Methylmercuric Chloride Research Articles

Methylmercuric chloride induces activation of neuronal stress circuitry and alters exploratory behavior in the mouse

Methylmercury (MeHg) is a well-known neurotoxicant, responsible for neurological and cognitive alterations. However, there is very little information available on the effects of MeHg administration on activation of murine neuronal pathways involved in the stress response, and whether this is altered as a function of repeated exposure to MeHg. Moreover, interactions between MeHg and other psychogenic and inflammatory stressors have yet to be fully determined. Acute i.p. exposure of male C57BL/6J mice to MeHg (2–8 mg/kg) dose-dependently attenuated exploratory behavior in the open field in the presence and absence of a novel object. In addition, increased numbers of c-Fos immunoreactive cells appeared in response to acute i.p. and i.c.v. MeHg within thalamic (anterior paraventricular nucleus of the thalamus (PVA)/posterior paraventricular nucleus of the thalamus (PV)), hypothalamic (paraventricular nucleus of the hypothalamus (PVN)), central amygdaloid nucleus (CeC), septal and hippocampal (dentate gyrus) nuclei, medial bed nucleus (BSTm) and the locus coeruleus (Lc). The increase in c-Fos positive cells in response to acute i.p. and i.c.v. MeHg did not appear to be influenced further by open field exposure. Repeated administration of MeHg led to an attenuation of most parameters of open field behavior altered by acute MeHg. However, increased c-Fos was significant in the CeC, Dg, supracapsular bed nucleus (BSTs), and Lc. Moreover, open field exposure after repeated treatments resulted in significant c-Fos responses in similar areas. Interestingly, 3 days after the final repeated MeHg dose (2 or 4 mg/kg) c-Fos increases to an immunogenic stressor (LPS) were not affected by MeHg pretreatment. These results demonstrate that systemic exposure to acute and repeated MeHg serves to activate the brain’s stress circuitry, and furthermore appears to engage normal neuronal habituation processes.

Changes in Biochemical Processes in Cerebellar Granule Cells of Mice Exposed To Methylmercury

At postnatal day 34, male and female C57BL/6J mice were exposed orally once a day to a total of five doses totaling 1.0 or 5.0 mg/kg of methylmercuric chloride or sterile deionized water in moistened rodent chow. Eleven days after the last dose cerebellar granule cells were acutely isolated to measure reactive oxygen species (ROS) levels and mitochondrial membrane potential using CM-H(2)DCFDA and TMRM dyes, respectively. For visualizing intracellular calcium ion distribution using transmission electron microscopy, mice were perfused 11 days after the last dose of methylmercury (MeHg) using the oxalate-pyroantimonate method. Cytosolic and mitochondrial protein fractions from acutely isolated granule cells were analyzed for cytochrome c content using Western blot analysis. Histochemistry (Fluoro-Jade dye) and immunohistochemistry (activated caspase 3) was performed on frozen serial cerebellar sections to label granule cell death and activation of caspase 3, respectively. Granule cells isolated from MeHg-treated mice showed elevated ROS levels and decreased mitochondrial membrane potential when compared to granule cells from control mice. Electron photomicrographs of MeHg-treated granule cells showed altered intracellular calcium ion homeostasis ([Ca(2+)](i)) when compared to control granule cells. However, in spite of these subcellular changes and moderate relocalization of cytochrome c into the cytosol, the concentrations of MeHg used in this study did not produce significant neuronal cell death/apoptosis at the time point examined, as evidenced by Fluoro-Jade and activated caspase 3 immunostaining, respectively. These results demonstrate that short-term in vivo exposure to total doses of 1.0 and 5.0 mg/kg MeHg through the most common exposure route (oral) can result in significant subcellular changes that are not accompanied by overt neuronal cell death.

Coordination Deficits Induced in Young Adult Mice Treated with Methylmercury

Male and female C57BL/6J mice starting at postnatal (P) day 34 were exposed orally to five divided doses totaling 1.0 or 5.0 mg/kg of methylmercury (MeHg; given as methylmercuric chloride) or sterile deionized water in moistened rodent chow. After a 5-day waiting period, control and MeHg-treated mice were subjected to a standard battery of behavior tests for balance and motor coordination. Latency to falling on the accelerating rota-rod was significantly decreased in 5.0 mg/kg MeHg-exposed mice when compared to control mice. In the open field, horizontal exploration with respect to total distance traveled during the first 5 min on the first test day was significantly reduced in 1.0 mg/kg MeHg-exposed mice when compared to control mice. Rearing activity was not affected by MeHg treatment. In the footprint analysis, angle of foot placement measured in 1.0 mg/kg MeHg-treated mice was significantly greater compared to control mice. Base stance and stride length were unaffected by MeHg treatment. On the vertical pole test, 10 mice from each treatment group fell off the pole during the time the pole was shifted from a horizontal position to a vertical position, whereas none of the control mice fell. These results indicate that short-term, low to moderate doses of MeHg in young adult mice can be detrimental to motor coordination and balance.

Assessment of Mercury Concentrations in Mouse Brain Using Different Routes of Administration and Different Tissue Preparations

ABSTRACTThe objective of this study was to determine the best method for preparing brain tissue for mercury analysis from mice exposed to methylmercury either through subcutaneous (SC) injection or through ingestion. C57BL/6 J mice at postnatal day 29 were exposed to 0.0 or 5.0 mg/kg methylmercuric chloride (MMC) given SC or through food containing MMC. Eighteen mice received vehicle (sodium bicarbonate; SC) and 18 additional mice received 5.0 mg/kg MMC (SC). Whole brain tissue was prepared using one of four tissue preparation methods: rapid freezing, saline perfusion, 4% paraformaldehyde perfusion fixation, or 4% paraformaldehyde immersion fixation. Brains from vehicle-treated mice exhibited minimal levels of mercury (0.0007 to 0.0018 ppm) in all preparation methods. Mercury content in rapidly frozen control brains differed statistically from immersion-fixed control brain tissue. There was no significant difference in mercury content from mice given 5.0 mg/kg MMC (SC) in all preparation methods (0.2660 to 0.3650 ppm). Additional mice were divided into groups of six mice each: single oral dose of 5.0 mg/kg MMC; total oral dose of 5.0 mg/kg MMC divided into five doses; and vehicle only. Forebrain (0.3243 ppm) and hindbrain (0.1908 ppm) mercury content in MMC-treated mice given multiple doses was 10 times higher than in brain tissue from mice given a single 5.0 mg/kg dose. Brain mercury content following administration of 5.0 mg/kg MMC via the oral route (0.5354 ppm) differed statistically from the SC route (0.3430 ppm). In conclusion, different tissue preparation methods do not significantly affect brain mercury content, but route of administration and dosing regimen can influence total brain mercury content.

Selective Effect of Mercury on Th2-Type Cytokine Production in Humans

Mercury induces autoimmune disease and increases IL-4 production and IgE levels in certain rodent strains. The object of this study was to determine if mercury was capable of inducing Th2 cytokine production in human leucocytes. Human peripheral blood mononuclear cells (PBMC) were incubated with PMA/ionomycin or Con A in the presence or absence of methyl mercury (CH3Hg) or mercuric chloride (HgCl2). IL-4 and gamma-IFN were measured by ELISA. RESULTS: IL-4 production significantly increased at low concentrations of CH3Hg (0.5 uM, p < 0.01), while gamma-IFN production was suppressed starting at CH3Hg 2 uM (p = 0.004). Inorganic mercury (HgCl2) increased IL-4 only at concentrations 10–20 times higher than CH3Hg. These findings suggest a mechanism by which mercury could trigger or potentiate TH2 cytokine production in humans.

Cell death and cytotoxic effects in YAC-1 lymphoma cells following exposure to various forms of mercury

The effects of 1 min–4 h exposures to four Hg compounds (mercuric chloride [HgCl 2], methyl mercuric chloride [CH 3HgCl], p-chloromercuribenzoate [p-CMB] and thimerosal [TMS; ethylmercurithiosalicylate]) on cell death, microtubules, actin, CD3 receptor expression, protein tyrosine phosphorylation (PTyr-P) and intracellular calcium ([Ca 2+] i) levels were investigated in YAC-1 lympoma cells using flow cytometry. YOPRO-1 (YP) and propidium iodide (PI) dye uptake indicated all forms of Hg tested were toxic at concentrations ranging from 25.8–48.4 μM, with two distinct patterns of effects. Early apoptosis was prolonged for CH 3HgCl- and TMS-treated cells, with more than 50% remaining YP +/PI − after 4 h. Both CH 3HgCl and TMS induced complete loss of β-tubulin fluorescence, indicative of microtubule depolymerization and inhibition of tubulin synthesis and/or β-tubulin degradation, while F-actin fluorescence diminished to a lesser degree and only after loss β-tubulin. CH 3HgCl and TMS induced an almost immediate two-fold increase in CD3 fluorescence, with levels returning to baseline within minutes. With continued exposure, CD3 fluorescence was reduced to approximately 50% of baseline values. Both compounds also increased PTyr-P two- to three-fold immediately, with levels returning to baseline at 4 h. Similarly, two- to three-fold increases in [Ca 2+] i were noted after 1 min exposure. [Ca 2+] i increased progressively, reaching levels five- to eight-fold greater than control values. In contrast, dye uptake was delayed with HgCl 2 and p-CMB, although cell death proceeded rapidly, with almost all non-viable cells being late apoptotic (YP +/PI +) by 4 h. p-CMB produced early reductions in F-actin, and after 4 h, complete loss of F-actin with only partial reduction of total β-tubulin was seen with both p-CMB and HgCl 2. HgCl 2 reduced CD3 expression and PTyr-P slightly within minutes, while p-CMB produced similar effects on CD3 only at 4 h, at which time PTyr-P was increased two- to three-fold. Both compounds increased [Ca 2+] i within minutes, though levels remained under twice the baseline concentration after 15 min exposure. With continued exposure, [Ca 2+] i increased to levels two- to five-fold greater than control values. These findings indicate the two groups of Hg compounds may induce cell death by distinct pathways, reflecting interactions with different cellular targets leading to cell death.

Crystallization and X-ray diffraction analysis of 6-aminohexanoate-dimer hydrolase fromArthrobactersp. KI72

To investigate the structure-function relationship between 6-aminohexanoate-dimer hydrolase (EII) from Arthrobacter sp. and a cryptic protein (EII') which shows 88% sequence identity to EII, a hybrid protein (named Hyb-24) of EII and EII' was overexpressed, purified and crystallized using the sitting-drop vapour-diffusion method with ammonium sulfate as a precipitant in MES buffer pH 6.5. The crystal belongs to space group P3(1)21 or P3(2)21, with unit-cell parameters a = b = 96.37, c = 113.09 A. Diffraction data were collected from native and methylmercuric chloride derivative crystals to resolutions of 1.75 and 1.80 A, respectively.

Salicylic acid triggers genotoxic adaptation to methyl mercuric chloride and ethyl methane sulfonate, but not to maleic hydrazide in root meristem cells of Allium cepa L.

Salicylic acid (SA), 0.01 mM, a signalling phytohormone, was tested for induction of adaptive response against genotoxicity of methyl mercuric chloride (MMCl), 0.013 mM; ethylmethane sulfonate (EMS), 2.5 mM, or maleic hydrazide (MH), 5 mM, in root meristem cells of Allium cepa. Induction of adaptive response to EMS by hydrogen peroxide (H 2O 2), 1 mM, and yet another secondary signal molecule was tested for comparison. Assessed by the incidence of mitoses with spindle and/or chromosome aberration and micronucleus, the findings provided evidence that SA-conditioning triggered adaptive response against the genotoxic-challenges of MMCl and EMS, but failed to do so against MH. H 2O 2, which is known to induce adaptive response to MMCl and MH, failed to induce the same against EMS in the present study. The findings pointed to the possible role of signal transduction in the SA-induced adaptive response to genotoxic stress that perhaps ruled out an involvement of H 2O 2.

Maximum limits of organic and inorganic mercury in fish feed

The relatively high levels of mercury found in fish feeds might form a fish health and food safety risk. The present study aims to establish sublethal toxic threshold levels in fish and assess feed-fillet transfer of dietary mercury. Atlantic salmon (Salmo salar L.) parr were fed for 4 months on fish meal-based diets supplemented with mercuric chloride (0, 0.1, 1, 10 or 100 mg Hg kg−1 dry weight (DW)) or methylmercuric chloride (0, 0.1, 0.5, 5 or 10 mg MeHg kg−1 DW). At the end of the experiment, dietary inorganic mercury mainly accumulated in intestine (80% of body burden) and assimilation was low (6%). In contrast, methylmercury readily accumulated in internal organs and muscle (80% of body burden) and had a relatively high assimilation (23%). Highest accumulation of dietary inorganic mercury was observed in the gut and kidney. Fish fed 10 mg Hg kg−1 had an early (after 2 months) significant increase in renal metallothionein (MT) level and intestinal cell proliferation, followed by intestinal pathological conditions after 4 months of exposure. At 100 mg Hg kg−1, intestinal and renal function were reduced as seen from the significantly reduced protein and glycogen digestibility and increased plasma creatinine levels. For dietary methylmercury (MeHg), highest accumulation was found in blood and muscle. Intestinal cell proliferation and liver MT significantly increased at 5 mg MeHg kg−1 after 2 months of exposure. At the end of the experiment, blood haematology was significantly affected in fish fed 5 mg MeHg kg−1 and these fish exceeded the current food safety limit for mercury. Tissue MT induction and intestinal cell proliferation appeared to be useful and quantifiable early indicators of toxic mercury exposures. Based on the absence of induction of these early biological markers such as MT and cell proliferation, nonobserved effect levels (NOELs) could be set to 0.5 mg Hg kg−1 for dietary methylmercury and 1 mg Hg kg−1 for inorganic mercury. Lowest observed effect levels (LOELs) levels could be set to 5 mg kg−1 for methylmercury and 10 mg Hg kg−1 for inorganic mercury.

Genetic variation of resistance to mercury poisoning in steelhead (Oncorhynchus mykiss) alevins.

Newly hatched steelhead alevins were obtained from the factorial breeding of 24 male and 10 female steelhead trout, Oncorhynchus mykiss. Each set of offspring were in a separate cell. They were tested for resistance to intoxication by methylmercuric chloride (CH3HgCl) in water at a nearly constant mercury concentration of 8 microg l(-1). High mortality (81% of the tested alevins) occurred within 2 weeks. Resistance to intoxication, as measured by the time to death, as well as by the survival rate, shared high paternal and maternal variation with negligible interaction. Heritability of time to death was 0.59 +/- 0.17; heritability of survival (all-or-none trait) was lower (0.26 +/- 0.09). Mercury in dead alevins increased with time to death, exhibiting a large environmental variation and (comparatively) negligible genetic influence. At the end of the bioassay, the mercury content in survivors varied widely (3-21 microg g(-1) wet weight). The content was greater than, but correlated with that of dead alevins from the same cells, and it showed little relation with survival rate. Thus, it seems that resistance to poisoning implies a tolerance to high levels of mercury rather than a limitation of its accumulation.

Persistence and prevention of aluminium- and paraquat-induced adaptive response to methyl mercuric chloride in plant cells in vivo

Induction and persistence of adaptive response by aluminium (Al), 1 or 10 μM, and paraquat (PQ), 5 or 10 μM, against genotoxicity of methyl mercuric chloride (MMCl), 1.26 μM, a standard environmental genotoxin, was investigated in root meristem cells of Allium cepa. Subsequently, three metabolic inhibitors, namely, 3-aminobezamide (3-AB, 10 or 100 μM), an inhibitor of poly(ADP-ribose) polymerase (PARP) implicated in DNA repair and/or apoptosis, cycloheximide (CH, 0.1 or 1 μM), an inhibitor of protein synthesis, and buthionine sulfoximine (BSO, 100 μM or 1 mM), an inhibitor of glutathione synthesis were tested for their ability to prevent the adaptive response induced by conditioning doses of Al, 10 or 100 μM; and PQ, 5 or 100 μM, against MMCl-challenge, 1.26 or 100 μM, in root meristems of A. cepa or embryonic shoots of Hordeum vulgare, respectively. The findings demonstrated that once triggered, the Al- or PQ-adaptive response to MMCl could persist for at least 48 h in root meristems of A. cepa. Furthermore, the adaptive response could effectively be prevented by 3-AB, to a lesser degree by CH, and the least by BSO, suggesting primarily the involvement of PARP and implicating DNA repair in the underlying mechanisms of adaptive response in plant cells in vivo.

Relationship between semen parameters and mercury concentrations in blood and in seminal fluid from subfertile males in Hong Kong

Relationship between semen parameters and mercury concentrations in blood and in seminal fluid from subfertile males in Hong Kong

Mercury-induced apoptosis in human lymphocytes: caspase activation is linked to redox status.

There is growing evidence that heavy metals, in general, and mercurial compounds, in particular, are toxic to the human immune system. We have previously shown that methyl mercuric chloride (MeHgCl) is a potent human T-cell apoptogen; moreover, mitochondria appear to be a target organelle for the induction of cell death. The objective of this study was to determine the impact of MeHgCl on mitochondrial function in lymphocytes in terms of modulating reactive oxygen species (ROS) generation, thiol status, and caspase activation. Using the fluorescent probe, 3,3'-dihexyloxacarbocyanine, we demonstrated that exposure to MeHgCl for 1 h resulted in a profound decrease in the mitochondrial transmembrane potential. We next observed the release of cytochrome c from mitochondria into the cytosol; significant translocation was noted between 4 and 8 h following treatment with mercury. ROS generation was monitored by following the conversion of dihydroethidium to the fluorescent product, ethidium. Kinetic analysis indicated that ROS generation was maximal after 16 h of exposure to MeHgCl. The toxicant also depleted the thiol reserves of the cell; glutathione levels were depleted in a dose-dependent fashion reaching minimal levels at 16 h. Real-time RT-PCR analysis demonstrated a significant reduction in both glutathione S-transferase and glutathione peroxidase gene expression in mercury-treated cells. Finally, after 16 h of treatment with MeHgCl, we observed activation of caspase-8, -9, and -3 along with increased expression of caspase-8 and -9. We propose that the target organelle for MeHgCl is the mitochondrion and that induction of oxidative stress is critical to activation of death-signaling pathways. Additonally, mercury acts as a genotoxin significantly altering the expression of genes that affect cell survival and apoptosis.

PROLONGATION OF HUMAN NEUTROPHIL SURVIVAL BY LOW-LEVEL MERCURY VIA INHIBITION OF SPONTANEOUS APOPTOSIS

Low levels of organic and inorganic mercury compounds have been reported previously to induce cell death by apoptosis in human peripheral blood mononuclear cells (MNC), but little is known about their potential effects on the viability and death of polymorphonuclear neutrophils (PMN). In contrast to MNC, PMN are known to undergo readily spontaneous apoptosis both in vivo and in vitro. Therefore, it was hypothesized that PMN may differ from MNC in their reactions to low mercury levels. The effects of methylmercuric chloride (MeHgCl) and mercuric chloride (HgCl 2 ) were evaluated in concentration- response and time-course studies on human PMN viability and on their modes of cell death after in vitro incubation at 37°C. Cell death by apoptosis or necrosis was assessed by annexin V-fluorescein isothiocyanate binding to externalized phosphatidylserine in conjunction with propidium iodide, and flow cytometry analysis. Morphologic counting of pyknotic nuclei and the fluorescence properties of the DNA-binding dye Hoechst 33342 in combination with propidium iodide were used to further confirm apoptotic cell death and to characterize the sequence of Hg-induced cell death. Results show that low concentrations of MeHgCl (1-7.5 µ M ) that were cytotoxic to MNC actually inhibited PMN spontaneous apoptosis. Low-level HgCl 2 reproduced the anti-apoptotic effects of MeHgCl on PMN, but to a lower extent. Higher concentrations of MeHgCl and HgCl 2 were necro-genic to PMN, but MeHgCl was about an order of magnitude more toxic, and discrete differences were observed in the modalities of cell death induced by both species. These data reveal for the first time that (1) low levels of organic and inorganic mercury species protect human PMN from cell death via inhibition of spontaneous apoptosis, and (2) PMN are more resistant than MNC to mercury-induced cytotoxicity. Since delayed apoptosis and increased resistance to toxicant-induced cell death may lead to excessive accumulation of senescent PMN, evidence indicates that findings of this study may have implications for mercury-induced autoimmunity and inflammation.

Cytotoxicity of ingredients of various dental materials and related compounds in L2- and A549 cells.

Various ingredients of dental materials and related compounds were tested for cytotoxicity in two alveolar epithelial cell lines (L2 and A549 cells). Release of lactate dehydrogenase (LDH) from cells was measured after incubation with the test substances for time intervals up to 48 h and expressed as percentage of total LDH content of lysed cells. Furthermore, the glutathione content of cells was determined in the nonmalignant L2 cells. Additionally, cell viability was assessed by microscopic examination. The highest cytotoxicity was observed with mercury compounds (methylmercuric chloride and mercury dichloride) in the range of 5-20 micromol/l. The composite components 2-hydroxyethylmethacrylate (HEMA) and triethleneglycoldimethacrylate (TEGDMA) showed time- and concentration-dependent effects of cytotoxicity at high concentrations (about 1-5 mmol/l). A time dependence for GSH decrease was mainly found for the composite components up to 12 h of cellular exposure. L2 cells were more sensitive to both mercury and composite compounds than A549 cells. Gold compounds (sodiumaurothiomalate and gold particles < 1.5 microm) did not produce any sign of toxic reactions. A time-dependent increased toxicity in pulmonary cell lines was found for the composite components HEMA and TEGDMA, but not for mercury and gold compounds.

Impairment of spermatogenesis in rats by methylmercury: involvement of stage- and cell- specific germ cell apoptosis

Methylmercury has been shown to affect the male reproductive organs. However, the specific mode of impairment of spermatogenesis during methylmercury exposure remains unknown. In this study, we characterized the induction of germ cell apoptosis and reproductive toxicity in Wistar male rats that had been exposed to methylmercuric chloride (MMC). Subcutaneous injection of MMC at a dose of 10 mg/kg per day for 8 days resulted in a 28% testicular weight loss at 14 days after the first injection. In addition, the ventral and dorso-lateral prostatic lobes showed a 65 and 52% decrease, respectively, at 14 days, although no effects were observed in the epididymis. Sperm production also was suppressed by the administration of MMC. After exposure to MMC, fragmentation of testicular DNA was found to be increased at 3 days after the first injection, with a 20-fold increase over control levels at 14 days. In situ detection of apoptosis by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) staining revealed that spermatocytes and spermatids at stages VII–VIII and IX–XI, respectively, steps which are considered to be highly sensitive to testosterone, were the major cell types affected. Consequently, a marked cell loss in elongated spermatids at stages XII–XIV and I was observed at 14 days. In addition, plasma testosterone levels were reduced at 6 days after exposure to MMC, and remained at approximately 20% of control levels during the 14-day observation period. Our results suggest that methylmercury impairs spermatogenesis by germ cell deletion via cell- and stage- specific apoptosis.

Screening of organomercurial-volatilizing bacteria in the mercury-polluted sediments and seawater of Minamata Bay in Japan

The special organomercurial-volatilizing bacteria found in the seawater and sediments of Minamata Bay were screened to develop a method for the removal of mercury to produce clean products. A total of 104 mercury-resistant bacteria that could grow on an agar plate containing 40 µg/ml of HgCl2 were isolated from Minamata Bay. Almost all strains were Gram-negative rods. Eight of the 104 strains volatilized only mercuric chloride, while 21 of the 104 strains volatilized all of the organomercurials used in this study. Four strains isolated from the seawater were most resistant to methyl mercuric chloride, ethyl mercuric chloride, thimerosal, and fluorescein mercuric acetate as well as HgCl2, and volatilized all of the organomercurials used in this study. We were able to screen the most mercury-resistant bacteria and organomercurial-volatilizing bacteria, which contained an organomercurial lyase with a particularly wide range of substrate specificity.

Selenite or selenomethionine interaction with methylmercury on uptake and toxicity showing a weak selenite protection: studies on cultured K-562 cells.

Selenium and methylmercuric chloride (MMC) interactions regarding cellular uptake and selenium protection on MMC toxicity have been studied. Human K-562 cells were pretreated or simultaneously treated with either selenite (5 or 50 microM) or selenomethionine (10 or 50 microM) together with (3.5 or 5 microM) MMC. Cells simultaneously treated with selenite or selenomethionine and 3.5 microM MMC showed a decreased mercury concentration with increased selenium dose especially seen in the selenite combinations. The simultaneous selenite and MMC 3.5 microM combinations showed growth curves with an increasing number of viable cells with increased selenite dose. All combinations with 5 microM MMC were toxic to the cells. Interactions between selenite or selenomethionine and MMC regarding cellular uptake of mercury and selenium were observed and indications of selenite protection against MMC toxicity in human K-562 cells were noticed.

Mercury volatilization by the most mercury-resistant bacteria from the seawater of Minamata Bay in various physiological conditions

The volatilization of mercuric chloride (HgCl2) and methyl mercuric chloride (CH3HgCl) by the 45 strains (35 Pseudoalteromonas sp., 2 Vibrio sp., 1 Aeromonas sp., and 7 unclassified) of the most mercury-resistant bacteria from Minamata Bay seawater was examined in various physiological conditions. The bacteria could grow and volatilize HgCl2 in the liquid medium containing 1–10% NaCl. Two Pseudoalteromonas strains could grow and volatilize HgCl2 at pH levels ranging from 5.0 to 10.0. The resting cells of 43 strains could volatilize HgCl2 at concentrations ranging from 30 to 68% after 1-h incubation at 30 °C. The resting cells of 41 strains could volatilize CH3HgCl at concentrations ranging from 13 to 88% after 1-h incubation at 30 °C. Ninety-two percent of mercury was removed from the phosphate buffer containing 0.1 μg/ml by a resting cell of Pseudoalteromonas strain H-4 after 30-min incubation at 30 °C. We were able to screen the special bacteria, which could volatilize mercury compounds at a high rate in various physiological conditions, for the purpose of developing mercury removal methods using bacteria.

Dynamics of mercury in blood and feathers of great skuas

AbstractMercury dynamics in the blood and feathers of captive great skuas, Catharacta skua, were monitored over 56 weeks. Prior to the onset of molt, mercury intake was solely from their maintenance ration of sprats, Sprattus sprattus. For the first half of molt, in addition to mercury intake from sprats, birds were fed different doses of methylmercuric chloride weekly for 20 weeks. During the second half of molt, dosing was stopped and mercury intake was solely from sprats. Blood was sampled throughout the study and feather growth was monitored. Prior to the onset of molt, mercury concentrations increased over the first 51 to 71 d and appeared to level off after this period. Repeated dosing models based on mammalian pharmacokinetics were, in general, too simplistic to be applicable to the birds in the study. During molt, the elimination of mercury from the blood is probably best described by a three‐compartment model. Mercury concentrations in feathers were significantly correlated with those in blood at the time of their growth, suggesting that blood and feathers reflect mercury intake over the same time period. Individuals varied in their ability to excrete ingested mercury into the feathers.