with smoking.

Adult↗
PubMed2000

Evaluation of indicators of cobalamin deficiency defined as cobalamin-induced reduction in increased serum methylmalonic acid.

BACKGROUND: Early detection of cobalamin deficiency is clinically important, and there is evidence that such deficiency occurs more frequently than previously anticipated. However, serum cobalamin and other commonly used tests have limited ability to diagnose a deficiency state. METHODS: We investigated the ability of hematological variables, serum cobalamin, plasma total homocysteine (tHcy), serum and erythrocyte folate, gastroscopy, age, and gender to predict cobalamin deficiency. Patients (n = 196; age range, 17-87 years) who had been referred from general practice for determination of serum cobalamin were studied. Cobalamin deficiency was defined as serum methylmalonic acid (MMA) >0.26 micromol/L with at least 50% reduction after cobalamin supplementation. ROC and logistic regression analyses were used. RESULTS: Serum cobalamin and tHcy were the best predictors, with areas under the ROC curve (SE) of 0. 810 (0.034) and 0.768 (0.037), respectively, but age, intrinsic factor antibodies, and gastroscopy gave additional information. CONCLUSIONS: When cobalamin deficiency is suspected in general practice, serum cobalamin should be the first diagnostic test, and the result should be interpreted in relation to the age of the patient. When a definite diagnosis cannot be reached, MMA and tHcy determination will provide additional discriminative information, but MMA, being more specific, is preferable for assessment of cobalamin status.

Adolescent↗
PubMed1999

[Analytical uncertainty--how wrong can a laboratory result be?].

Some uncertainty encumbers the outcome of all laboratory tests. Patient conditions and handling of specimens, as well as analytical variation and systematic error will affect the results. In order not to confuse the interpretation of test results, the analytical standard deviation should not exceed one half of the intraindividual biological standard deviation, and systematic error should not exceed 1/16 of the reference interval. However, these goals cannot always be achieved. Moreover, analytical control procedures have limited ability to detect errors in the analytical process. After one analysis of control material, using +/- 2 standard deviations (analytical) from the mean as acceptance limits, the magnitude of a systematic error must be 3.3 times the analytical standard deviation in order to be detected with 90% probability. As a result of such error, patients' results can be released with a total error up to five times the analytical standard deviation. More complicated control procedures may give smaller total error. Practising physicians should be familiar with the variations in lab results, and interpret the results accordingly. Lab results that conflict with results of other investigations should be used with caution.

Blood Chemical Analysis↗
PubMed1997

[Quality assurance of laboratories outside hospitals. Use of internal control].

Norway has a national programme for quality assurance of laboratory analyses performed in general practice. A central laboratory distributes control material, and a local team gives practical assistance in each county. To perform laboratory tests properly, the use of quality control material ("internal control") is essential. The users' control results provide a basis for finding both systematic error and the analytical coefficient of variation. The analytical and biological coefficients of variation can be used to calculate the confidence intervals around laboratory test results, and around medical decision thresholds. It is also possible to calculate the magnitude of significant changes in serial results ("critical difference"). In Rogaland county, 11-14 general practitioners showed an analytical coefficient of variation ranging from 0.5 to 5.0% on haemoglobin determination, from 1.2 to 9.9% on glucose, and from 3.1 to 10.5% on prothrombin time. Five general practitioners showed an analytical coefficient of variation from 3.3 to 9.7% for cholesterol. This gives a critical difference ranging from 7.8 to 15.8% for haemoglobin and 18.8 to 31.6% for cholesterol. We present a diagram that can be used to find the critical difference for any test. Such an evaluation of laboratory analyses should become routine in all near-patient testing.

Chemistry, Clinical↗
PubMed1997

[How do antioxidants work?].

Reactive oxygen species, formed by incomplete reduction of molecular oxygen, may cause oxidative stress in the organism and be involved in the pathogenesis of many diseases. A number of anti-oxidants are necessary to counteract the harmful effects. Some antioxidants are enzymes which catalyze the breakdown of reactive oxygen species, some act by chelating transition metals, which makes them non-reactive, while chain-breaking antioxidants act by halting the cascade of free radical reactions. The effect of redox active antioxidants depends on their redox status. In some circumstances antioxidants can have pro-oxidant effects. The mechanisms may be reductive release of metals, accumulation of the oxidized form of redox active antioxidants, or merely an unfavourable equilibrium between various antioxidants. At present there is no basis for recommending the prophylactic use of commercially produced antioxidants. In particular, the optimal combinations of antioxidants are not yet known. If the aim is to improve the antioxidant defence of the body, our advice is still a mixed diet and regular physical activity.

Antioxidants↗
PubMed1996

Determination of manganese superoxide dismutase activity by direct spectrophotometry.

A method to determine Mn-superoxide dismutase activity by measuring directly the rate of decay of O2- in a spectrophotometer, is described. Decay of O2- generated by KO2 at pH 9.5, was monitored as the fall in absorbance (A250nm-A360nm). Mn-superoxide dismutase was determined as the activity of cyanide-resistant superoxide dismutase, calculated from the rate of O2- dismutation. Mn-superoxide dismutase could be determined in the presence of a 700 times higher Cu,Zn-superoxide dismutase activity. The alkaline pH did not cause analytical problems. The assay was used to measure both Mn- and Cu,Zn-superoxide dismutase activity in mitochondrial preparations. The assay had a detection limit of 2.8 ng/ml when Mn-superoxide dismutase from E. coli was used, and the between-day CV was 5.8%. The assay is an alternative to indirect methods for detecting superoxide dismutase activity.

Animals↗
PubMed1993

Stimulated decay of superoxide caused by ferritin-bound copper.

The redox interaction between O2.- and ferritin cannot solely be regarded as as a Fe(II) release reaction. We demonstrate that native copper bound to horse spleen ferritin and apoferritin, stimulated the decay of O2.- in a catalytic reaction. Copper was determined by atomic absorption spectrophotometry. Decay of O2.- was monitored spectrophotometrically as the decrease in (A250-A360) at pH 9.5. The catalytic effect was linearly related to the copper content of the protein. Ferritin copper was less efficient than equimolar CuCl2, and iron-poor ferritin was more efficient than iron-rich ferritin. The results support a direct antioxidant function of ferritin.

Animals↗
PubMed1993

Decay of superoxide catalyzed by ferritin.

Ferritin iron can be reduced by O2.-, released, and form a Fe(II)-chelator complex. However, the thermodynamic influence of the chelator may disturb the reaction balance. We therefore excluded the chelator and measured instead the effect of ferritin on the decay of O.2-, monitored by direct spectrophotometry at pH 9.5. Ferritin, but not apoferritin, accelerated the decay of O.2-. Ferritin iron was apparently the responsible agent. The effect of ferritin was maintained after several bursts of O.2-, and the ratio degraded O.2-/released Fe(II) greatly exceeded one, consistent with a catalytic reaction.

Animals↗
PubMed1992

Decay kinetics of O2.- studied by direct spectrophotometry. Interaction with catalytic and non-catalytic substances.

The kinetic behaviour of O2.- during spontaneous dismutation and in the presence of Cu,Zn-superoxide dismutase and other compounds, was studied by monitoring the decrease in absorbance (A250nm-A360nm) on a time-scale of > or = 1 min, at pH 9.5. O2.- was generated from KO2, and calculations were performed between 25 and 4 microM of O2.-. An algorithm for the simultaneous calculation of the 1st and 2nd-order rate constants from the decay curve, was evolved. The respective fractions of O2.- which interacted with catalysts or disappeared spontaneously, in various experimental situations, could be estimated. Substances could be classified as inert, catalysts or scavengers. The high assay pH excluded examination of the effect of alkali sensitive substances, e.g., Mn-superoxide dismutase. However, the high pH minimized the interfering effect of trace amounts of Cu(II). Therefore a metal chelator was superfluous and even the effect of metals and metal complexes could be tested. The extremely high sensitivity of the method allowed minute concentrations of reagents to be used, including proteins absorbing in the UV-region. The rate constants found by this simple method, agreed with those obtained by more sophisticated and inaccessible techniques like pulse radiolysis and stopped-flow spectrophotometry.

Hydrogen-Ion Concentration↗
PubMed1991

Improvement of a direct spectrophotometric assay for routine determination of superoxide dismutase activity.

The growing interest in measuring superoxide dismutase (EC 1.15.1.1) in many diseases calls for useful routine assays. For this purpose, the direct spectrophotometric method of Marklund (J Biol Chem 1976;251:7504-7) was improved to offer an alternative to the imprecise, indirect assays currently used. The decay of O2.- (from KO2) at pH 9.5 was monitored as the decrease in delta A (delta A = A250nm-A360nm). Superoxide dismutase was determined from the pseudo-first-order rate constant of O2.- dismutation. The precision of the assay was improved by increasing the concentration of O2.- and expanding the interval for measurements of O2.- concentrations to 4-16 mumol/L. Other assay characteristics, including temperature, were also optimized. In hemolysate the assay had a within-day CV of 5.5-13% and a between-day CV of 4%. Mn-superoxide dismutase and some superoxide dismutase mimics are inhibited at alkaline pH. Therefore, the method is primarily recommended for Cu,Zn-superoxide dismutase.

Animals↗
PubMed1990

On the limited ability of superoxide to release iron from ferritin.

Reductive release of iron from ferritin may catalyze cytotoxic radical reactions like the Haber-Weiss reaction. The ability of .O2- to mobilize Fe(II) from ferritin was studied by using the xanthine/xanthine oxidase reaction, with and without superoxide dismutase, and with bathophenanthroline sulphonate as the chelator. Not more than one or two Fe(II)/ferritin molecules could be released by an .O2(-)-dependent mechanism, even after repeated exposures of ferritin to bursts of .O2-. The amount of releaseable iron depended on the size and the age of the iron core, but not on the iron content of the protein shell of ferritin which was manipulated by chelators and addition of FeCl3. The kinetic characteristics of the .O2(-)-mediated iron release indicated the presence of a small pool of readily available iron at the surface of the core. The very limited .O2(-)-dependent release of iron from ferritin is compatible with a protective role of ferritin against toxic iron-catalyzed reactions.

Chelating Agents↗
PubMed1989

Implications of probability analysis for interpreting results of leukocyte esterase and nitrite test strips.

We examined 288 urine samples, using test strips, sediment microscopy, and culture. The ability of the leukocyte esterase and nitrite test strips to detect or exclude urinary tract infection, as defined by a positive culture, was evaluated by probability analysis. We found that the diagnostic efficiency of the esterase-nitrite combination was similar to that of sediment microscopy. Moreover, once the strip test results had been obtained, little additional information was given by microscopy. The importance of estimating the prevalence, or pre-test probability, of infection before the test result is evaluated is emphasized. We conclude that, for detecting or excluding urinary-tract infection, microscopy can be replaced by the esterase and nitrite test strips. If the probability of infection predicted by the test strips is not high (or low) enough compared with medical decision limits, the samples should be cultured.

Esterases↗
PubMed1987

Release of iron from ferritin by xanthine oxidase. Role of the superoxide radical.

Mobilization of iron from ferritin by xanthine oxidase was studied under aerobic and anaerobic conditions. Aerobic iron release amounted to approx. 3.7 nmol/ml in 10 min. This amount was decreased by approx. 30% under anaerobic conditions. Aerobic iron mobilization involved two mechanisms. About 70% was released by O2.- generated by xanthine oxidase. The rest was released by O2(.-)-independent mechanisms, which also accounted for the total iron release when O2 was absent. A possible transfer of reducing equivalents directly from xanthine oxidase to ferritin is discussed. The results imply that, in pathological conditions with increased formation of O2.-, iron may be released from ferritin. Furthermore, in hypoxic tissues xanthine oxidase can release iron from ferritin by an O2(.-)-independent process. Free iron is liable to catalyse the formation of the extremely reactive and damaging OH. radical.

Anaerobiosis↗