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Biomedical subjects

M Vahter

Publications and source records attributed to M Vahter.

At least 55 records · Page 3Linked to original sources
PubMed1996

Concentrations of mercury, cadmium and lead in brain and kidney of second trimester fetuses and infants.

The concentrations of mercury (Hg), cadmium (Cd) and lead (Pb) in brain (cerebrum) and kidney during fetal (second trimester terminations or abortions, n = 20) and postnatal (infants deceased before three months of age, n = 15) development have been studied. Information on possible sources of exposure was obtained from the mothers of the fetuses, but not from those of the infants. The median concentration of Hg in the brain was 4 micrograms/ kg wet weight in both fetuses and infants (total range < or = 2-23 micrograms/kg). The concentrations of Hg in the kidneys were significantly higher than in brain, median of Hg 6 micrograms/kg (range < or = 5-34 micrograms/kg) in fetuses and 10 micrograms/kg (< or = 7-37) in infants. There was a tendency of increasing concentration of Hg in the fetal kidney, but not in the brain, with increasing number of amalgam fillings in the mothers. The concentration of Cd in the brain was less than 1 microgram/kg in most cases, both in fetuses and infants. The concentration of Cd in the kidneys was significantly higher, with a median of about 2 micrograms/kg (1-8 micrograms/kg) in both groups. There was no detectable association between tissue Cd concentrations and the smoking habits of the mothers. The concentration of Pb in brain was below 10 micrograms/kg in most cases. In the kidneys, the concentrations of Pb were significantly higher, with a median of 12 micrograms/kg in the fetuses (range < or = 6-20 micrograms/kg) and 15 micrograms/kg (< or = 9-36 micrograms/kg) in the infants. In general, the concentrations of Cd and Pb were lower than in previously reported studies.

Brain Chemistry↗
PubMed1996

Sample collection guidelines for trace elements in blood and urine. IUPAC Commission of Toxicology.

This paper presents an organized system for element-specific sample collection and handling of human blood (whole blood, serum or plasma, packed cells or erythrocytes) and urine also indicating a proper definition of the subject and sample. Harmonized procedures for collection, preparation, analysis and quality control are suggested. The aim is to assist scientists worldwide to produce comparable data which will be useful on a regional, national and international scale. The guidelines are directed to the elements aluminium, arsenic, cadmium, chromium, cobalt, copper, lead, lithium, manganese, mercury, nickel, selenium and zinc. These include the most important elements measured for their occupational or clinical significance, and serve as examples of principles that will guide development of methods for other elements in the future.

Blood Specimen Collection↗
PubMed1995

A unique metabolism of inorganic arsenic in native Andean women.

The metabolism of inorganic arsenic (As) in native women in four Andean villages in north-western Argentina with elevated levels of As in the drinking water (2.5, 14, 31, and 200 micrograms/1, respectively) has been investigated. Collected foods contained 9-427 micrograms As/kg wet weight, with the highest concentrations in soup. Total As concentrations in blood were markedly elevated (median 7.6 micrograms/1) only in the village with the highest concentration in the drinking water. Group median concentrations of metabolites of inorganic As (inorganic As, methylarsonic acid (MMA) and dimethylarsinic acid (DMA)) in the urine varied between 14 and 256 micrograms/1. Urinary concentrations of total As were only slightly higher (18-258 micrograms/1), indicating that inorganic As was the main form of As ingested. In contrast to all other populations studied so far, arsenic was excreted in the urine mainly as inorganic As and DMA. There was very little MMA in the urine (overall median 2.2%, range 0.0-11%), which should be compared to 10-20% of the urinary arsenic in all other populations studied. This may indicate the existence of genetic polymorphism in the control of the methyltransferase activity involved in the methylation of As. Furthermore, the percentage of DMA in the urine was significantly higher in the village with 200 micrograms As/1 in the water, indicating an induction of the formation of DMA. Such an effect has not been observed in other studies on human subjects with elevated exposure to arsenic.

Adult↗
PubMed1995

Relation of a seafood diet to mercury, selenium, arsenic, and polychlorinated biphenyl and other organochlorine concentrations in human milk.

Human transition milk was sampled from 88 mothers at the Faroe Islands, where the seafood diet includes pilot whale meat and blubber. Milk mercury concentrations (median, 2.45 micrograms/liter) were significantly associated with mercury concentrations in cord blood and with the frequency of pilot whale dinners during pregnancy. Milk selenium concentrations (mean, 19.1 micrograms/liter) correlated significantly with concentrations in cord blood but not with seafood consumption. Arsenic concentrations were very low. Twenty-four of the milk samples were separated into four pools based on fish intake and milk mercury concentrations. The polychlorinated biphenyl (PCB) concentrations (1.8-3.5 micrograms/g lipid) were high and mainly due to congener numbers 153, 180, and 138. One pool contained a congener 77 concentration of 1380 ppt, which is the highest ever reported in a human specimen for a coplanar PCB. The highest PCB concentrations were seen in the pools from women who had eaten frequent whale dinners and whose milk contained high mercury concentrations. The concentrations of chlorinated dibenzo-p-dioxins and furans were not similarly elevated. Given the advantages associated with breast-feeding, advice to nursing mothers in this population should take into regard the possible risks associated with long-term exposure to milk contaminants.

Adult↗
PubMed1995

Lack of methylation of inorganic arsenic in the chimpanzee.

Most mammals methylate inorganic arsenic (As) to methylarsonic acid (MMA) and dimethylarsinic acid, which are rapidly excreted in the urine. Previous studies have shown that, in contrast to humans, all experimental animals excrete very little MMA. With the aim of finding an appropriate animal model for studies on inorganic As metabolism and toxicity, we have investigated the metabolism of As in two male chimpanzees after a single iv dose of [73As]arsenate (5.8 micrograms As/kg body wt). The initial clearance from plasma was rapid with an apparent half-time of about 1 hr. Urine was found to constitute the major excretory pathway with very little excretion in the feces. About 60% of the administered 73As dose was excreted in the urine within 96 hr in a biphasic manner. The second phase of slow urinary excretion was characterized by first-order kinetics with a half-time of about 7 days. Upon ion-exchange chromatography of ultrafiltrated plasma and urine, only inorganic As could be detected, a finding confirmed by thin-layer chromatography. Thus, the results indicate that the chimpanzee, as previously shown for the marmoset monkey, but unlike all other mammals studied so far, including humans, is unable to methylate and detoxify inorganic As.

Animals↗
PubMed1995

Selenium concentrations in brain after exposure to methylmercury: relations between the inorganic mercury fraction and selenium.

Three groups of female monkeys (Macaca fascicularis) were exposed to methylmercury (MeHg, p.o. 50 micrograms Hg/kg body wt per day) for 6, 12, or 18 months. One group was exposed to MeHg for 12 months and kept unexposed for 6 months before sacrifice. Another group of three monkeys was exposed to HgCl2 i.v. for 3 months. Total and inorganic mercury concentrations in occipital pole and thalamus were determined by cold vapor atomic absorption spectroscopy. Selenium concentrations were analyzed by hydride generation atomic absorption spectroscopy. The results indicated an association between concentrations of inorganic mercury and selenium in both occipital pole and thalamus in the MeHg-exposed animals. A linear regression model using concentrations of inorganic mercury (nmol/g wet wt) as independent variable, and selenium concentrations (nmol/g wet wt) as the dependent variable showed significant correlations between the variables in both occipital pole and thalamus (r = 0.85 and r = 0.91, P < 0.0001). The intercept of the regression line was slightly lower (about 2 nmol Se/g wet wt) than the selenium concentrations found in control monkeys (about 3 nmol Se/g wet wt). There was a tendency to a "hockey stick"-shaped relationship between concentrations of selenium and inorganic mercury in the thalamus of monkeys with ongoing exposure to MeHg. An important role for selenium in the retention of mercury in brain is indicated.

Animals↗
PubMed1995

Lactational exposure to methylmercury in the hamster.

Syrian Golden hamster dams were administered 203Hg-labelled methyl mercury (MeHg; 1.6 mumol/kg) 1 day after parturition and milk was collected twice during the 1st week. The excretion of 203Hg in milk and the uptake, retention and tissue distribution of 203Hg in the pups was studied using gamma counting. The fraction of inorganic Hg in milk and in the kidneys of the pups was determined following separation of inorganic Hg and MeHg by ion exchange chromatography. The concentration of 203Hg in milk on the 1st day after MeHg administration was 0.12 nmol/g. 203Hg was mainly (80-90%) excreted as MeHg during the first 6 days of lactation. The whole body and tissue concentration of 203Hg in the pups increased for 10-15 days and decreased thereafter. The content of 203Hg in the pelt and the fraction of inorganic Hg in the kidney increased throughout the study period (4 weeks). The excretion of MeHg in milk corresponded to at least 5% of the dose administered to the dam. Our study demonstrates that breast milk may be a significant source of MeHg exposure during the critical neonatal period.

Animals↗
PubMed1995

Metabolism of mercury in hamster pups administered a single dose of 203Hg-labeled methyl mercury.

Golden Syrian hamster pups were administered a single subcutaneous dose of 203Hg-labeled methyl mercury (MeHg), 0.4 nmol/g body weight, seven days after birth, and were sacrificed 2, 7, 14, 21 or 28 days later. The excretion of 203Hg followed a biphasic elimination pattern with an average half-time of 8.7 days for the rapid component. The slow component had a much longer half-time and probably reflects binding of 203Hg to growing hair. The concentration of 203Hg in the liver, kidneys and brain two days after administration was 0.44, 0.38 and 0.19 nmol/g, respectively. The retention of 203Hg was higher in the kidney than in the liver and the brain. The content of inorganic 203Hg in the liver and kidneys increased the first weeks after administration, demonstrating that hamsters are able to demethylate MeHg before two weeks of age.

Aging↗
PubMed1995

Transplacental and lactational exposure to mercury in hamster pups after maternal administration of methyl mercury in late gestation.

Pregnant Syrian golden hamsters were given a single oral dose of 203Hg-labelled methyl mercury (MeHg), 1.6 mumol/kg body weight, on day 12 of gestation. The uptake, retention and tissue distribution of 203Hg in the dams and pups was studied by gamma-counting during the following three weeks. The average transplacental transfer of 203Hg was 1.1% of the administered dose per pup, corresponding to 11% of the administered dose to a whole litter. This was considerably more than in our previous studies when the dams were treated on gestational day 2 (1.3%) or 9 (4.6%). The amount of 203Hg transferred to each pup in utero was independent of the litter size. The average additional transfer of 203Hg to a litter via milk was 1.7% of the administered dose. In the pups, the content of 203Hg in the liver and brain decreased, while the content in the kidneys and pelt increased during the second and third week. The highest amount of 203Hg was generally found in the pelt, which indicated that unweaned hamster pups primarily excrete MeHg by binding to hair. The chemical form of mercury in the liver and kidneys of the pups was determined by ion-exchange separation of inorganic Hg and MeHg followed by gamma-counting. The amount of inorganic Hg in the liver of the pups remained constant throughout the experiment, while it increased in the kidneys after one week due to the demethylation of MeHg. The inorganic Hg in the liver of newborn pups was probably due to maternal demethylation of MeHg and transplacental transfer of inorganic Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury.

Total (T-Hg) and inorganic (I-Hg) mercury in blood and brain of female Macaca fascicularis monkeys, exposed to daily peroral doses of methyl mercury (MeHg; 50 micrograms Hg/kg body wt) for 6, 12, or 18 months, or to continuous iv infusion of HgCl2 (200 micrograms Hg/kg body wt) for 3 months, were determined. In normal weight monkeys (2.4-4.1 kg body wt) exposed to MeHg, steady state of T-Hg in blood (1.1 micrograms Hg/g) was reached in about 4 months. The elimination T1/2 in blood was 26 days. I-Hg constituted 7% of T-Hg in blood. The average concentration of MeHg in occipital pole and thalamus was about 3 micrograms Hg/g at 6 months and 4.5 micrograms Hg/g at 12-18 months. Accumulation in brain seemed to be biphasic. Following termination of 12 months exposure, elimination T1/2 for MeHg in brain was 35 days. I-Hg constituted about 9% of T-Hg in brain at 6-12 months, 18% at 18 months, and 74% at 6 months after termination of exposure. The I-Hg concentrations were somewhat higher in thalamus than in occipital pole. The elimination T1/2 for I-Hg was extremely long, on the order of years. Most likely, the I-Hg was formed by demethylation of MeHg in the brain. In monkeys exposed to HgCl2, blood levels of 0.6 micrograms I-Hg/g gave rise to brain I-Hg levels of about 0.1 micrograms/g only. In three heavy weight monkeys (5.0-6.1 kg body wt) exposed to MeHg, blood Hg increased to about 2 micrograms Hg/g, indicating a limited distribution of MeHg to fat. The Hg concentrations in brain (7-22 micrograms Hg/g) were considerably higher than those in normal weight monkeys, due to the high blood Hg levels in combination with a high brain-to-blood distribution ratio.

Administration, Oral↗
PubMed1994

A pilot study of lead and cadmium exposure in young children in Stockholm, Sweden: methodological considerations using capillary blood microsampling.

A capillary blood microsampling technique was tested among urban young children in Stockholm. Blood lead (BPb) and hemoglobin (Hb) concentrations were determined in capillary blood obtained by fingerstick from 41 children, 13-20 months old, and the accompanying parent. The quality control included control for lead (Pb) and cadmium (Cd) contamination of material and equipment used for blood sampling, washing procedures for the hands and fingers to be punctured, comparisons of Pb and Cd concentrations in blood obtained by fingerstick and by brachial vein puncture from the same individuals, analysis of external quality control samples for Pb and Cd in blood together with the collected samples, and evaluation of the analytical performance using linear regression analysis. The results showed that blood sampling material may contaminate the blood samples with amounts of Pb and Cd that would seriously influence the monitoring results in the low concentration range (< 100 micrograms Pb/L and < 1 microgram Cd/L). However, it is possible to obtain reliable BPb concentrations (> 10 micrograms Pb/L), but not BCd concentrations (< 1 microgram Cd/L), with the capillary blood microsampling technique tested provided that a strict quality control is applied. The sampling procedure tested was well accepted by the children and their parents. The children's median BPb concentration (27 micrograms/L; range 9-73 micrograms/L) was similar to the median BPb concentration of their parents (27 micrograms/L; range 7-74 micrograms/L). However, the correlation between child and parent BPb concentrations was poor (R2 = 0.20), which may indicate different sources to Pb exposure in children and parents.

Adult↗
PubMed1994

Effect of methyl mercury exposure on the uptake of radiolabeled inorganic mercury in the brain of rabbits.

Exposure to mercuric compounds at high dose levels has previously been shown to alter the integrity and function of the blood-brain barrier in laboratory animals. In the present study, we have investigated the distribution of intravenously administered inorganic 203Hg in rabbits additionally exposed to MeHg. A single dose of 203HgCl2 was administered together with or 5 min. or 24 hr after administration of a single dose (10 or 37.5 mumol/kg b.wt.) of MeHg. In another experiment, 203HgCl2 was administered to rabbits subchronically exposed to MeHg (1 mumol/kg b.wt. daily for three weeks) 24 hr after cessation of treatment. The integrity of the blood-brain barrier was assayed by measuring the uptake of 203Hg in the brain, as the blood-brain barrier usually serves to exclude inorganic Hg from the brain. The concentration of 203Hg within the brain was similar in all MeHg-treated rabbits, corresponding to 0.02% of the administered dose, and not different from that of control animals. Under these conditions, no obvious damage to the blood-brain barrier by MeHg could be observed.

Animals↗
PubMed1994

Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake.

Measurements of intake and uptake of cadmium in relation to diet composition were carried out in 57 nonsmoking women, 20-50 years of age. A vegetarian/high-fiber diet and a mixed-diet group were constructed based on results from a food frequency questionnaire. Duplicate diets and the corresponding feces were collected during 4 consecutive days in parallel with dietary recording of type and amount of food ingested for determination of the dietary intake of cadmium and various nutrients. Blood and 24-hr urine samples were collected for determination of cadmium, hemoglobin, ferritin, and zinc. There were no differences in the intake of nutrients between the mixed-diet and the high-fiber diet groups, except for a significantly higher intake of fiber (p < 0.001) and cadmium (p < 0.002) in the high-fiber group. Fecal cadmium corresponded to 98% in the mixed-diet group and 100% in the high-fiber diet group. No differences in blood cadmium (BCd) or urinary cadmium (UCd) between groups could be detected. There was a tendency toward higher BCd and UCd concentrations with increasing fiber intake; however, the concentrations were not statistically significant at the 5% level, indicating an inhibitory effect of fiber on the gastrointestinal absorption of cadmium. Sixty-seven percent of the women had serum ferritin < 30 micrograms/l, indicating reduced body iron stores, which were highly associated with higher BCd (irrespective of fiber intake). BCd was mainly correlated with UCd, serum ferritin, age, anf fibre intake. UCd and serum ferritin explained almost 60% of the variation in BCd.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Modifications of Ca2+ signaling by inorganic mercury in PC12 cells.

The effects of different levels of inorganic mercury (Hg2+) on depolarization- or agonist-stimulated Ca2+ signals were studied in PC12 cells. Exposure to 50-300 nM Hg2+ did not alter the resting cytosolic free Ca2+ concentration ([Ca2+]i), but enhanced the Ca2+ response to KCL-induced depolarization. Patch-clamp experiments revealed that these Hg2+ concentrations increased the voltage-dependent Ca2+ current through L-type channels. Also, Hg2+ treatment amplified the intracellular [Ca2+]i transients elicited by extracellular ATP. In contrast, the Ca2+ increase stimulated by bradykinin was unaffected. At slightly higher concentrations (1 to 2 microM), Hg2+ caused a sustained rise of the resting [Ca2+]i. This increase did not occur in Ca(2+)-free medium and was prevented by pretreatment with NiCl2 or with the L-type Ca2+ channel blockers, verapamil and nifedipine. Hg2+ did not mobilize Ca2+ from intracellular stores sensitive to thapsigargin, 2,5-di-(tert-butyl)-benzohydroquinone, or caffeine. At 2 microM, Hg2+ inhibited the [Ca2+]i transients elicited by bradykinin, ATP, or KCl-induced depolarization. The loss of the intracellular Ca2+ response to bradykinin was independent from the Ca2+ overload elicit by Hg2+; instead, it was associated with inhibition of polyphosphoinositide generation. Exposure to the lower Hg2+ concentrations (0.3-0.5 microM) greatly potentiated NGF-induced PC12 cell differentiation. Conversely, treatment with 2 microM Hg2+ caused cell death. Our results show that inorganic mercury has selective and different effects on Ca2+ signaling in PC12 cells depending on the concentration, within a narrow range.

Adenosine Triphosphate↗
PubMed1993

Fatal cadmium-induced pneumonitis.

A previously relatively healthy 78-year-old man was exposed to cadmium fumes during brazing with cadmium-containing silver solder. He developed severe chemical pneumonitis and died 25 d after exposure.

Aged↗
PubMed1992

Faecal elimination of lead and cadmium in subjects on a mixed and a lactovegetarian diet.

Faecal elimination of lead and cadmium in 16 subjects who changed from a mixed diet to a lactovegetarian diet has been studied. The faecal weight increased significantly following the change to the vegetarian diet, partly because of increased water content. There was a large inter-individual variation in faecal elimination of lead and cadmium during both the mixed-diet period (range 14 to 118, median 31 micrograms Pb/day; range 4.5 to 21, median 12 micrograms Cd/day) and the vegetarian diet period (range 19 to 136, median 42 micrograms Pb/day; range 6.1 to 24, median 14 micrograms Cd/day). There was a tendency towards increased faecal elimination of lead and cadmium following the change to the vegetarian diet, but the differences were not statistically significant.

Adult↗
PubMed1992

Integrated personal monitoring of cadmium exposure in Sweden.

Methods for the personal monitoring of human exposure to cadmium from air, food and beverages were studied in a group of 15 non-smoking women in Stockholm. Particles in the breathing zone air and duplicates of all food and beverages ingested were collected during seven consecutive days, as were faeces corresponding to the food ingested. Spot samples of blood and urine were also taken. The main sampling problems were caused by the noise of the personal air monitors and the short operation time of the batteries. On average, dietary cadmium (8.5 micrograms per day) contributed 99% of the total cadmium absorbed. There were large day-to-day variations in intake, most peaks corresponding to the consumption of seafood. Faecal cadmium was shown to reflect the total amount of cadmium ingested. There was a significant (p < 0.05) correlation between cadmium concentrations in blood (median 0.3 microgram/l) and average daily dietary intake of cadmium, but the blood cadmium levels could vary by a factor of four at one and the same average daily intake. The median urinary cadmium level was 0.2 microgram/l.

Adult↗