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At least 19 recordsLinked to original sources
PubMed2001

Volatilization of mercury under acidic conditions from mercury-polluted soil by a mercury-resistant Acidithiobacillus ferrooxidans SUG 2-2.

Volatilization of mercury under acidic conditions from soil polluted with mercuric chloride (1.5 mg Hg/kg soil) was studied with resting cells of a mercury-resistant strain, Acidithiobacillus ferrooxidans SUG 2-2. When resting cells of SUG 2-2 (0.01 mg of protein) were incubated for 10 d at 30 degrees C in 20 ml of 1.6 mM sulfuric acid (pH 2.5) with ferrous sulfate (3%) and mercury-polluted soil (1 g), which contained 7.5 nmol of Hg, approximately 4.1 nmol of mercury was volatilized, indicating that 54% of the total mercury in the soil was volatilized. The amount of mercury volatilized from the soil was dependent on the concentration of Fe2+ added to the medium. When elemental sulfur, sodium tetrathionate, and pyrite were used as an electron donor for the mercury reduction, 16, 2.4 and 0.84%, respectively, of the total mercury added to the solution were volatilized. The optimum pH and temperature for mercury volatilization were 2.5 and 30 degrees C. Approximately 92% of the total mercury in a salt solution (pH 2.5) with resting cells of SUG 2-2 (0.01 mg of protein), ferrous sulfate (3%) and mercury-polluted soil (1 g) was volatilized by further addition of both resting cells and Fe2+ and by incubating for 30 d at 30 degrees C.

Hydrogen-Ion Concentration↗
PubMed1987

Cytochemical demonstration of mercury deposits in trout liver and kidney following methyl mercury intoxication: differentiation of two mercury pools by selenium.

The amount and the ultrastructural distribution of mercury was studied in seven different organs of rainbow trout (Salmo gairdneri) fingerlings following exposure to methyl mercury (MeHg)-contaminated fodder for periods of 2 and 7 weeks. The amounts of mercury retained by the whole fish and the selected organs were determined by measuring the uptake of 203Hg-labeled MeHg. Spleen, liver, and kidney had the highest concentrations after both experimental periods, while the largest relative increases were found in brain, muscle, and kidney. The subcellular distribution of mercury accumulations was demonstrated cytochemically in liver and kidney using the silver enhancement method by which accumulations of mercury-sulfides and/or mercury-selenides are made visible for light and electron microscopy. When sections prepared from the liver and kidney from fish, injected with selenium 2 hr prior to being killed, were compared with those of fish not treated with selenium, two distinct pools of mercury could be demonstrated, the HgS pool, and the HgSe pool. The HgS pool, supposed to represent inorganic mercury, was found exclusively within lysosomes. The increase of this pool from 2 to 7 weeks was most pronounced in the kidney. The HgSe pool, supposed to represent methyl mercury, was shown by the presence of silver deposits at new locations as well as by an increase in the amount of deposits within lysosomes. The new locations included (1) secretory-like vesicles and the bile canaliculi of the liver, suggesting a biliary excretion of this mercury pool; (2) microvilli and endosomes of kidney tubular cells, suggesting a glomerular filtration and subsequent reabsorption; and (3) mitochondria of proximal tubule cells.

Animals↗
PubMedDate not supplied

Mercury uptake in vivo by normal and acatalasemic mice exposed to metallic mercury vapor (203Hg degrees) and injected with metallic mercury or mercuric chloride (203HgCl2).

Levels of mercury in the brain and liver of acatalasemic mice immediately following exposure to metallic mercury vapor or injection of metallic mercury were higher than those found in normal mice. Acatalasemic mice had decreased levels of mercury in the blood and kidneys when the levels were compared with those of normal mice, which indicated that catalase plays a role in oxidizing and taking up mercury. Thus, the brain/blood or liver/blood ratio of mercury concentration in acatalasemic mice was significantly higher than that of normal mice. These results suggest that metallic mercury in the blood easily passed through the blood-brain or blood-liver barrier. The levels of mercury distribution to the kidneys of normal and acatalasemic mice, 1 hr after injection of mercuric chloride solution, were higher than that of normal and acatalasemic mice, respectively, 1 hr after injection of metallic mercury.

Animals↗
PubMed1999

Removal of mercury from mercury-contaminated sediments using a combined method of chemical leaching and volatilization of mercury by bacteria.

A method for the removal of mercury sulfide from mercury-contaminated sediments was developed, which consists of chemical leaching and volatilization of mercury by bacteria. More than 85% of the mercury in sediment containing 0.11-37.4 mg/kg of mercury was efficiently extracted with 3 M HCl and 74 mM FeCl3. Subsequent volatilization by bacteria resulted in the removal of 62.9-75.1% of mercury from mercury-contaminated Minamata Bay sediments. Methylmercury was also eliminated from soil at a high efficiency. Thus, this combined method of chemical and microbial treatments could be used for efficient removal of both organic and inorganic mercurials from natural sediments.

Bacteria↗
PubMed1993

Subjective symptoms and neurobehavioral performances of ex-mercury miners at an average of 18 years after the cessation of chronic exposure to mercury vapor. Mercury Workers Study Group.

In order to determine if there are any residual effects of long-term exposure to mercury vapor, neurobehavioral tests were given to ex-mercury miners about 18 years after the cessation of mercury exposure. Seventy-six male ex-mercury miners who had been exposed to relatively high concentrations of mercury vapor (over 1.0 mg/m3) and with a past history of mercury intoxication were compared to age (+/- 3 years)-, sex-, and years of education-matched controls. Although the extent of the workers' symptoms caused by mercury poisoning, termed erethismus merculialis, markedly decreased after the cessation of exposure, the prevalence of neurological symptoms (such as hand tremors, headaches, and slurred speech) and symptoms of senility (such as low-back pain, loss of sexual desire) in the ex-miners was significantly higher than those in the controls. Matched-pair analysis showed that performances of motor coordination, Simple reaction time, and Short-term memory in the ex-miners were significantly deteriorated compared to those of controls. There are slight but persistent effects on neurobehavioral function, especially on motor coordination function, among mercury miners more than 10 years after the cessation of exposure.

Aged↗
PubMed1992

An acute mercuric mercury poisoning: chemical speciation of hair mercury shows a peak of inorganic mercury value.

A woman ingested a dose of sublimate (approximately 0.9 g) in an attempted suicide. She survived and recovered in response to a combination of therapies including chelate (BAL) therapy, plasma exchange, haemodialysis and peritoneal dialysis. Serum inorganic mercury concentration, urinary inorganic mercury excretion and hair inorganic and organic mercury and selenium concentrations, along the length from the scalp to the distal part, were measured. Longitudinal analysis of hair, revealed a peak in inorganic mercury corresponding to the time of mercury ingestion. Organic mercury and selenium in the hair had different patterns of longitudinal variation from that of inorganic mercury. The biological half-life (23.5 d) of serum inorganic mercury levels was in good agreement with values previously reported in the literature.

Adult↗
PubMed1999

Mercury accumulations in brains from populations exposed to high and low dietary levels of methyl mercury. Concentration, chemical form and distribution of mercury in brain samples from autopsies.

Autopsy samples from 17 Greenlanders and 12 Danes were analysed for total and organic mercury by atomic absorption spectrophotometry, and for cellular localisation by autometallography. The concentration of total mercury in the Greenlanders (median: 174 micrograms Hg/kg wet weight brain tissue, range 59-4782, highest in cerebellum: 492) was found to be significantly higher than in the Danish group (3.7 micrograms Hg/kg w.w., range 1.2-11.8). Furthermore, the total concentration of mercury was positively correlated to age (rho = 0.56, p < 0.05), and the fraction of methyl mercury was negatively correlated to age (rho = -0.66, p < 0.01) among the Greenlanders. This suggests an age dependent accumulation of total mercury and a slow transformation of methyl mercury to inorganic mercury in the brain. The autometallographically demonstrable mercury was primarily located in glia cells.

Adult↗
PubMed2003

Continuous analysis of dissolved gaseous mercury (DGM) and mercury flux in two freshwater lakes in Kejimkujik Park, Nova Scotia: evaluating mercury flux models with quantitative data.

Diurnal patterns for dissolved gaseous mercury (DGM) concentration, mercury flux, several water variables (pH, oxidation reduction potential (ORP), water temperature), and meteorological variables (wind speed, air temperature, % relative humidity, solar radiation) were measured in two lakes with contrasting dissolved organic carbon (DOC) concentrations in Kejimkujik Park, Nova Scotia. A continuous analysis system made it possible to measure quick changes in DGM over time. Consistently higher DGM concentrations were found in the high DOC lake as compared to the low DOC lake. An examination of current mercury flux models using this quantitative data indicated some good correlations between the date and predicted flux (r ranging from 0.27 to 0.83) but generally poor fit (standard deviation of residuals ranging from 0.97 to 3.39). Cross-correlation analysis indicated that DGM dynamics changed in response to solar radiation with lag-times of 65 and 90 min. This relationship with solar radiation was used to develop new predictive models of DGM and mercury flux dynamics for each lake. We suggest that a generalized approach using time-shifted solar radiation date to predict DGM can be incorporated into existing mercury flux models. It is clear from the work presented that DOC and wind speed may also play important roles in DGM and mercury flux dynamics, and these roles have not been adequately accounted for in current predictive models.

Air Pollutants↗
PubMed2001

A methylene blue-mediated enzyme electrode for the determination of trace mercury(II), mercury(I), methylmercury, and mercury-glutathione complex.

A methylene blue-mediated enzyme biosensor has been developed for the detection of inhibitors including mercury(II), mercury(I), methylmercury, and mercury-glutathione complex. The inhibition to horseradish peroxidase was apparently reversible and noncompetitive in the presence of HgCl2 in less than 8 s and irreversibly inactivated when incubated with different concentrations of HgCl2 for 1-8 min. The binding site of horseradish peroxidase with HgCl2 probably was a cysteine residue SH. Mercury compounds can be assayed amperometrically with the detection limits 0.1 ng ml(-1) Hg for HgCl2 and methylmercury, 0.2 ng ml(-1) Hg for Hg2(NO3)2 and 1.7 ng ml(-1) Hg for mercury glutathione complex. Inactivation of the immobilized horseradish peroxidase was displayed in the AFM images of the enzyme membranes.

Biosensing Techniques↗
PubMed2001

Synthesis and characterization of the dimercury(I)-linked compound [PPn]4[(Re7C(CO)21Hg)2]. Oxidative cleavage of the mercury-mercury bond leading to carbidoheptarhenate complexes of mercury(II), including [PPN][Re7C(CO)21Hg(S=C(NME2)2)].

The reaction of [PPN](3)[Re(7)C(CO)(21)] with Hg(2)(NO(3))(2).2H(2)O in dichloromethane formed the complex [PPN](4)[(Re(7)C(CO)(21)Hg)(2)] ([PPN](4)[1]), isolated in 60% yield. Analogous salts of [1](4-) with [PPh(4)](+) and [NEt(4)](+) were also prepared. The crystal structure of [PPN](4)[1] showed that two carbidoheptarhenate cores are linked by a dimercury(I) unit (d(Hg-Hg) = 2.610(4) A), with each individual mercury atom face-bridging. Oxidative cleavage of the Hg-Hg bond in [1](4-) was effected by 4-bromophenyl disulfide to form [Re(7)C(CO)(21)HgSC(6)H(4)Br](2-) ([4](2-)), by I(2) to form [Re(7)C(CO)(21)HgI](2-) ([5](2-)), and by Br(2) to form [Re(7)C(CO)(21)HgBr](2-) ([6](2-)). Oxidation of [1](4-) by ferrocenium ion (2 equiv) in the presence of tetramethylthiourea resulted in the derivative [Re(7)C(CO)(21)HgSC(NMe(2))(2)](-) ([7](-)). The molecular structure of [PPN][7] was determined by X-ray crystallography. This is the first example of a carbidoheptarhenate-mercury complex with a neutral ligand on mercury, and ligand exchange was demonstrated by displacement with triethylphosphine. Complex [7](-) can also be prepared by protonating [Re(7)C(CO)(21)HgO(2)CCH(3)](2-) in the presence of tetramethylthiourea. Cyclic voltammetry data to calibrate and compare the redox properties of compounds [1](4-) and [7](-) have been measured.

Indicators and Reagents↗
PubMed1995

The dental amalgam mercury controversy--inorganic mercury and the CNS; genetic linkage of mercury and antibiotic resistances in intestinal bacteria.

Mercury (Hg) vapor exposure from dental amalgam has been demonstrated to exceed the sum of all other exposure sources. Therefore the effects of inorganic Hg exposure upon cell function in the brain and in the intestinal bacteria have recently been examined. In rats we demonstrate that ADP-ribosylation of tubulin and actin brain proteins is markedly inhibited, and that ionic Hg can thus alter a neurochemical reaction involved with maintaining neuron membrane structure. In monkeys we show that Hg, specifically from amalgam, will enrich the intestinal flora with Hg-resistant bacterial species which in turn also become resistant to antibiotics.

Animals↗
PubMed1988

[Nucleotide sequences of mercury resistance determinants in bacteria isolated from mercury mines: detection of a family of recombinant mercury transposons in plasmids from Acinetobacter species].

Partial nucleotide sequences were determined for mer operons located on large and small plasmids previously described in Acinetobacter spp. isolated from different mercury mines of the USSR. Inspection of the sequences shows that: 1. All Acinetobacter mer operons studied belong to a family of transposons homologous to transposons found in clinical isolates. 2. The transposons located on the small plasmids originated by recombinations between the transposons from the large plasmids and Tn501, a transposon found in a Pseudomonas hospital strain isolated in Australia. The left arm of each hybrid transposon was donated by a transposon of a large Acinetobacter plasmid and the right arm - by the Tn501.

Acinetobacter↗
PubMed1995

Renal disposition of mercury in rats after intravenous injection of inorganic mercury and cysteine.

The disposition of mercury in the blood, kidneys and liver was evaluated and compared in rats 5 min, 1 h, and 24 h after the intravenous administration of a 0.25 mumol/kg dose of inorganic mercury or a 0.25 mumol/kg dose of inorganic mercury plus a 0.5 mumol/kg dose of cysteine to determine the possible role of extracellular cysteine and complexes of cysteine and inorganic mercury in the renal uptake and transport of inorganic mercury. More inorganic mercury was present in the blood of the rats injected with inorganic mercury alone than in the blood of the rats injected simultaneously with both the inorganic mercury and cysteine during the first hour after injection. In addition, significantly more mercury was in the plasma fraction of blood in the rats injected with both inorganic mercury and cysteine than in the rats injected with inorganic mercury alone. These findings indicate that much of the mercury injected with cysteine was in some form of a complex that allowed the mercury to be cleared from the blood more readily and prevented the mercury from entering readily into the cellular components of blood. The renal concentration of mercury was significantly greater in the rats injected with both inorganic mercury and cysteine than in the rats injected with inorganic mercury alone 1 h, but not 24 h, after injection. This increased renal accumulation of mercury during the initial hour after injection was due mainly to enhanced uptake and/or retention of mercury in the renal cortex, although some of the enhanced accumulation of mercury also occurred in the outer stripe of the outer medulla during the first hour after injection. These data indicate that coadministration of a nontoxic dose of inorganic mercury with a twofold higher amount (in moles) of cysteine increases significantly the clearance of mercury from the blood and increases the accumulation of inorganic mercury in the renal cortex and outer stripe of the outer medulla during the initial 1 h after injection. In conclusion, the data in this study are consistent with the hypothesis that complexes of inorganic mercury and cysteine in the blood and/or ultrafiltrate probably play a role in the renal uptake of some of the mercury in blood after exposure to mercuric compounds.

Animals↗
PubMed2000

Mercury distribution in the neonatal and adult cerebellum after mercury vapor exposure of pregnant squirrel monkeys.

The objectives of the study were (1) to map the detailed localization of mercury in the monkey cerebellum after mercury vapour exposure; (2) to investigate whether there is any difference in mercury distribution between neonatal and adult cerebellum after mercury vapor exposure; (3) to investigate the ability of mercury to accumulate in the cerebellum years after the end of exposure. Pregnant squirrel monkeys were exposed 5 days/week to mercury vapor at a concentration of 0.5 mg Hg/m(3) air 4 or 7 h/day or 1 mg Hg/m(3) air for 4 or 7 h/day. Mercury concentration in the offspring and maternal brains was examined by cold vapor, flameless atomic absorption spectrophotometry. Mercury distribution was examined by processing cerebellar sections for autometallographic (AMG) silver enhancement. Mercury concentration in the offspring cerebral occipital pole ranged between 0.20 and 0.70 microg Hg/g tissue, and in the maternal between 0.80 and 2.58 microg/Hg tissue in animals killed immediately after the end of exposure. AMG revealed that the external granule cell layer of offspring cerebellar tissue contained small amounts of mercury. The molecular layer contained mercury in some of the mercury-exposed monkeys. In the Purkinje cell layer, the Bergmann glial cells together with the Purkinje cells contained mercury. The granule cells and the Golgi cells contained small amounts of mercury. The astrocytes of the medullary layer, identified by immunohistochemistry, contained considerable amounts of mercury, but the cerebellar nuclei accumulated the highest amounts of mercury. No correlation was found between cellular accumulation and maturity of the brain; that is, the cellular localization of mercury did not differ between adult and neonatal brain, except for the amount of visualized mercury. This pattern corresponded well to the mercury concentrations found in the cerebral occipital pole. The differences found in mercury accumulation were instead considered to be dose-related. The results demonstrate that the distribution of mercury in the cerebellum after mercury vapor exposure is similar to the distribution pattern obtained after methyl mercury exposure and that mercury is trapped in the cerebellum over a long period of time.

Animals↗
PubMed1986

Sexual differences in the distribution and retention of organic and inorganic mercury in methyl mercury-treated rats.

At 56 days of age, male and female Long-Evans rats received 1 mumole of 203Hg-labeled methyl mercuric chloride per kilogram sc and total, organic, and inorganic mercury contents and concentrations in tissues were determined for up to 98 days postdosing. Whole body clearance of mercury was faster in females than in males, and females attained higher peak percentages of the methyl mercury dose in kidney and brain than did males. Females had significantly higher mean percentages of the mercury dose present in the kidney and brain as organic or total mercury and in brain as inorganic mercury than did males. Males had significantly higher mean percentages of the dose present as organic or total mercury in pelt and whole body than did females. When expressed on a concentration basis, the only significant sexual difference was in the higher average concentration of organic mercury in the kidneys of females. When expressed on a tissue content basis, significant male-female differences in the kinetics (sex X time interactions) of organic mercury retention were found in kidney, brain, skeletal muscle, pelt, and whole body. Significant sex X time interactions in the concentrations of organic mercury were found in kidney, skeletal muscle, and whole body. Kinetics of retention and concentration of inorganic Hg in the pelt differed significantly for males and females. Discordance in degree of statistical significance of differences in mercury contents and concentrations reflected in part differences in relative body composition of males and females. Integrated exposures of tissues of males and females to organic or inorganic mercury were determined by fitting multiexponential retention functions to retention data. Differences in integrated exposure were estimated by the female-to-male ratio of areas under retention curves. Reconstruction of whole body organic and inorganic mercury burdens from constituent tissues indicated that integrated exposures of males and females to inorganic mercury were equal but females had a lower integrated exposure to organic mercury. Integrated exposure of liver to either form of mercury was about equal in males and females. However, the integrated exposure of the brain of females to inorganic mercury was 2.19 times that of males suggesting a sexual difference in accumulation or retention of inorganic mercury in the nervous system. These sexual differences in distribution and retention of organic and inorganic mercury after methyl mercury exposure may underlie reported sexual differences in sensitivity to the toxic effects of methyl mercury.

Animals↗