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Biomedical subjects

F Adlkofer

Publications and source records attributed to F Adlkofer.

At least 37 records · Page 2Linked to original sources
PubMed1990

Dietary influences on urinary excretion of hydroxyphenanthrenes, thioethers and mutagenicity in man.

Our study indicates that large differences in dietary polycyclic aromatic hydrocarbon (PAH) content in humans are not reflected by urinary and faecal excretion of hydroxyphenanthrenes, although significant increases in 3-hydroxybenzo[a]pyrene and 3-hydroxychrysene in faeces were observed after consumption of a diet rich in PAHs. The question therefore arises whether urinary hydroxyphenanthrenes are a reliable marker for exposure to PAHs. As expected, the elevated mutagenicity of the diet rich in PAHs led to increased mutagenic activity in urine. The increased urinary excretion of thioethers after this diet was probably due to its higher thioether content. Therefore, an elevated thioether excretion does not always indicate exposure to electrophilic compounds.

Adult↗
PubMed1989

Biomonitoring after controlled exposure to environmental tobacco smoke (ETS).

A rough estimation of the amounts of tobacco smoke components taken up by active and passive smoking suggests that, in the case of passive smoking, gas phase constituents in ETS are of greater relevance than particle-bound substances. Since this aspect is of importance for the risk evaluation of passive smoking, it was decided that it should be investigated further in a series of exposure studies with human volunteers. The ETS exposure conditions were characterized by measuring tobacco smoke components such as carbon monoxide (CO), nitrogen oxides (NOx), nicotine, formaldehyde, tobacco-specific nitrosamines (N-nitrosonornicotine (NNN), 4-methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), benzo(a)pyrene (BaP) and particulate matter in the air of the exposure room. The biomonitoring covered carboxyhemoglobin (COHb), thioethers and mutagenic activity in urine. These parameters were compared to those observed after controlled active smoking. It was found that urinary thioether excretion increased in non-smokers after extremely high ETS exposure. This effect could be attributed to gas phase ETS components. Urinary mutagenicity was not measurably increased in non-smokers under these conditions. This indicates that in passive smoking, as opposed to smoking, the gas phase might be more important in terms of possible effects than the particulate matter. It would, therefore, be misleading to make extrapolations based on the burden of smoking to establish the burden of passive smoking.

Adult↗
PubMed1988

Pharmacokinetics of nicotine, cotinine, and 3'-hydroxycotinine in cigarette smokers.

The trans-isomer of 3'-hydroxycotinine has recently been identified as a major metabolite of nicotine in urine of cigarette smokers. We, therefore, investigated the pharmacokinetics of 3'-hydroxycotinine in six male smokers after intravenous infusion of nicotine, cotinine, and 3'-hydroxycotinine. Serum concentrations of 3'-hydroxycotinine were lower than those of cotinine throughout the observation period of 60 h after infusion of nicotine or cotinine, whereas the amounts excreted in the urine were similar or higher than those of cotinine. The following means and ranges for the pharmacokinetic parameters were derived from the 3'-hydroxycotinine infusion experiment: half-life (t1/2 beta) = 5.9 (4.2-9.5) h; apparent volume of distribution (Vd) = 0.87 (0.51-1.14) l/kg; total clearance (Cl total) = 1.79 (1.08-2.59) ml/min/kg; renal clearance (Clr) = 1.31 (0.85-1.78) ml/min/kg; percentage of renal clearance (Clr/Cl total) = 75.4 +/- 12.8 (60.3-98.2). The high percentage of renal clearance suggests that further metabolization of this compound is limited. No evidence for a mutagenic activity of 3'-hydroxycotinine or of urine extracts from subjects dosed with hydroxycotinine was found with the S. typhimurium (TA 98) microsome assay.

Adult↗
PubMed1987

Determination of nicotine and cotinine in human serum and urine: an interlaboratory study.

An interlaboratory study aimed at determining nicotine and cotinine in human serum and urine was carried out. 11 laboratories from 6 countries, all experienced in performing nicotine and cotinine determinations in biological fluids by radioimmunoassay (RIA) and/or gas chromatography (GC) were involved. Each of them received 18 serum and 18 urine samples. The specimens were obtained from 8 smokers and 10 non-smokers; 2 samples from non-smokers were spiked with defined amounts of nicotine and cotinine. All the laboratories distinguished perfectly between the smokers and the non-smokers and according to cotinine levels in serum the laboratories ranked the samples with good agreement. There were systematic differences in the absolute values between the laboratories. The ratios of urinary cotinine concentrations between active and passive smokers differed widely from laboratory to laboratory. The reasons for this are not yet known and necessitate further investigation.

Chromatography, Gas↗
PubMed1987

Hydroxy-phenanthrenes in the urine of non-smokers and smokers.

Urinary hydroxy-phenanthrene (HO-PHE) excretion in non-smokers exposed to environmental tobacco smoke (ETS) is not increased. There is no significant difference in HO-PHE excretion between smokers (S) and non-smokers (NS), though excretion seems to be slightly elevated in smokers. A diet rich in polycyclic aromatic hydrocarbons leads to a rise in urinary HO-PHE excretion as compared to a diet low in polycyclic aromatic hydrocarbons (PAH), coming close to significance. HO-PHE excretion is not correlated with the mutagenic activity in urine.

Diet↗
PubMed1987

Urinary mutagenicity after controlled exposure to environmental tobacco smoke (ETS).

20 non-smokers on a defined diet low in polycyclic aromatic hydrocarbons (PAH) were exposed to environmental tobacco smoke (ETS) in an unventilated room for 8 h. The urinary mutagenicity in the 24-h urine samples as tested with the Salmonella (TA98) microsome assay did not significantly increase after exposure to either 10 ppm CO or 20-25 ppm CO. We conclude that exposure of non-smokers to ETS does not lead to an increase in their urinary mutagenicity, provided the exposure conditions are within a realistic range.

Adult↗
PubMed1985

Urinary hydroxyproline excretion in smokers, non-smokers and passive smokers.

The hydroxyproline/creatinine ratio in urine was investigated in 200 cigarette smokers, 199 pipe and/or cigar smokers and 24 non-smokers. For cigarette smokers a statistically significant positive correlation is found between this ratio and daily cigarette consumption, COHb, serum cotinine and nicotine excretion in urine. This smoking-related increase in the hydroxyproline/creatinine ratio is, for the most part or completely, due to the fact that creatinine urine concentrations inversely correlate with the smoke uptake variables. Neither pipe and/or cigar smoking nor passive smoke exposure of non-smokers seem to affect the hydroxyproline/creatinine ratio. A seasonal influence is found in these studies as well as in two experiments with limited numbers of subjects: the hydroxyproline/creatinine ratio is higher in winter than in summer for both smokers and non-smokers. Our data do not favour the idea that measuring hydroxyproline/creatinine ratios in urine is an accurate method of investigating early effects of smoking, passive smoking and air pollution in man.

Adolescent↗
PubMed1984

Hydroxyproline excretion in urine of smokers and passive smokers.

Urinary hydroxyproline excretion was investigated in 125 male cigarette smokers, 194 male pipe and/or cigar smokers, and 24 male nonsmokers. Hydroxyproline excretion was calculated either as hydroxyproline/creatinine ratio or as body surface-standardized amounts of hydroxyproline excreted in urine sampled during day, during night, or over 24 hr. The association of hydroxyproline excretion with smoke uptake variables such as daily cigarette consumption, carboxyhemoglobin, serum cotinine, and nicotine in urine and with self-reported passive smoking exposure in nonsmokers was analyzed. The hydroxyproline/creatinine ratio was found to be unsuitable as a measure of hydroxyproline excretion since creatinine urine concentrations correlate inversely with smoke uptake in cigarette and pipe/cigar smokers. The amount of hydroxyproline excreted in 24-hr urine and standardized for body surface was not significantly associated with smoke uptake in pipe/cigar smokers or exposure to passive smoking in nonsmokers. In cigarette smokers the situation appeared similar, although the results were less clear-cut. The data do not favor the premise that measuring urinary hydroxyproline excretion is an accurate method of investigating a lung-damaging effect of smoking, passive smoking, or air pollution.

Adult↗
PubMed1983

Thyroid function in patients with proteinuria and normal or increased serum creatinine concentration.

The thyroid function of 13 patients with proteinuria and normal serum creatinine level (Group 1) and 15 patients with proteinuria and increased creatinine level (Group 2) was investigated. The daily urinary T41- and T3 excretion was much higher in Group 1 patients than in Group 2 patients (37.1 +/- 25.9 nmol T4 vs 17.5 +/- 8.7 nmol T4, 3.3 +/- 1.6 nmol T3 vs 1.1 +/- 0.8 nmol T3, respectively) and correlated in both groups with the protein loss. None of the patients suffered from hypothyroidism as a consequence of this hormone loss. Although the mean serum T4-, T3-, FT4-, FT3-, TBG- and TBPA concentrations in both groups of patients were within the normal range, the urinary hormone loss appeared to influence these values considerably. It was striking that the rT3 concentration in the patients with the highest hormone loss was frequently less than 0.08 nmol/l, the lower limit of detectability. The basal TSH levels in serum of the nephrotic patients were similar to those of normal individuals. The thyroid function of patients with proteinuria accompanied by retention of creatinine due to renal failure was more difficult to assess because different pathological mechanisms may exert their influence on the thyroidal hormone secretion as well as on the peripheral hormone metabolism.

Aged↗
PubMed1980

Binding of thyrotrophin to low molecular weight fragments of human thyroid membranes.

The LATS absorbing activity from thyroid homogenates which is associated with the soluble thyroid fraction (4S-LAA) binds TSH in addition to LATS. This may indicate that 4S-LAA originates from the receptor sites for TSH at the thyroid cell surface. The affinity of 4S-LAA for TSH is much lower than that of thyroid membranes suggesting that 4S-LAA represents incomplete receptor sites or receptor sites which are altered in their structure.

Absorption↗
PubMed1978

[Diagnostic significance of heat-induced inhibition of erythrocyte sedimentation (author's transl)].

Heat-induced inhibition of erythrocyte sedimentation (HIES) was examined in 158 cases. HIES is significantly lower in patients with a liver cell damage isolated or due to metastases of a neoplastic process in comparison to that in patients suffering from inflammation or malign tumor not involving the liver. Generally, HIES depends upon the concentration of lysophosphatidyl choline (lysolecithin) which is set free in plasma by lecithin-cholesterol-acyltransferase (LCAT) during incubation. In patients with lever cell damage, LCAT is diminished. HIES is being influenced by several factors: Lysophosphatidyl choline is bound to albumin, and this prevents its reaction on the erythrocyte surface. Lysophospholipase reduces the concentration of lysophosphatidyl choline in the plasma by splitting off its fatty acid in the alpha-position. Specific serum proteins, the so-called agglomerines, which are responsible for the acceleration of erythrocyte sedimentation, are counteracting the HIES. The concentration of albumin and agglomerines in plasma and the activity of lysophospholipase are subject to physiologically and pathologically caused deviations. Thereby, HIES is being influenced individually at varying degrees. This makes it difficult to estimate the LCAT activity which represents the principal cause of HIES. As a consequence, HIES seems not to be suitable for clinical diagnostics.

Blood Proteins↗
PubMed1978

Relationship between thyroid status and Graves' disease-specific immunoglobulins.

The prevalence of TSI in Graves' disease was investigated with a radioligand receptor assay using human thyroid membranes and highly purified labeled porcine TSH or bovine TSH in 110 patients before treatment and in 39 patients after successful treatment with antithyroid drugs. In 11 patients, the assay was performed before, during, and after therapy. The results in the radioligand receptor assay were compared to thyroid function tests (TRH test, free T4 index, serum %3 level, and thyroid suppression test). Normal IgG inhibits nonspecifically, but dose dependently, the binding of [125I]TSH to thyroid membranes. IgG samples from patients were only considered to be positive if they reduced the binding of the labeled hormone below the mean value minus 2 SD of the controls. TSI activity was found in 50% of the patients with untreated diffuse toxic goiter, in 3 out of 27 cases who regained suppressible thyroid function, and in 5 out of 12 cases who were off therapy for more than 6 weeks and showed normal TRH tests and normal hormone levels but in whom the suppression test was not performed. Our data cannot prove the hypothesis that only humoral antibodies are responsible for the thyroid stimulation in Graves' disease, but of course they cannot exclude it; furthermore, they suggest the existence of antibodies which bind to the human thyroid cell membrane without necessarily stimulating thyroid cellular activity.

Antigen-Antibody Complex↗
PubMed1977

Metabolism of thyroid hormones by the isolated perfused rabbit kidney.

The metabolism of thyroxine and triiodothyronine in the isolated perfused rabbit kidney was monitored by specific radioimmunoassay for each hormone. The amount of thyroxine catabolised was proportional to the amount added initially and no saturation effects were observed over a wide range (3.9-82 nmol). After addition of thyroxine alone, triiodothyronine could be detected in the perfusion medium within 10 minutes but only much later in the urine. It was proposed that circulating thyroxine contributes indirectly to the level of urinary triiodothyronine.

Animals↗