Search PubMed⌕ Search

Biomedical subjects

M Vahter

Publications and source records attributed to M Vahter.

At least 73 records · Page 4Linked to original sources
PubMed1991

Methods for integrated exposure monitoring of lead and cadmium.

An international pilot monitoring study on exposure to lead (Pb) and cadmium (Cd) has been implemented in Beijing, Yokohama, Stockholm, and Zagreb as part of the UNEP/WHO human exposure assessment locations (HEAL) Program. The main objective was to develop and test methods, including methods for quality assurance, for monitoring of personal exposure to Pb and Cd. The study included analytical training for Pb and Cd in blood, air filters, dust, diets, and feces, as well as exposure monitoring activities in small groups of nonsmoking women, 23-53 years of age, during 7 consecutive days. Airborne particulates, duplicate diets, feces, and blood were collected. An extensive quality assurance program was implemented in order to assure the reliability and comparability of the monitoring data. The main problem in the sample collection was associated with the air monitoring. The pumps were noisy, and the batteries had to be recharged every 6-8 hr. Collection of duplicate diets during 1 week gave good estimates of average dietary intakes of Pb and Cd. The metal contents in feces were found useful for evaluation of total peroral intakes. The methods used made it possible to demonstrate that the diet was the main source of Cd exposure at all the HEAL sites.

Adult↗
PubMed1991

Modifications of cell signalling in the cytotoxicity of metals.

Many metals act on biological systems at low concentrations and recent epidemiological and experimental research indicates that toxic effects of certain metals occur at levels only marginally higher than those found in healthy subjects. Despite a large number of studies describing metal cytotoxicity, the molecular mechanisms involved are still poorly understood. However, it now seems evident that several metals can interact with enzyme functional groups and that proteins involved in signal transduction, including Ca2+ channels and pumps, may be especially sensitive to this interaction. Impairment of the ability of cells to adequately respond to the stimulation by hormones and growth factors may result in the loss of important cell functions or activation of mechanisms that compromise cell survival. In the following sections we will briefly describe the effects of various metals on cell signalling and present our recent findings on the mechanism by which inorganic mercury affects signal transduction.

Animals↗
PubMed1991

Distribution of mercury in rabbits subchronically exposed to low levels of radiolabeled methyl mercury.

The metabolism of methyl mercury (MeHg) has been studied in rabbits administered 203Hg-labeled methyl mercuric chloride, 0.125 mumol/kg body weight, twice a week for 9 weeks, by intravenous injection. Twelve weeks after cessation of treatment, about 54% of the administered dose had been excreted in faeces and 5% in urine. After one week, the highest concentration of 203Hg was found in fur (8.6 nmol Hg/g). Substantially lower concentrations were found in kidney (2.5 nmol/g), liver (0.9 nmol/g), brain (0.4 nmol/g), muscle (0.3 nmol/g) and blood (0.1 nmol/g). The rate of elimination of 203Hg from brain, muscle and blood was faster (t1/2 about 12 days) than that from kidney and liver (t1/2 about 28 days). The relative amount of inorganic Hg in kidney and liver increased with time after cessation of treatment. The highest fractions were 85 and 70%, respectively. In brain, no significant demethylation of MeHg could be detected.

Animals↗
PubMed1991

Personal monitoring of lead and cadmium exposure--a Swedish study with special reference to methodological aspects.

Methods for determining personal exposure to lead and cadmium were tested in Stockholm in 1988. Lead and cadmium in breathing-zone air, 24-h duplicate diets, and feces of 15 nonsmoking women (27-46 years of age) were studied. Blood was collected at the beginning of and immediately after the test period (seven consecutive days). An extensive quality assurance program was included. Most technical problems were encountered in the 24-h collection of airborne particles. The pumps were noisy, and the batteries had to be recharged every 6-8 h. The lead and cadmium levels in feces were found to be useful indicators of the total ingested amounts of these metals. Because of the large day-to-day variation in the dietary intake of lead and cadmium, the sampling period for duplicate diets and feces should be at least 5-6 d.

Adult↗
PubMed1988

Environmental exposure to lead and arsenic among children living near a glassworks.

Concentrations of lead (Pb) in blood (B-Pb, geometric mean 34.6 micrograms l-1, n = 127) and inorganic arsenic (As) and its metabolites in urine (U-As, mean 5.1 micrograms/g creatinine, n = 35) did not differ between children living in a village close to a glassworks emitting both Pb and As and children living in a reference area. There was no significant effect on B-Pb and U-As related to parents working at the glassworks or consumption of domestically grown vegetables. Neither was there any significant effect upon B-Pb of sex, age, potentially lead-exposing hobbies, or consumption of canned foods. Boys had higher U-As than girls (5.8 vs 4.2 micrograms/g creatinine, p = 0.005), and there was a decrease with age (range 8.4-10.4 years, 27% per year, p = 0.01). Further, parental smoking habits had a significant effect on both B-Pb and U-As. In children of non-smoking parents the B-Pb was 30 micrograms l-1, in children with one parent who smoked 39 micrograms l-1 (smoking father 37, smoking mother 41 micrograms l-1) and in children with two parents who smoked 47 micrograms l-1 (p less than 0.001). The corresponding values for U-As were 4.2, 5.5, and 13 micrograms/g creatinine, respectively (p = 0.01).

Adult↗
PubMed1987

Biotransformation of dimethylarsinic acid in mouse, hamster and man.

The metabolism of dimethylarsinic acid (DMA) a common pesticide and the main metabolite of inorganic arsenic in mammals, has been studied in mice, hamsters and man. Mice and hamsters were administered a single dose of 74As-DMA (40 mg As/kg body weight) orally, while a human subject ingested DMA corresponding to 0.1 mg As/kg body weight. Ion exchange chromatography, paper electrophoresis, thin layer chromatography as well as arsine generation--gas chromatography combined with atomic absorption spectrophotometry or mass spectrometry were used to characterize the arsenic metabolites in urine and feces collected over 48 hours after treatment. In mice and hamsters 3.5% and 6.4% of the dose, respectively, were excreted in urine in the form of trimethylarsine oxide (TMAO). No TMAO was found in feces. A DMA-complex was detected in urine and feces. It amounted to about 13% of the dose in mice and 15% in hamsters. About 80-85% of the dose was eliminated in urine and feces in the form of unmetabolized DMA. No demethylation of DMA to inorganic arsenic was observed. In man, about 4% of the dose was excreted in urine as TMAO and about 80% as DMA.

Adult↗
PubMed1987

Dissolution of two arsenic compounds by rabbit alveolar macrophages in vitro.

The ability of rabbit alveolar macrophages to dissolve two arsenic compounds, 74As-labeled lead arsenate and arsenic trisulfide, was studied in vitro. The solubilities in water of these two compounds are related differently to pH. The solubility of lead arsenate increases and that of arsenic trisulfide decreases with decreasing pH. The radiolabeled particles were incubated with and without macrophages for up to 3 days, whereafter the amount of 74As in soluble form and the amount in particle form and/or bound to macrophages were determined. The results strongly support the hypothesis that the dissolution of particles by macrophages is influenced by the acid milieu in the phagosomes. About 14% of the 74As-labeled lead arsenate particles incubated for 3 days with the macrophages was released into the culture medium, compared with about 2% of the particles incubated with the culture medium without macrophages. With the arsenic trisulfide particles, less soluble 74As was released into the medium in samples with macrophages than in samples without macrophages, although the solubility in all incubations was considerably greater than that for lead arsenate. The results indicate that dissolution in the phagosomes of the macrophages may be of great importance for the clearance of particles such as lead arsenate, which are more soluble at pH 4 than at pH 7.

Animals↗
PubMed1987

Effects of low dietary intake of methionine, choline or proteins on the biotransformation of arsenite in the rabbit.

The effects of 6 weeks feeding with diets low in methionine, choline, or proteins on the biotransformation and retention of 76As-labelled arsenite (0.4 mg As/kg bw) in rabbits have been studied. All test diets caused a significant decrease in the urinary excretion of dimethyl[76As]-arsinic acid, the main metabolite of inorganic arsenic. This gave rise to an increased retention of arsenic in the tissues, especially liver and lung. The test diets also caused a specific increase of the arsenic concentration in liver microsomes. The results indicate that subjects with a poor nutritional status have a lower capacity of methylating and thereby detoxifying inorganic arsenic.

Animals↗
PubMed1987

Solubility, retention, and metabolism of intratracheally and orally administered inorganic arsenic compounds in the hamster.

The absorption, biotransformation, and tissue retention of arsenic following intratracheal and oral administration of 74As-labeled sodium arsenite, sodium arsenate, arsenic trisulfide (suspension), and lead arsenate (suspension) have been studied in hamsters, and correlated to the in vitro and in vivo solubility of the compounds. After intratracheal instillation, the clearance of 74As from the lungs was positively correlated to the in vivo solubility. Less than 0.1% of the sodium arsenite and sodium arsenate was retained in the lungs after 3 days, compared to 1.3% of the arsenic trisulfide particles and 45% of the lead arsenate particles. The latter showed a very low solubility both in vivo and in vitro. In general, orally administered arsenic had a shorter biological half-life than intratracheally administered, especially when given in the form of arsenic trisulfide or lead arsenate particles, which seemed to be absorbed to only 20-30% in the gastrointestinal tract. Reduction, oxidation, and methylation of arsenic varied to a great extent with the arsenic compound and the route of exposure. Trivalent arsenic was methylated to a greater extent than pentavalent and less soluble compounds (suspended particles) more than dissolved compounds. The trivalent arsenic compounds caused higher concentrations than the pentavalent in the upper gastrointestinal tract but not in other tissues.

Administration, Oral↗
PubMed1986

Airborne arsenic and urinary excretion of metabolites of inorganic arsenic among smelter workers.

The relationship between airborne concentrations of arsenic and the urinary excretion of inorganic arsenic metabolites (inorganic arsenic + methylarsonic acid + dimethylarsinic acid) have been studied among smelter workers exposed to arsenic trioxide. The urinary concentrations of arsenic metabolites were found to increase steadily during the first day of the working week (after 2-3 d off from work), whereafter they reached a steady state. The concentration in the late evening after a day of exposure was very similar to that in the early morning after. Both were well correlated to the total daily excretion. In the second part of the study, comprising 18 subjects, the first-void morning urine of each participant was collected for 2 to 3 d during the steady-state phase. Total concentration of arsenic in the breathing zones was measured by personal air samplers. Airborne arsenic (8-h values) varied between 1 and 194 micrograms As/m3, and urinary arsenic between 16 and 328 micrograms As/g creatinine. With the urinary arsenic concentrations (mean values of 2-3 d for each subject) plotted against the corresponding airborne arsenic concentrations, the best fit was obtained by a power curve with the equation y = 17 X X0.56. However, four of the participants were found to excrete far more (105-260%) arsenic in the urine than possibly could have been inhaled, most likely due to oral intake of arsenic via contaminated hands, cigarettes or snuff. If these four were excluded, the best fit was obtained by a straight regression line with the slope 2.0 and the intercept 29 micrograms As/g creatinine (coefficient of correlation 0.92; P less than 0.001).

Air Pollutants, Occupational↗
PubMed1986

Concentrations of arsenic in urine of the general population in Sweden.

The concentration of the sum of the metabolites of inorganic arsenic (inorganic arsenic, methylarsonic acid and dimethylarsinic acid) as well as the concentration of organic arsenic compounds, mainly in the form of arsenobetaine, in the urine of human subjects from two cities in Sweden have been studied. The median concentration of metabolites of inorganic arsenic was approximately 8 micrograms As/g creatinine, independent of place of residence, sex, smoking and consumption of beer and wine. However, subjects who frequently ate flatfish and crustacea had somewhat higher (1.5 times) concentrations than those who very seldom ate such food. Flatfish, mainly in the form of plaice, and crustacea were found to be the main source of organic arsenic compounds. Subjects eating this type of seafood more than once a week had approximately 40 micrograms organic As/g creatinine (median value), compared with about 12 micrograms organic As/g creatinine in subjects who very seldom ate it. Other types of seafish or freshwater fish did not give rise to elevated concentrations of arsenic in the urine. The total range of organic arsenic compounds in urine was less than 1 to 525 micrograms As/g creatinine.

Adult↗
PubMed1985

The role of the methylation in the detoxication of arsenate in the rabbit.

The biotransformation, tissue retention, intracellular binding and biokinetics of arsenic were studied in rabbits exposed to [74As]arsenate (0.4 mg As/kg body wt., i.v.). Inhibition of the methyltransferase activity by injection of periodate-oxidized adenosine (PAD) caused a marked decrease of the formation of [74As]dimethylarsinic acid (DMA), which gave rise to 1.5-4 times increased tissue levels of 74As. This is almost the same as reported for rabbits given arsenite in combination with PAD and was due to a rapid reduction of the arsenate to arsenite which bound to the tissues. Only about 30% of the arsenate given was excreted unchanged in the urine, indicating that a large part was reduced to AsIII. Thus the methylation to DMA seems to be almost as important for the detoxication following exposure to arsenate as that following exposure to arsenite. In the rabbits with normal methylating capacity 50-70% of the produced AsIII was methylated to DMA. The liver was the only organ in which DMA was present 1 h after the administration, indicating that this is the main site of the methylation. The DMA was rapidly cleared from all tissues except the thyroid.

Animals↗
PubMed1985

Reduction and binding of arsenate in marmoset monkeys.

The metabolism of 74As-arsenate (As V, 0.4 mg As/kg body weight, IV) in marmoset monkeys (two males and two females) was studied. Unlike all other animal species studied so far, the marmoset was found to be unable to metabolize the arsenate to dimethylarsinic acid. Most of the absorbed arsenate was reduced to arsenite (As III) in vivo. Only 20% was excreted in the urine as unchanged As V. A further 20% of the dose was excreted as As III. The rest of the As III produced was bound to the tissues, giving a distribution picture very similar to that reported earlier for marmoset monkeys given arsenite. The tissues with longest retention of arsenic were the liver, upper gastrointestinal tract (oral cavity and esophagus), skin, kidneys and gall bladder. The pronounced accumulation in the liver resulted from specific binding of arsenic to the rough microsomal membranes, unique to this animal species.

Animals↗
PubMed1984

Metabolism of arsenocholine in mice, rats and rabbits.

The distribution, retention and biotransformation of arsenocholine, an organic arsenic compound present in certain seafood, have been studied in rats, mice and rabbits by use of synthesized 73 As-labelled arsenocholine. Orally administered arsenocholine was almost completely absorbed from the gastro-intestinal tract in mice and rats. In all species 70--80% of the administered dose was excreted in the urine within 3 days, [73 As] arsenobetaine was the main urinary metabolite; [73 As] arsenocholine was found in the urine of the first day only. No degradation to inorganic arsenic, mono- or dimethylarsenic acids, or trimethylarsine oxide was observed. In the tissues the 73 As activity retained was found in the form of [73 As] arsenobetaine and [73 As arsenophospholipids. Tissues with longest retention times were prostate, epididymis, testes, myocardium, liver, adrenal cortex, pancreas, dental pulp and pituitary gland.

Animals↗