Histochemical demonstration of two mercury pools in trout tissues: Mercury in kidney and liver after mercuric chloride exposure

Juvenile rainbow trout (Salmo gairdneri) were exposed to 100 ppb mercury (as HgCl2) in the water for 14 days. Concentrations of mercury in water and fish organs were monitored using radiolabeled mercury. Tissues from kidney and liver were fixed, and sections were developed by autometallography, a method whereby accumulations of mercury sulfides and/or mercury selenides are silver amplified. In the kidney, mercury was found within lysosomes and extracellularly in the basal lamina of proximal tubules. In the liver, mercury was found within lysosomes of the hepatocytes. Additional groups of mercury-exposed trout were subjected to selenium (as Na2SeO3), administered intraperitoneally 2 hr before fixation. Following this treatment, additional mercury could be visualized in the kidney circulatory system, including glomeruli, and in the nucleus and endoplasmic reticulum of liver cells. It is suggested that the mercury visualized prior to selenium treatment represents inorganic mercury, while additional mercury visualized after selenium administration represents an organic form.     

Health effect of long-term diet mercury contaminated tuna. Part II. Accumulation and retention of mercury and selenium in organs and clinical symptoms (author's transl)]

Health effects of long-term tuna diet in cats were examined. The cats were fed daily with three kinds of tuna, containing different concentrations of mercury and selenium. The following results were obtained. 1) A high correlation was noted between the amount of fish intake and the mercury level in hair and blood samples of cats. 2) Mercury levels in organs were elevated corresponding with the amount of tuna consumption, but the distribution of mercury in organs of cats exposed to mercury in tuna flake differed from that in tuna fresh meat. In the liver, the ratio of methyl mercury to the total mercury was very low with an average of 11.5% of the ratio. 3) With regard to selenium, there was no correlation between intake of selenium and selenium levels in the cerebrum, celebellum, and kidneys, exept in the liver (r=0.766). 4) None of the cats had definite methyl mercury poisoning, but some slight disturbances were noted in several cats.     

Role of selenium in mercury intoxication in mice

Studies were conducted to examine the effect of pre and post-treatment of selenium in mercury intoxication (20 micromole/ kg b.w. each given intraperitoneally) in mice in terms of lipid peroxidation (LPO), glutathione (GSH) content, activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and mercury concentration in liver, kidney and brain. No significant alteration was observed in all the organs examined after mercury or selenium treatment in LPO and GSH but administration of selenium (pre and post) resulted in an increase in the level of LPO and GSH. The activity of SOD was depleted in liver and kidney while that of GPx was lowered in liver of mercury exposed animals. Selenium administration resulted in restoration of the depletion of these enzymatic activities. The activity of CAT in liver and brain was enhanced both in mercury and selenium treated animals. Administration of selenium significantly arrested enhanced CAT activity. Kidney showed the highest mercury concentration among the organs examined. Administration of selenium resulted in further enhancement of mercury concentration in the tissues. An increase in selenium level in liver was observed after mercury treatment, which was also restored by mercury selenium co-administration. Our results indicate that the prooxidant effect of selenium was greater by its pretreatment.     

Methyl mercury and inorganic mercury in Swedish pregnant women and in cord blood: influence of fish consumption

We studied exposure to methyl mercury (MeHg) in Swedish pregnant women (total mercury [T-Hg] in hair) and their fetuses (MeHg in cord blood) in relation to fish intake. The women were recruited at antenatal care clinics in late pregnancy to participate in an exposure study of environmental pollutants. Fish consumption was evaluated using food frequency questionnaires including detailed questions on fish consumption. In addition, we determined inorganic mercury (I-Hg) and selenium (Se) in cord blood. On average, the women consumed fish (all types) 6.7 times/month (range 0-25 times/month) during the year they became pregnant. They reported less consumption of freshwater fish--species that might contain high concentrations of MeHg--during than before pregnancy. T-Hg in maternal hair (median 0.35 mg/kg; range 0.07-1.5 mg/kg) was significantly associated (R2 = 0.53; p < 0.001) with MeHg in cord blood (median 1.3 microg/L; range 0.10-5.7 microg/L). Both hair T-Hg and cord blood MeHg increased with increasing consumption of seafood (r = 0.41; p < 0.001 and r = 0.46; p < 0.001, respectively). Segmental hair analysis revealed that T-Hg closer to the scalp was lower and more closely correlated with MeHg in cord blood than T-Hg levels in segments corresponding to earlier in pregnancy. We found a weak association between Se (median 86 microg/L; range 43-233 microg/L) and MeHg in cord blood (r = 0.26; p = 0.003), but no association with fish consumption. I-Hg in cord blood (median 0.15 microg/L; range 0.03-0.53 microg/L) increased significantly with increasing number of maternal dental amalgam fillings.     

Inorganic mercury and methylmercury in placentas of Swedish women

We determined levels of inorganic mercury (I-Hg) and methylmercury in placentas from 119 Swedish women, not selected with respect to high exposure of mercury. Our objective was to relate placental Hg species with maternal and fetal blood concentrations and to evaluate possible associations with selenium. We performed the analyses using automated alkaline solubilization/reduction and cold-vapor atomic fluorescence spectrophotometry. I-Hg levels in placenta increased with an increasing number of maternal dental amalgam fillings (p < 0.001). Despite placental accumulation (median, 1.3 microg/kg; range, 0.18-6.7 microg/kg wet weight), a substantial fraction of maternal blood I-Hg, probably as Hg(0), reached the fetus. Although MeHg transferred easily to the fetus, it also accumulated in the placenta. On average, 60% of placental Hg was in the form of MeHg. The median concentration was 1.8 microg/kg (range, 0-6.2 microg/kg wet weight), more than twice the maternal blood concentration. We found significant associations between MeHg and selenium in both maternal and umbilical cord blood but not in the placenta. The associations were particularly obvious in freshwater fish consumers, probably reflecting that fish is a source of both MeHg and selenium. We found no correlations between I-Hg and selenium. This study increases the understanding of Hg, in its different forms, in human placenta and how they are related to maternal and fetal exposure.     

New evidence on the effects of tea on mercury metabolism in humans

The authors present the results of an experiment in which they explored the role of tea in human metabolic processing of methylmercury (MeHg) from fish consumption. The experiment involved 50 scientists from the Collaborative Mercury Research Network (COMERN) who agreed to eat fish for 2 daily meals for 3 consecutive days. Half of the participants also drank 6 cups of tea daily, starting a week before and continuing through the experiment. The authors calculated the total amount of MeHg that each participant ingested from (1) the measured mercury (Hg) level in fish and (2) the quantity of fish eaten, and compared it with the total increases of Hg and MeHg levels in participants' blood. Results indicated that the control group metabolized roughly 100% of the available fish MeHg, whereas the tea-exposed group showed blood levels of MeHg at more than 40% than that available in the fish provided, suggesting that an external MeHg pool supplied part of the measured blood MeHg increase. The authors conclude that tea may accelerate the enterohepatic MeHg cycle and contribute to a temporary bioamplification of MeHg in the bloodstream.     

Comparison of Elements in Bottlenose Dolphins Stranded on the Beaches of Texas and Florida in the Gulf of Mexico over a One-Year Period

We analyzed tissue samples from bottlenose dolphins (Tursiops truncatus) that had stranded on beaches in Texas and Florida over a 1-year period starting in September 1991. The concentrations of 10 elements plus methyl mercury (MeHg) were determined in brain, kidney, and liver, and we examined these results for differences based upon age, site, sex, and tissue type. A strong inverse relationship between total mercury (Hg) and the percentage that was MeHg was found in liver, kidney, and brain tissue, presumably due to demethylation of MeHg. A threshold concentration was found for total Hg in brain tissue, indicating that most Hg was present as MeHg up to about 8 years of age. Increases in total Hg after this age were accompanied by an increase in the ratio of total Hg to MeHg, indicating demethylation. Strong relationships were found between total Hg in liver and age and between total Hg and selenium in liver, which have been observed before in many fish- and squid-eating marine mammals. The only difference based on sex of the animals was observed for MeHg, which was higher in females and contrary to the pattern often observed for organic contaminants. Several elements (copper, Hg, lead, zinc) exhibited intersite differences, which were not consistent. Bottlenose dolphin from Florida exhibited the highest levels of MeHg and total Hg, while animals from Texas exhibited the highest levels of lead, copper, and zinc. The essential elements copper and zinc were expected to be the same for the Texas and Florida animals; however, observed differences may indicate population differences in basic physiological levels, dietary intake, or health status. Received: 10 April 1998/Accepted: 27 July 1998     

Sexual differences in the excretion of organic and inorganic mercury by methyl mercury-treated rats

Adult male and female Long Evans rats received 1 mumole of methyl (203Hg) mercuric chloride per kilogram sc. Whole-body retention of mercury and excretion of organic and inorganic mercury in urine and feces were monitored for 98 days after dosing. Females cleared mercury from the body more rapidly than did males. The major route of mercury excretion was feces. By 98 days after dosing, cumulative mercury excretion in feces accounted for about 51% of the dose in males and about 54% of the dose in females. For both sexes, about 33% of the dose was excreted in feces as inorganic mercury. Cumulative excretion of organic mercury in feces accounted for about 18 and 21% of the dose in males and females, respectively. Urinary excretion of mercury was quantitatively a smaller route for mercury clearance but important sexual differences in loss by this route were found. Over the 98-day experimental period, males excreted in urine about 3.2% of the dose and females excreted 7.5%. Cumulative organic Hg excretion in urine accounted for 1.8% of the dose in males and 5.3% of the dose in females. These sexual differences in urinary and fecal excretion of organic and inorganic mercury following methyl mercury treatment were consistent with previous reports of sexual differences in mercury distribution and retention in methyl mercury-treated rats, particularly sexual differences in organic mercury uptake and retention in the kidney. Relationships between body burdens of organic or inorganic Hg and output of these forms of Hg in urine and feces were also found to be influenced by the interval after MeHg treatment and by sex. Relationship between concentration of Hg in liver and feces and in kidney and urine differed for organic and inorganic Hg and depended upon sexual status and interval after MeHg treatment. These findings emphasize that sexual differences in distribution, retention, and metabolism of methyl mercury are factors to be considered in estimations of hazards associated with exposure to this agent.     

A quantitative analysis of prenatal methyl mercury exposure and cognitive development

Although a rich source of n-3 polyunsaturated fatty acids (PUFAs) that may confer multiple health benefits, some fish also contain methyl mercury (MeHg), which may harm the developing fetus. U.S. government recommendations for women of childbearing age are to modify consumption of high MeHg fish to reduce MeHg exposure, while recommendations encourage fish consumption among the general population because of the nutritional benefits. The Harvard Center for Risk Analysis convened an expert panel (see acknowledgements) to quantify the net impact of resulting hypothetical changes in fish consumption across the population. This paper quantifies the impact of prenatal MeHg exposure on cognitive development. Other papers quantify the beneficial impact of prenatal intake of n-3 PUFAs on cognitive function and the extent to which fish consumption protects against coronary heart disease mortality and stroke in adults. This analysis aggregates results from three major prospective epidemiology studies to quantify the association between prenatal MeHg exposure and cognitive development as measured by intelligence quotient (IQ). It finds that prenatal MeHg exposure sufficient to increase the concentration of mercury in maternal hair at parturition by 1 microg/g decreases IQ by 0.7 points. This paper identifies important sources of uncertainty influencing this estimate, concluding that the plausible range of values for this loss is 0 to 1.5 IQ points.     

Neurobehavioral assessment of Mohawk Indians for subclinical indications of methyl mercury neurotoxicity

A total of 200 male and 200 adult female Mohawk Indians were examined by means of performance tests as part of a total health evaluation of participants in a medical field survey on the St. Regis Reserve. Age-corrected performance test scores were studied in relation to blood, urinary, and hair methyl mercury (MeHg) levels, and local fish consumption. Males were found to eat more fish than females and had relatively higher MeHg levels than females. Blood and hair MeHg levels were significantly correlated with local fish consumption for both sexes. Biological indicators of MeHg absorption suggested low exposure levels but did not correlate significantly with performance test scores. These findings indicate that the time of examination, St. Regis residents were exposed to almost "background" levels of MeHg and did not exhibit either subclinical or clinical manifestations of MeHg neurotoxicity.     

Selenium as a potential protective factor against mercury developmental neurotoxicity

Experimental studies suggest that selenium (Se) may decrease methylmercury (MeHg) toxicity under certain exposure regimens. In epidemiological studies, the exposure to MeHg occurs from fish and seafood, which are also a source of beneficial nutrients such as selenium. However, little is known about the potential protective effects of dietary Se against MeHg neurotoxicity in humans. The possible interaction was assessed in two birth cohorts in the Faroe Islands, consisting of singleton term births from 1986 to 1987 (N=1,022), and 1994 to 1995 (N=182), respectively. Dietary habits in this fishing population included frequent consumption of seafood, including whale meat high in mercury. Both Hg and Se were measured in cord whole blood. Neurodevelopmental outcomes were evaluated at age 7 years in both cohorts, and the smaller cohort also included neurological assessment on several prior occasions. Each outcome was modeled as a function of Hg and Se interactions (with adjustments for potential risk factors) by expressing the effects of log10(Hg) within the lowest 25%, the middle 50%, and the highest 25% of the Se distribution. Surplus Se was present in cord blood, the average being a 10-fold molar excess above MeHg. Regression analyses failed to show consistent effects of Se, or statistically significant interaction terms between Se and MeHg. Overall, no evidence was found that Se was an important protective factor against MeHg neurotoxicity. Prevention, therefore, needs to address MeHg exposures rather than Se intakes. Because of the benefits associated with fish intake during pregnancy, consumers should be advised to maintain a high fish and seafood intake that is low in Hg contamination. Additional research is needed to determine the identity of the nutrients responsible for the beneficial effects.     

Mercury concentrations in three species of fish from North Atlantic offshore waters

Mercury concentrations were determined in tissues and organs of spiny dogfish (Squalus acanthias), cusk (Brosme brosme), and blackbellied redfish (Helicolenus dactylopterus) collected from Atlantic Ocean waters off the northeastern coast of the United States. Information was obtained on the spatial and temporal distribution of mercury in the organs and tissues of these fish.Cusk were obtained from 2 locations and blackbellied redfish from 4 locations. The mercury levels in both muscle and liver of cusk averaged about 0.30 ppm for one and 0.16 ppm for the second location. Gills and kidneys of cusk had mercury levels that averaged 0.08 ppm for both collections. In blackbellied redfish mercury levels in muscle and liver averaged about 0.08 ppm for all locations; gill and kidney tissues of this fish were less than 0.2 ppm.Spiny dogfish were obtained from 5 areas. No significant difference in mercury levels was found in muscle tissue as related to geographic area. Mercury levels ranged from 0.21 to 0.62 ppm. The kidneys of dogfish contained about 54% of the mercury level of muscle. The mercury level in gills of dogfish ranged from 0.06 to 0.21 ppm.Spiny dogfish pups were obtained from 6 adult females. Samples of muscle, liver, gill, kidney, and yolk of pups were analyzed for mercury. These same samples, except for the yolk, were obtained from the adult females. Mercury levels in all pup samples were less than 0.03 ppm, while mercury levels in adult females ranged from 0.03 to 1.1 ppm in all tissues and organs.     

Histopathological evidence of inorganic mercury and methyl mercury toxicity in the arctic charr (Salvelinus alpinus)

In our sustained effort to understand mechanisms of mercury toxicity in fish, the histopathological effects of a 96-h acute exposure to water-borne inorganic mercury (inorganic Hg) (15 micro gL(-1)), as well as those of a single dietary dose of inorganic and methyl mercury (methyl Hg) (0.260.05 micro g.Hgg(-1) body weight), over 30 days were examined. Samples of gills, olfactory epithelium, kidneys, and liver of arctic charr, Salvelinus alpinus, were studied using light and electron microscopy. The distribution of dietary inorganic and methyl Hg in the intestinal epithelium was determined using 203Hg microautoradiography. Gills of fish exposed to water-borne inorganic Hg presented a severe disorganization of epithelial cells after 12h and modifications of cilia of ciliated olfactory cells appeared after 24h. Nevertheless, a partial recovery was seen in both tissues by the end of the 96-h exposure period. Liver was little affected by water-borne and single-trophic-dose contamination of inorganic Hg, but dietary methyl Hg had drastic effects, despite its low dosage, with severe necrosis and alterations of cytoplasmic organization. Microautoradiograms showed that inorganic Hg was distributed evenly in the intestinal epithelium, whereas methyl Hg was found at very specific locations on the epithelial surface.     

Mercury concentration in organs of contemporary Japanese

Concentrations of inorganic mercury (IHg), methylmercury (MeHg), and total mercury (THg) were determined for autopsy samples from 46 Japanese subjects. Two laboratories (Labs A and B) participated in Hg analyses: Lab A for THg and IHg and Lab B for THg and MeHg. Total mercury concentration values were in good agreement between the two laboratories: the averages were several hundreds of ng/g in kidney cortex, kidney medulla, and liver, and were several tens of ng/g in cerebrum, cerebellum, heart, and spleen. Inorganic mercury accumulated more in kidney and liver: its percentage THg was 81-84% in the kidney, 67% in the liver, 25% in the heart, 22% in the spleen, 20% in the cerebrum, and 14% in the cerebellum. Methylmercury levels in tissues were uniform through all organs except the liver. Approximately 80% was in the form of MeHg in the cerebrum, cerebellum, heart, and spleen, whereas the values were 33%, 15%, and 11% in the liver, kidney medulla, and kidney cortex, respectively. Age was a significant factor in increased IHg concentrations in the cerebrum and heart, decreased values of %MeHg in the cerebrum, cerebellum, and heart, and increased values of %IHg in the cerebrum and heart.     

Evaluation of protective effects of fish oil against oxidative damage in rats exposed to methylmercury

The present study evaluates a possible protective effect of fish oil against oxidative damage promoted by methylmercury (MeHg) in sub-chronically exposed rats. Reduced glutathione peroxidase and catalase enzyme activity and reduced glutathione levels were observed in MeHg-exposed animals compared to controls. Methylmercury exposure was also associated with DNA damage. Administration of fish oil to the methylmercury-exposed animals did not ameliorate enzyme activity or glutathione levels. On the other hand, a significant DNA protective effect (about 30%) was observed with fish oil treatment. There were no differences in the total mercury concentration in rat liver, kidney, heart or brain after MeHg administration with or without fish oil co-administration. Histopathological analyses showed a significant leukocyte infiltration in rat tissues after MeHg exposure, but this effect was significantly reduced after co-administration of fish oil.Taken together, our findings demonstrate oxidative damage even after low-level MeHg exposure and the protective effect of fish oil. This protection seems not to be related to antioxidant defenses or mercury re-distribution in rat tissues. It is probably due to the anti-inflammatory effects of fish oil.     

Total and Methyl Mercury Concentrations in Antarctic Toothfish (<Emphasis Type="Italic">Dissostichus mawsoni</Emphasis>): Health Risk Assessment

The concentrations of total mercury (THg) in different organs of the Antarctic toothfish (Dissostichus mawsoni) collected from CCAMLR research blocks in Subarea 88.3 and Division 58.4.1 off the coast of Antarctica were determined. The results revealed THg concentrations of 0.165?±?0.095 mg/kg (0.023–0.454 mg/kg, wet weight) in the Antarctic toothfish. In muscle, methyl mercury (MeHg) accounted for approximately 40% of the THg. In a comparison analysis, muscle and liver tended to bioaccumulate the highest levels of THg, and both THg and MeHg contents showed correlations with fish length and weight. Compared with international guidelines, fish contained 2.5–6.4% and 4.0–10.3% of the provisional tolerable weekly intake for THg recommended by the Joint FAO/WHO Expert Committee on Food Additives and the tolerable weekly intake for MeHg proposed by the European Food Safety Authority, respectively. These results suggest that consumption of the Antarctic toothfish presents no health risk to humans.     

Nutrient and methyl mercury exposure from consuming fish

There is controversy about the risks and benefits of consuming fish. Fish consumption provides nutrients, some of which are essential for brain growth and development. All fish, however, contain methyl mercury (MeHg), a known neurotoxicant. The toxic effect of MeHg seems most damaging during brain development, and thus, prenatal exposure is of greatest concern. At present the level of prenatal exposure associated with risk to a child's neurodevelopment is not known. Balancing the rewards and possible risks of fish consumption presents a dilemma to consumers and regulatory authorities. We review the nutrients in fish that are important in brain development and the current evidence of risk from MeHg at exposure levels achieved by consuming fish. We then review the findings from a large prospective cohort study of a population that consumes fish daily, the Seychelles Child Development Study. The MeHg content of the fish consumed in the Seychelles is similar to that of ocean fish available in industrialized countries, so they represent a sentinel population for any risk from fish consumption. In the Seychelles, evaluations of the children through 9 y of age show no consistent pattern of adverse associations with prenatal MeHg exposure. Recent studies in the Seychelles have focused on nutrients in fish that might influence a child's development, including long-chain polyunsaturated fatty acids, iodine, iron, and choline. Preliminary findings from this study suggest that the beneficial influence of nutrients from fish may counter any adverse effects of MeHg on the developing nervous system.     

Generation and dose as modifying factors of inorganic mercury accumulation in brain, liver, and kidneys of rats fed methylmercury

Through three generations, male rats were fed a commercial chow supplemented with four levels of methyl mercury; the average mercury concentrations were 0.038, 0.18, 7.23, and 33.92 nmol Hg/g food for control, low, middle, and high dose groups, respectively. No clinical abnormalities except enlarged kidneys were found in these animals. The effects of dose and generation on tissue distribution and accumulation of inorganic mercury and total mercury were studied in the brain, kidneys, and liver. The dose level of methyl mercury greatly determined the organ accumulation of total mercury and inorganic mercury, as well as the ratio of inorganic mercury concentration to total mercury concentration (I/T) in organs. The I/T ratio was inversely related to the dose level of methyl mercury. With generational procession, the most notable change was found in the liver, i.e., the increasing I/T ratio and the decreasing total mercury accumulation at any dose level. In contrast, the I/T ratio in the kidney showed no constant tendency with generation. The present results suggest that the generational enhancement of inorganic mercury formation from methyl mercury occurs mainly in the liver.     

Mercury in the dorsal root ganglia of rats treated with inorganic or organic mercury

Autometallographic silver amplification has been used to demonstrate the localization of mercury deposits in rat dorsal root ganglia after repeated intraperitoneal injections of mercuric chloride or methylmercuric chloride. The silver-enhanced mercury deposits were demonstrated with the light and electron microscope. The degree of intracellular staining of the individual cells depended on the mercury compound and total dosage. Ganglion cells (types A and B) and macrophages were found to accumulate mercury after a total dosage of 400 micrograms HgCl2. After 600 micrograms HgCl2, satellite cells, endothelial cells and fibroblasts were additionally found to contain mercury deposits. Treatment with 6000 micrograms CH3HgCl caused faint staining of type A and B ganglion cells and fibroblasts. Macrophages, however, were the most heavily stained cells after treatment with CH3HgCl. Ultrastructurally, mercury was exclusively located in lysosomes. This was irrespective of the cell type and mercury compound used for treatment.     

Effects of dietary methylmercury on liver and kidney histology in the neotropical fish Hoplias malabaricus

Methylmercury is a potent toxic present in Amazonian fish species due to gold mining activities. In the present work, we investigated the morphological effects of methylmercury in liver and kidney of Hoplias malabaricus feeding contaminated prey fish over 70 days. Two groups of nine mature fish (tested and control) were acclimatized for four weeks to laboratory conditions and then the tested group fed prey fish previously contaminated at an additional level of 0.075 microg MeHg g(-1) at 5-day intervals and over 14 successive intervals whereas control group fed uncontaminated fish. H. malabaricus specimens were then dissected for chemical and morphological analyses. The low and realistic level of MeHg in the prey fish induced a low increase of total mercury in liver (1.8-fold) and muscle (2.2-fold). The biomagnification factor (Hg in predator/Hg in prey) reached 142 in liver and 21 in muscle and was indicative of a relatively fast contamination of internal organs by dietary exposure. The liver of exposed individuals presented leukocyte infiltration, increased number of melano-macrophage centers, necrotic areas and lesions in Disse's space. Evident disorder and chaos in cytoskeleton organization suggest a strong toxic effect in hepatocytes, such as organelles positioning and movement, vesicles traffic and secretion. Head kidney showed large necrosis areas, increased number of melano-macrophages centers, phagocytic areas, intercellular space among parenquimal cells and atypical cells. Injuries and damages to tissues suggest too slow defense mechanisms to immobilize or eliminate ingested methylmercury, demonstrating that the sensitivity of fish cells to methylmercury exposure is higher than it has been previously described in the literature.