Accumulation Of Inorganic Mercury Research Articles

Understanding reduced inorganic mercury accumulation in rice following selenium application: Selenium application routes, speciation and doses

Selenium (Se) has recently been demonstrated to reduce inorganic mercury (IHg) accumulation in rice plants, while its mechanism is far from clear. Here, we aimed at exploring the potential effects of Se application routes (soil or foliar application with Se), speciation (selenite and selenate), and doses on IHg-Se antagonistic interactions in soil-rice systems. Results of our pot experiments indicated that soil application but not foliar application could evidently reduce tissue IHg concentrations (root: 0–48%, straw: 15–58%, and brown rice: 26–74%), although both application routes resulted in comparable Se accumulation in aboveground tissues. Meanwhile, IHg distribution in root generally increased with amended Se doses in soil, suggesting antagonistic interactions between IHg and Se in root. These results provided initial evidence that IHg-Se interactions in the rhizosphere (i.e., soil or rice root), instead of those in the aboveground tissues, could probably be more responsible for the reduced IHg bioaccumulation following Se application. Furthermore, Se dose rather than Se speciation was found to be more important in controlling IHg accumulation in rice. Our findings regarding the importance of IHg-Se interactions in the rhizosphere, together with the systematic investigation of key factors affecting IHg-Se antagonism and IHg bioaccumulation, advance our understanding of Hg dynamics in soil-rice systems.

Inorganic mercury accumulation in brain following waterborne exposure elicits a deficit on the number of brain cells and impairs swimming behavior in fish (white seabream—Diplodus sargus)

The current study contributes to fill the knowledge gap on the neurotoxicity of inorganic mercury (iHg) in fish through the implementation of a combined evaluation of brain morphometric alterations (volume and total number of neurons plus glial cells in specific regions of the brain) and swimming behavior (endpoints related with the motor activity and mood/anxiety-like status). White seabream (Diplodus sargus) was exposed to realistic levels of iHg in water (2μgL−1) during 7 (E7) and 14 days (E14). After that, fish were allowed to recover for 28 days (PE28) in order to evaluate brain regeneration and reversibility of behavioral syndromes. A significant reduction in the number of cells in hypothalamus, optic tectum and cerebellum was found at E7, accompanied by relevant changes on swimming behavior. Moreover, the decrease in the number of neurons and glia in the molecular layer of the cerebellum was followed by a contraction of its volume. This is the first time that a deficit on the number of cells is reported in fish brain after iHg exposure. Interestingly, a recovery of hypothalamus and cerebellum occurred at E14, as evidenced by the identical number of cells found in exposed and control fish, and volume of cerebellum, which might be associated with an adaptive phenomenon. After 28 days post-exposure, the optic tectum continued to show a decrease in the number of cells, pointing out a higher vulnerability of this region. These morphometric alterations coincided with numerous changes on swimming behavior, related both with fish motor function and mood/anxiety-like status. Overall, current data pointed out the iHg potential to induce brain morphometric alterations, emphasizing a long-lasting neurobehavioral hazard.

Accumulation properties of inorganic mercury and organic mercury in the red-crowned crane Grus japonensis in east Hokkaido, Japan

The red-crowned (Japanese) crane Grus japonensis is native to east Hokkaido, Japan, in contrast to the East Asia mainland. Previously, we reported that red-crowned cranes in Hokkaido were highly contaminated with mercury in the 1990s and that the contamination rapidly decreased to a moderate level in the 2000s. In the present study, we determined levels of organic mercury (O–Hg) in the liver and kidney of cranes in east Hokkaido in comparison with levels of total mercury (T–Hg). T–Hg levels in the kidneys were higher than those in the livers in adults but not in subadults and juveniles; however, the reverse was the case for O–Hg even for adults. The ratio of O–Hg to T–Hg in both the liver and kidney decreased as T–Hg increased in the three developmental stages. While the ratios of O–Hg to T–Hg in the liver and kidney of adults were significantly lower than those of juveniles, the ratios were similar for adults and juveniles in a lower range of T–Hg. The ratio of selenium (Se) to T–Hg decreased as T–Hg increased in both the liver and kidney, irrespective of stages. Mercury burdens in feathers were about 59% and 67% of the total body burdens for juveniles and adults, respectively. Furthermore, ratios of carbon and nitrogen stable isotopes to T–Hg varied greatly, with no relation to mercury level in the liver. The results suggest slow accumulation of inorganic mercury in the kidney of red-crowned cranes in east Hokkaido, Japan.

Selenium modulates mercury uptake and distribution in rice (Oryza sativa L.), in correlation with mercury species and exposure level.

Rice cultured in Hg- and/or Se-contaminated fields is an important food source of human Hg/Se intake. There are elevated Hg and Se levels in the soil of the Wanshan District, Guizhou Province. Here we attempted to explore how a Hg antagonist, Se, modulates the absorption and accumulation of inorganic mercury (IHg) and methylmercury (MeHg) in rice. The effects of Se on the content and transportation of Hg in hydroponic and soil cultured rice plants were examined. The results show that IHg mainly accumulated in the rice roots, but some also accumulated in the rice grain. In comparison to IHg, MeHg can be concentrated in the rice grain, and the proportion of MeHg in the rice grain may account for above 40% of the total Hg. Se can protect against Hg phytotoxicity in rice and inhibit IHg accumulation in rice tissues, but was not remarkable for MeHg at a low dosage exposure level in this study. These discrepancies imply mechanistic differences between IHg and MeHg absorption and accumulation in rice. This study illustrates that Se plays an important role in modulating Hg uptake, transportation and accumulation in rice. Therefore, Se is considered to be a naturally existing element that effectively reduces Hg accumulation in rice, which may have significant implications for food safety.

Differential Sex, Morphotype and Tissue Accumulation of Mercury in the Crab Carcinus maenas

Carcinus maenas is an invasive species of recognised economical and ecological importance in which mercury accumulation could be a pathway for bioamplification through food webs. Little information is available about differential accumulation between crab sexes and morphotypes. Taking this in mind, a set of different industrial discharge scenarios were investigated in 96-h laboratory experiments for assessing the accumulation of inorganic mercury from contaminated seawater into the tissues of C. maenas. Three groups of crabs (green males, green and red females) where exposed to 5, 50 and 250 μg Hg L−1. Differences among sexes, morphotypes and tissues were detected, depending on the mercury concentration. The muscle did not show differential accumulation between sexes or morphotypes. For mercury-exposed crabs, the contaminant was accumulated preferably in the gills (more than 75%) while, in control experiments, it was in the internal organs, muscle and hepatopancreas, and gills corresponded to less than 31% of the total mercury quantified. The different tissue contamination seems dependent on the major pathway of exposure, diet or water. Mercury accumulation by the crab was a rapid process and could represent a risk for the environment only after 96 h. In a scenario of a discharge point of 250 μg L−1, all tissues of crabs exposed would attain a very close, or even exceed the threshold concentration value for human consumption (0.5 mg kg−1).

Induction by mercury compounds of metallothioneins in mouse tissues: inorganic mercury accumulation is not a dominant factor for metallothionein induction in the liver

Among the naturally occurring three mercury species, metallic mercury (Hg(0)), inorganic mercury (Hg(II)) and methylmercury (MeHg), Hg(II) is well documented to induce metallothionein (MT) in tissues of injected animals. Although Hg(0) and MeHg are considered to be inert in terms of directly inducing MT, MT can be induced by them after in vivo conversion to Hg(II) in an animal body. In the present study we examined accumulations of inorganic mercury and MT inductions in mouse tissues (brain, liver and kidney) up to 72 hr after treatment by one of three mercury compounds of sub-lethal doses. Exposure to mercury compounds caused significant mercury accumulations in mouse tissues examined, except for the Hg(II)-treated mouse brain. Although MeHg caused the highest total mercury accumulation in all tissues among mercury compounds, the rates of inorganic mercury were less than 10% through the experimental period. MT inductions that depended on the inorganic mercury accumulation were observed in kidney and brain. However, MT induction in the liver could not be accounted for by the inorganic mercury accumulation, but by plasma IL6 levels, marked elevation of which was observed in Hg(II) or MeHg-treated mouse. The present study demonstrated that MT was induced in mouse tissues after each of three mercury compounds, Hg(0), Hg(II) and MeHg, but the induction processes were different among tissues. The induction would occur directly through accumulation of inorganic mercury in brain and kidney, whereas the hepatic MT might be induced secondarily through mercury-induced elevation in the plasma cytokines, rather than through mercury accumulation in the tissue.

Multidrug Efflux Transporters Limit Accumulation of Inorganic, but Not Organic, Mercury in Sea Urchin Embryos

Mercuric compounds are persistent global pollutants that accumulate in marine organisms and in humans who consume them. While the chemical cycles and speciation of mercury in the oceans are relatively well described, the cellular mechanisms that govern which forms of mercury accumulate in cells and why they persist are less understood. In this study we examined the role of multidrug efflux transport in the differential accumulation of inorganic (HgCl(2)) and organic (CH(3)HgCl) mercury in sea urchin (Strongylocentrotus purpuratus) embryos. We found that inhibition of MRP/ABCC-type transporters increases intracellular accumulation of inorganic mercury but had no effect on accumulation of organic mercury. Similarly, pharmacological inhibition of metal conjugating enzymes by ligands GST/GSH significantly increases this antimitotic potency of inorganic mercury, but had no effect on the potency of organic mercury. Our results point to MRP-mediated elimination of inorganic mercury conjugates as a cellular basis for differences in the accumulation and potency of the two major forms of mercury found in marine environments.

Laboratory studies on the accumulation of inorganic mercury and methylmercury by the mussel (Mytilus galloprovincialis Lam) in relation to the presence of sediment

A comparative study on the accumulation of inorganic mercury and methylmercury by the mussel Mytilus galloprovincialis was based on nine days of exposure to 25 µg L−1 HgCl2 or to 2.5 µg L−1 methylmercury in laboratory microcosms. Mercury (Hg) content was evaluated in the gills, digestive gland, and mantle. A higher accumulation occurred in the gills than in other tissues. The effect of the sediment on the bioaccumulation of the Hg species was evaluated. The results showed that the sediment accumulated the inorganic Hg more efficiently than the methylmercury. In both cases, the bioaccumulation in the tissues was reduced. The observed differences emphasized the need for caution when field results are compared with the results of laboratory experiments. The fate of either inorganic or organic Hg was depicted considering the absolute total amount given and the amount found in all the matrices (organism, sediment, and seawater).

Cystine alters the renal and hepatic disposition of inorganic mercury and plasma thiol status

In the present study, we determined whether cystine can inhibit, under certain conditions, the renal tubular uptake of inorganic mercury in vivo. We co-injected (i.v.) cystine with a non-toxic dose of mercuric chloride to rats and then studied the disposition of inorganic mercury during the next 24 h. We also determined if pretreatment with cystine influences the disposition of administered inorganic mercury. Moreover, plasma thiol status was examined after the intravenous administration of cystine with or without mercuric chloride. During the initial hour after co-injection, the renal tubular uptake of mercuric ions was diminished significantly relative to that in control rats. The inhibitory effects of cystine were evident in both the renal cortex and outer stripe of the outer medulla. In contrast, the renal accumulation of mercury increased significantly between the 1st and 12th hour after co-treatment. Urinary excretion and fecal excretion of mercury were greatly elevated in the rats co-treated with cystine and mercuric chloride. Thus, when cystine and mercury are administered simultaneously, cystine can serve as an inhibitor of the renal tubular uptake of mercury during the initial hour after co-treatment. In rats pretreated with cystine, the renal uptake of inorganic mercury was enhanced significantly relative to that in rats not pretreated with cystine. This enhanced accumulation of inorganic mercury correlated with the increased circulating concentrations of the reduced cysteine and glutathione. Additionally, the present findings indicate that thiol status is an important determinant of renal and hepatic disposition, and urinary and fecal excretion, of inorganic mercury.

Accumulation of Inorganic Mercury in Hair of Rats Exposed to Methylmercury or Mercuric Chloride

The concentration of methylmercury (MeHg) in human hair is an excellent marker for its exposure, since a portion of MeHg is taken up from the blood circulation to the hair protein in a dose-dependent manner. However, a small portion of the mercury in human hair is found in the inorganic form, though the mechanism of its occurrence is not well established. Here, we examined the hair uptake of inorganic mercury in the rat. Male Wistar rats were exposed to MeHg (1 microg Hg/ml) or HgCl(2) (20 microg Hg/ml) for 84 days through drinking water. The hair, grown from 49 to 84 days, was collected from the MeHg-exposed rats, and the hair samples showed 54.5 microg/g hair of the total mercury concentration, 6.1% of which was in the inorganic form. The inorganic mercury in the plasma (0.022 microg/ml), which would probably be formed from MeHg in rat tissues, accounted for as high as 29% of the total mercury (0.076 microg/ml). The hair uptake rate of inorganic mercury estimated from the hair/plasma ratio was about 1/6 lower than that of MeHg. On the other hand, the total hair mercury level in the HgCl(2)-exposed group at the same time point was 2.86 microg/g, with the inorganic portion being as high as 62%. These findings suggest that the inorganic mercury is also taken up by rat hair from the blood circulation, as is the MeHg, irrespective of the consequences of the biotransformation of MeHg or exposure to inorganic mercury itself. Accordingly, a selective quantification of inorganic mercury in human hair may be useful in detecting inorganic mercury exposure.

Interaction between cadmium and mercury accumulation by Daphnia magna Straus (Crustacea, Branchiopoda)

The objective of this study was to evaluate the effects and interactions of various factors on the simultaneous accumulation of cadmium and mercury contaminants. Two chemical forms of mercury (HgCl2 and CH3HgCl) were used in conjunction with inorganic cadmium (as CdCl2). The effects of direct and trophic modes of accumulation were investigated. Daphnids (Daphnia magna) were exposed for 5 days to cadmium (CdCl2) and mercury (HgCl2 or CH3HgCl) in different combinations and concentrations. Exposure was provided either directly via water, or indirectly by providing contaminated algae (Chlorella vulgaris) as a food source. As it is often the case for aquatic organisms, methylmercury was found to be the form of mercury most efficiently accumulated by D. magna. The way of exposure to mercury was also a determinant, with the results depending on the chemical form used. Therefore, even though the preferential way of inorganic mercury accumulation was through the water, the preferential way for D. magna contaminated with methylmercury was through contaminated algae. However, accumulation of Cadmium was not significantly affected by the exposure way. Both cadmium and mercury were able to inhibit each other accumulation. Even though HgCl2 was normally the mercury form that most efficiently inhibited cadmium accumulation, inhibition of CH3HgCl was more efficient in the presence of cadmium.

Simultaneous Coexposure to Inorganic Mercury and Cadmium: A Study of the Renal and Hepatic Disposition of Mercury and Cadmium

This study was designed to evaluate the effects of simultaneous coexposure to inorganic mercury and cadmium on the renal and hepatic disposition of each metal. Dispositional changes were assessed in rats 1 h and 24 h after the coexposure to relatively low doses of the metals (which individually are nonnephrotoxic in rats). The rational for studying mercury and cadmium is that both of these metals are encountered frequently in the same contaminated areas. Coadministration of a 0.5-µmol/kg dose of mercuric chloride with a 10-µmol/kg dose of cadmium chloride resulted in a decrease in the net renal accumulation of inorganic mercury at 1 and 24 h after exposure. Assessment of the disposition of both metals in renal zones indicates that the decreased renal accumulation of inorganic mercury was due specifically to changes in the accumulation of mercury in the renal cortex. Coexposure to inorganic mercury and cadmium also caused both the hepatic accumulation of mercury and the urinary excretion of mercury to increase during the initial 24 h after coexposure. During the initial 1 h after coexposure, the content of mercury in the blood was enhanced significantly. However, by the end of the first 24 h after exposure, the content of mercury in the blood was lower than that in animals treated with only inorganic mercury, likely due to the increased urinary excretion of mercury. Interestingly, with the exception of decreased fecal excretion of cadmium, no other changes in the disposition of cadmium were detected in the animals treated with both mercury and cadmium. These novel findings indicate that at the doses of inorganic mercury and cadmium used in the present study, cadmium has profound effects on the renal and hepatic handling of mercury. Based on the present findings, it appears that cadmium [by some currently unknown mechanism(s)] interferes with the luminal and/or basolateral uptake and/or net accumulation of mercury along S 1 and S 2 segments of the proximal tubules, which results in an overall decrease in the renal burden of mercury and an increased rate in the urinary excretion of mercury.

Relationships between alterations in glutathione metabolism and the disposition of inorganic mercury in rats: effects of biliary ligation and chemically induced modulation of glutathione status

Influences of biliary ligation and systemic depletion of glutathione (GSH) or modulation of GSH status on the disposition of a low, non-nephrotoxic i.v. dose of inorganic mercury were evaluated in rats in the present study. Renal and hepatic disposition, and the urinary and fecal excretion, of inorganic mercury were assessed 24 h after the injection of a 0.5-μmol/kg dose of mercuric chloride in control rats and rats pretreated with acivicin (two 10-mg/kg i.p. doses in 2 ml/kg normal saline, 90 min apart, 60 min before mercuric chloride), buthionine sulfoximine (BSO; 2 mmol/kg i.v. in 4 ml/kg normal saline, 2 h before mercuric chloride) or diethylmaleate (DEM; 3.37 mmol/kg i.p. in 2 ml/kg corn oil, 2 h before mercuric chloride) that either underwent or did not undergo acute biliary ligation prior to the injection of mercury. Among the groups that did not undergo biliary ligation, the pretreatments used to alter GSH status systemically had varying effects on the disposition of inorganic mercury in the kidneys, liver, and blood. Biliary ligation caused the net renal accumulation of mercury to decrease under all pretreatment conditions. By contrast, biliary ligation caused significant increases in the hepatic burden of mercury in all pretreatment groups except in the acivicin-pretreated group. Blood levels of mercury also increased as a result of biliary ligation, regardless of the type of pretreatment used. The present findings indicate that biliary ligation combined with methods used to modulate GSH status systemically have additive effects with respect to causing reductions in the net renal accumulation of mercury. Additionally, the findings indicate that at least some fraction of the renal accumulation of inorganic mercury is linked mechanistically to the hepato-biliary system.

Disposition of Inorganic Mercury Following Biliary Obstruction and Chemically Induced Glutathione Depletion: Dispositional Changes One Hour after the Intravenous Administration of Mercuric Chloride

Influences of biliary obstruction and systemic depletion of glutathione (GSH) on the disposition of a low nontoxic iv dose of inorganic mercury were evaluated in rats in the present study. Specifically, the disposition of mercury in the kidneys, liver, small and large intestines, and blood was assessed 1 h after the injection of 0.5 μmol/kg mercuric chloride in control rats and rats pretreated with acivicin, buthionine sulfoximine (BSO), or diethylmaleate (DEM) that did or did not undergo acute biliary ligation prior to the injection of mercury. Among the groups that did not undergo biliary ligation, the pretreatments used to alter GSH status systemically had varying effects on the disposition of inorganic mercury in the kidneys, liver, intestines, and blood. Biliary ligation caused the net renal accumulation of mercury to decrease under all pretreatment conditions. By contrast, biliary ligation caused significant increases in the hepatic burden of mercury in all pretreatment groups except the acivicin-pretreated group. Blood levels of mercury also increased as a result of biliary ligation, regardless of the type of pretreatment used. Evidence for a secretory-like movement of mercury into the lumen of the intestines is also provided in the animals that underwent biliary ligation. The present findings indicate that biliary ligation combined with methods used to alter GSH status systemically have additive effects with respect to causing reductions in the net renal accumulation of mercury. In addition, the findings indicate that at least some fraction of the renal accumulation of inorganic mercury is linked mechanistically to the hepatobiliary system.

Accumulation of mercury in estuarine food chains

To understand the accumulation of inorganic mercury and methylmercury at the base of the estuarine food chain, phytoplankton (Thalassiosira weissflogii) uptake and mercury speciation experiments were conducted. Complexation of methylmercury as methylmercury-bisulfide decreased the phytoplankton uptake rate while the uptake rate of the methylmercury-cysteine and -thiourea complexes increased with increasing complexation by these ligands. Furthermore, our results indicated that while different ligands influenced inorganic mercury/methylmercury uptake by phytoplankton cells, the ligand complex had no major influence on either where the mercury was sequestered within the phytoplankton cell nor the assimilation efficiency of the mercury by copepods. The assimilation efficiency of inorganic mercury/methylmercury by copepods and amphipods feeding on algal cells was compared and both organisms assimilated methylmercury much more efficiently; the relative assimilation efficiency of methylmercury to inorganic mercury was 2.0 for copepods and 2.8 for amphipods. The relative assimilation is somewhat concentration dependent as experiments showed that as exposure concentration increased, a greater percentage of methylmercury was found in the cytoplasm of phytoplankton cells, resulting in a higher concentration in the copepods feeding on these cells. Additionally, food quality influenced assimilation by invertebrates. During decay of a T. weissflogii culture, which served as food for the invertebrates, copepods were increasingly less able to assimilate the methylmercury from the food, while even at advanced stages of decay, amphipods were able to assimilate mercury from their food to a high degree. Finally, fish feeding on copepods assimilated methylmercury more efficiently than inorganic mercury owing to the larger fraction of methylmercury found in the soft tissues of the copepods.

Accumulation and handling of inorganic mercury in the kidney after coadministration with glutathione

The accumulation and handling of mercury in the blood, kidneys, and liver were evaluated and compared in rats 5 min, 1 h, and 24 h after the intravenous administration of either 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 glutathione (GSH) to determine the possible role of extracellular GSH and complexes of GSH and inorganic mercury in the renal uptake and transport of inorganic mercury. Significantly more of the injected dose of 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 inorganic mercury and GSH at all times evaluated after injection. Of the mercury remaining in the blood, however, significantly more mercury was in plasma fraction of blood in the rats injected with both inorganic mercury and GSH than in the plasma fraction of blood in the rats injected with inorganic mercury alone. The blood and plasma findings indicate that much of the mercury injected with GSH was in some complex that allowed the mercury to be cleared from the blood more readily and prevented the mercury from entering readily into red blood cells. The renal concentration of mercury was significantly greater in the rats injected with both inorganic mercury and GSH than in the rats injected with inorganic mercury alone at 5 min and 1 h, but not 24 h, after injection. This increased renal accumulation of mercury during the initial hours after injection was due mainly to enhanced uptake and/or retention of mercury in the renal cortex. Urinary excretion of mercury, over 24 h, was also slightly, but significantly, greater in the rats injected with both inorganic mercury and GSH simultaneously. These data indicate that coadministration of a nontoxic dose of inorganic mercury with a twofold higher amount (in moles) of GSH increases significantly the clearance of mercury from the blood and increases the renal cortical accumulation of inorganic mercury during the initial 1 h after injection. Moreover, the data in this study are consistent with the hypothesis that extracellular GSH is an important ligand to which mercuric ions bind, and that complexes of inorganic mercury and GSH 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.

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.

Lack of luminal or basolateral uptake and transepithelial transport of mercury in isolated perfused proximal tubules exposed to mercury-metallothionein.

The lumen-to-bath and bath-to-lumen transport, cellular uptake, and toxicity of inorganic mercury bound to metallothionein (203Hg-MT) were studied in isolated perfused S1, S2, and S3 segments of the renal proximal tubule of rabbits. Evidence of very mild toxicity was displayed in some of the segments perfused through the lumen with 18.4 microM inorganic mercury in the form of Hg-MT. The toxic response was restricted primarily to mild swelling of the epithelial cells localized at the end of the tubular segments where the perfusion pipette was inserted into the lumen. The cells in the proximal portions of perfused S2 segments appeared to be most severely affected in that a few blebs would on occasion come off the epithelial cells. Mild cellular swelling was also observed in some S2 and S3 segments that were exposed to 18.4 microM inorganic mercury in the form of Hg-MT in the bath. The swelling was more generalized, involving all the epithelial cells along the perfused segment. Very little, or no, measurable lumen-to-bath or bath-to-lumen transport of Hg as Hg-MT could be detected in any of the 3 perfused segments of the proximal tubule during 40-45 min of perfusion. The complex of Hg-MT appeared to behave in a manner similar to that of the volume marker [3H]-L-glucose. The lack of tubular transport of Hg as Hg-MT was confirmed by little or no measurable uptake and accumulation of inorganic mercury in the tubular epithelial cells. Thus, our findings indicate that the Hg-MT complex is not taken up avidly in isolated perfused S1, S2, or S3 segments of the proximal tubule.

Early aspects of the intrarenal distribution of mercury after the intravenous administration of mercuric chloride

The present study was designed to evaluate the early aspects of the renal accumulation and intrarenal distribution of inorganic mercury in rats given a nontoxic 0.5 μmol/kg or a moderately nephrotoxic 2.0 μmol/kg intravenous dose of mercuric chloride. Each dose of mercuric chloride contained between 1.0–1.5 μCi 203Hg 2+ in order to make it possible to follow the pattern for the intrarenal accumulation of inorganic mercury with standard gamma-counting techniques. Within the first 5 min after injection of either dose of mercuric chloride, about 70% of the dose of mercury was abstracted from blood. About 10% of the dose was in the combined renal mass, with the greatest fraction in the cortex. The liver contained about 5% of the dose. By the end of the first 3 h after injection of either dose, greater than 90% of the dose of mercury had been abstracted from the blood. At this time, about 8% of the dose was in the liver and more than 50% of the dose was found in the total renal mass. Again, the concentration of mercury in the renal cortex was greater than that in any other zone. The concentration of mercury in the outer stripe of the outer medulla also increased markedly over the first 3 h after injection, but was half that in the cortex. No change in the concentration of mercury was detected in the inner stripe of the outer medulla and inner medulla over the 3-h time period. Findings from the present study indicate that the pattern for intrarenal distribution of mercury does not change significantly during the initial 3 h after injection of the moderately nephrotoxic dose of mercuric chloride. Normally, the concentration of mercury in the outer stripe of the outer medulla increases above that in the cortex sometime during the first 24 h after a low or moderately nephrotoxic dose of inorganic mercury. The present findings indicate that this shift occurs sometime after the first 3 h.

Accumulation of organic and inorganic mercury from food in the tissues of Carcinus maenas: effect of waterborne selenium

Accumulation of organic and inorganic mercury from contaminated food into the tissues of seleniumand non-selenium-exposed shore crabs Carcinus maenas were investigated in the laboratory. Crabs fed homogenates of Cardiurn edule collected in the mercury-contaminated Nissum Bredning, Jutland, Denmark, assimilated 50 to 60 % of ingested inorganic and organic mercury. Muscle and midgut gland contained approxin~ately 50 to 60 % and 40 % respectively of both asslmilated mercury species. Simultaneous exposure to selenite augmented accumulation of organic mercury in muscle and increased assimilation of organic mercury from the food. Accumulation of inorganic mercury was not affected by exposure to selenite. When the mercury concentration of the food was increased 10-fold (by the addition of HgClz and CH3HgCl directly to the cockle homogenate), a higher percentage of the ingested inorganic mercury was assimilated by the crabs, 95 % of the inorganic mercury being accumulated in the rnidgut gland. Percent assimilation and tissue distribution of organic mercury was less affected by increasing the concentration in the diet. The subcellular distribution of the 2 mercury species was almost identical. In the soluble fraction both mercury species were bound predominantly to proteins with a molecular weight (MW) of ca 12 000 Da. In the soluble fraction, exposure to selenite diverted mercury from the 12 000 Da region to high (MW > 70 000 Da) or very low (MW c 4000 Da) molecular weight proteins. Injected organic mercury was cleared from the haemolymph more rapidly than inorganic mercury, and clearance of both mercury species from the haemolymph proceeded faster in selenite-exposed crabs.