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Biomedical subjects

H Remmer

Publications and source records attributed to H Remmer.

At least 19 recordsLinked to original sources
PubMed1990

Generation of volatile hydrocarbons from amino acids and proteins by an iron/ascorbate/GSH system.

Incubation of free, but not of peptide-bound methionine in an iron/ascorbate system resulted in ethylene generation, which was inhibited by glutathione. Leucine and isoleucine, however, when incubated in an iron/ascorbate/GSH system, released small amounts of propane and ethane, respectively. Peptide-bound leucine additionally yielded butane, as did bovine serum albumin or casein. Hydrocarbon generation from amino acids was inhibited by hydroxyl radical scavengers, but catalase and superoxide dismutase were more efficient. Additionally, ethane and propane generation in this system was optimal at pH 6.2 suggesting the involvement of protonated superoxide besides OH-radicals which attack the side chains of Leu and Ile and very probably produce carbon-centered radicals, which should abstract a hydrogen atom from the thiol group of GSH resulting in the formation of saturated hydrocarbons.

Amino Acids↗
PubMed1987

In vitro aging of red blood cells and lipid peroxidation.

Incubating isolated erythrocytes in phosphate buffered saline supplied with sufficient glucose (20 mM) for several days resulted in methemoglobin formation and decrease in glycolytic and antioxidant enzyme activities. Volatile hydrocarbon gas release (ethane, ethylene, propane, butane, isobutane, pentane) and loss of the polyunsaturated fatty acids, arachidonic acid (20:4) and docosahexaenoic acid (22:6) in the erythrocyte membrane indicated possible involvement of peroxidative reactions in cellular aging processes.

Erythrocyte Aging↗
PubMed1987

Alcohol consumption and hepatic fibrosis affect the fatty acid composition of red blood cells and their susceptibility to lipid peroxidation.

Erythrocytes from alcoholics with and without liver cirrhosis and from rats treated either with ethanol or thioacetamide, the latter treatment resulting in hepatic fibrosis, were analysed for their membrane fatty acid composition and their susceptibility to lipid peroxidation. Red cells containing less arachidonic acid than controls, as found in alcoholics with liver cirrhosis, were less susceptible to lipid peroxidation than controls. This observation was confirmed by experiments with rat erythrocytes obtained from animals with hepatic fibrosis. However, red cells containing less linoleic acid than controls, as found in alcoholics without liver cirrhosis, exhibited a normal degree of lipid peroxidation upon oxidant stress induced by hydrogen peroxide. The results demonstrated that in red cells only fatty acids with four double bonds seem to be involved in membrane peroxidation reactions under the condition chosen. This observation might be of relevance for in vivo aging of red cells.

Animals↗
PubMed1987

Passively inhaled tobacco smoke: a challenge to toxicology and preventive medicine.

The difficulties in defining the exposure of a passive smoker might explain the controversial results regarding an association between passive smoking on one hand and lung cancer, tumors of all sites and ischemic heart diseases on the other. The plausibility of these epidemiological observations will be discussed in the light of analytical, toxicological, biochemical and oncological data. The minute amounts of nicotine and particulate matter, even the much higher concentrations of volatile substances, such as nitrosamines, NOx, acroleine and formaldehyde, present in diluted sidestream compared to mainstream smoke and breathed by involuntarily smoking people, cannot explain their relatively high cancer risk. It is plausible if one considers the high capacity of cigarette smoke to induce drug metabolizing enzymes. Diluted sidestream smoke, however, lacks compounds which induce several iso-enzymes of cyt. P-450 monooxygenase in the tissues. The best evidence is the up to 100-fold increase in placental enzymes if pregnant women smoke, whereas passively inhaled tobacco smoke is ineffective as inducer. The small amounts of paternal smoke inhaled by pregnant women, containing teratogenic and carcinogenic compounds, which are supposedly not detoxified in the placenta, seem to explain the higher risk for malformations of the fetus and the same or even increased risk for perinatal mortality, compared with the outcome of pregnancy if the mother smoked. The induction of placental enzymes very probably protects the fetus against the much higher amounts of toxic agents inhaled by the smoking mother. The increased activity of placental enzymes seems to be a model for the probably greater capacity of certain cyt. P-450 iso-enzymes in the lung and other tissues to convert carcinogens to inactive metabolites when the individual smokes actively. It is well known that concomitant administration of carcinogens with inducing agents inhibits tumor growth in animals because of a shift in the metabolism which favours the formation of ineffective substances. The negligible amounts of nicotine and CO in passively inhaled tobacco smoke cannot be responsible for the surprisingly high risk for ischemic heart diseases of passive smokers. A plausible explanation is offered by experiments with doves and chicken, which develop atherosclerotic lesions due to the action of carcinogens which are metabolized by certain inducible cyt. P-450 iso-enzymes in the aortic wall. Much circumstantial evidence will be presented, indicating that PAHs, contrary to the propagated opinion, play a minor role for the initiation of cancer in active smokers.(ABSTRACT TRUNCATED AT 400 WORDS)

Female↗
PubMed1986

Induction of cytochrome P-448 iso-enzymes and related glucuronyltransferases in the human liver by cigarette smoking.

Human liver 10-20 mg from biopsy samples removed for diagnostic purposes from selected patients has been used for the preparation of microsomes. The activity of certain mono-oxygenases and UDP-glucuronyltransferases, as well as certain other enzymes involved in drug metabolism, has been determined using different substrates as indicators. Smokers oxidized benzo(a)pyrene and 7-ethoxyresorufin and also conjugated alpha-naphthol at a significantly increased rate compared to non-smokers. This indicates induction of certain mono-oxygenases and glucuronyltransferases which differs from the induction produced by phenobarbital. The findings can account for the reduced activity and increased elimination rate of certain drugs prescribed to smokers.

Benzopyrene Hydroxylase↗
PubMed1985

Decreased susceptibility of red blood cells to lipid peroxidation in patients with alcoholic liver cirrhosis.

Red blood cells from alcoholics with and without liver cirrhosis and control subjects were examined for the susceptibility to lipid peroxidation. Red blood cells of patients with liver cirrhosis were found to be less sensitive to hydrogen peroxide-induced peroxidation measured by a new, reliable and sensitive method: the release of pentane during red blood cell lipid peroxidation. Changes of sensitivity to lipid peroxidation correlated with the severity of the liver malfunction, but not with abnormalities of the lipid composition of red cell membranes which are apparent in patients with liver disease. In alcoholics without liver cirrhosis, only minor changes in the susceptibility of red cells to peroxidation were observed.

Erythrocytes↗
PubMed1985

Formation and metabolism of nitrosamines in vivo, monitored by 14N-stable isotope labelling.

Microsomal metabolism of N-nitrosodimethylamine entails release of molecular nitrogen; the extent is determined by 15N stable isotope labelling and mass-spectrometric isotope ratio measurements. Exhalation of labelled nitrogen by rats treated with 15N-dimethylamine and nitrite or 15N-nitrite alone indicates that nitrogen may arise from nitrite via two pathways: either directly from nitrosation of primary amines or from secondary and tertiary amines with subsequent enzymic N-demethylation. The overall yield of nitrosamine formation, N-demethylation and nitrogen-release represent about 0.3-6% or the administered dose of dimethylamine (1.1 mmol/kg), depending upon the dose of nitrite (0.55-2.2 mmol/kg). 15N-stable isotope labelling and mass-spectrometric isotope ratio measurements are powerful tools for assessment of endogenous nitrosamine formation from nitrite. One hundred nmol of labelled nitrogen are easily detectable in vivo; with further methodological refinement the limit of detection may be lowered by two orders of magnitude.

Animals↗
PubMed1985

Effect of ascorbate on red blood cell lipid peroxidation.

The present study investigates the effect of ascorbate on red cell lipid peroxidation. At a concentration between 0.2 mmol - 20 mmol/1 ascorbic acid reduces hydrogen peroxide-induced red blood cell lipid peroxidation resulting in a marked decrease in ethane and pentane production as well as in haemolysis. Ascorbic acid also shows an antioxidant effect on chelated iron-catalyzed hydrogen peroxide-induced peroxidation of erythrocyte membranes. At a concentration of 10 mmol/1 ascorbic acid totally inhibits oxidative break-down of polyunsaturated fatty acids by radicals originating from hydrogen peroxide. Our results indicate that ascorbate at the chosen concentration has an antioxidant effect on red blood cell lipid peroxidation.

Ascorbic Acid↗
PubMed1984

Phenylhydrazine-induced lipid peroxidation of red blood cells in vitro and in vivo: monitoring by the production of volatile hydrocarbons.

Human red blood cells and male Sprague-Dawley rats were treated in vitro and in vivo, respectively, with phenylhydrazine in order to determine whether the release of volatile hydrocarbons can serve as a suitable index for phenylhydrazine-induced red blood cell peroxidation. Lipid peroxidation following phenylhydrazine administration (in vitro experiments: dosage calculated at 0.5-50 mM; in vivo experiments: intraperitoneal injection of 2.8 mg/100 g body wt) was monitored by the release of ethane and pentane measured by gas chromatography. Further hydrocarbons such as ethylene, propane, n-butane, iso-butane and iso-butene were monitored to form a basis of comparison. In vitro haemolysis was also determined during the course of incubation. Red blood cell suspensions yielded more than 15-fold concentrations of propane and more than 2-fold concentrations of iso-butane compared to pentane and ethane yields. Haemoglobin solutions also produced propane and iso-butane in the presence of phenylhydrazine, whereas pentane and ethane were not detectable. Time-course studies revealed that ethane and pentane reached maximum in vitro levels after red blood cell suspensions had been incubated for 2 hr whereas the maximum degree of haemolysis (approximately 60%) was attained between 60 and 90 min following the beginning of phenylhydrazine treatment. The dosage did not affect the final degree of haemolysis. Rats treated with phenylhydrazine exhaled greater concentrations of ethane (6-fold increase) and pentane (2-fold increase) compared to control animals. Exhaled propane showed a 30-fold increase in concentration following drug treatment. Our results suggest that the release of pentane and ethane may be useful in assessing red blood cell lipid peroxidation in the presence of phenylhydrazine in vitro and in vivo.

Alkanes↗
PubMed1984

Metabolism of low concentrations of N-nitrosodimethylamine in isolated liver cells of the guinea pig.

Freshly isolated liver cells of guinea pig were used to study the metabolism of NDMA in the concentration range 0.05 to 100 microM. Analysis was performed using the gas chromatograph-thermal energy analyzer nitrosamine detector method and with radiolabeled NDMA. At concentrations below 10 microM, NDMA was degraded by liver cells (10 mg of protein in 2.5 ml of medium) within 20 min (at 100 microM in 80 min). The majority of metabolized methyl groups were initially associated with volatile compounds and were subsequently integrated into nonvolatile, acid-soluble molecules (57%) or liberated as CO2 (14%). Less than 2% were bound to cellular macromolecules. Ethanol inhibited NDMA degradation competitively, with a Ki of 0.8 mM ethanol. It is concluded that low concentrations of NDMA are metabolized in liver cells, primarily by the high-affinity demethylase and that there are no additional catalytic activities with Km values below 5 microM. Most of the methyl groups, released during metabolism, enter the C1 pool.

Animals↗