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PubMed1995

Environmental contaminants in the food chain.

Both terrestrial and aquatic food chains are capable of accumulating certain environmental contaminants to toxic concentrations. This article focuses on the aquatic food chain because we have less control over contaminant entry into this chain than we have for the terrestrial chain. In general, at least three special properties are required for a contaminant to bioaccumulate in an aquatic food chain: 1) a high octanol-water partition coefficient, 2) chemical and metabolic stability in water and in organisms in the food chain, and 3) a low toxicity to organisms in the chain so that the chain is not broken by loss of an intermediate species. Few of the thousands of chemicals produced by human industry meet these requirements. In terms of organic chemicals, the best known examples of bioaccumulation in aquatic food chains are the polychlorinated biphenyls (PCBs), dioxins, and organochlorine pesticides such as dichlorodiphenyltrichloroethane (DDT). Few examples exist of bioaccumulation of metal compounds. Methylmercury is arguably the most dramatic and best documented example of high bioaccumulation.

Animals↗
PubMedDate not supplied

Organic mercury: an environmental threat to the health of dietary-exposed societies?

As a natural element, mercury is ubiquitous in the environment. The largest amount of mercury, amounting to approximately 100,000 tons per year, originates from the degassing of the earth's crust. To this amount, such anthropogenic activities as combustion of fossil fuels and releases from industrial activities add approximately 20,000 tons of mercury every year. The emitted mercury, both natural and anthropogenic, is in an inorganic form, predominantly as the metallic vapor (Hgzero). In aquatic environments, however, inorganic mercury is microbiologically transformed into the lipophilic organic compound, methylmercury. The transformation from the hydrophilic to the lipophilic state makes mercury more prone to biomagnification in aquatic food chains. Consequently, populations with a traditionally high dietary intake of food originating from either fresh-water or marine environments have the highest exposure to methylmercury. Because of their traditional pursuit of marine mammals, the Inuits belong to the highest dietary exposure group /1/. This situation is particularly true for the Polar Eskimos in North West Greenland. This population has the most traditional lifestyle among the Inuits and hunts predatory species of whales, such as beluga and narwhal, a combination that results in a high level of exposure to methylmercury. Polar Eskimos in North West Greenland, living in areas with no 'accidental' mercury pollution, but with a high dietary access to methylmercury thus exemplify a population group with a current potential environmental health problem.

Carcinogens, Environmental↗
PubMed2001

The effect of thiolate organic compounds on methylmercury accumulation and redistribution in sheepshead minnows, Cyprinodon variegatus.

Methylmercury (CH3Hg(II)) was measured in various tissues and whole body of sheepshead minnows; Cyprinodon variegatus, following exposure to 100 ng/L methylmercury chloride (CH3HgCl) alone or in combination with one of the organic compounds cysteine (CH3Hg-Cys), thiourea (CH3Hg-Thu), or thioglycolate (CH3Hg-Thg). Overall, the CH3Hg(II) concentration in sheepshead minnows in all the treatments increased with time and was significantly different from the unspiked controls after 24 h. Addition of the organic compounds increased the bioavailability of CH3Hg(II) in the whole body of the fish after 72 h. In particular, the CH3Hg(II) concentration after CH3Hg-Thg and CH3Hg-Thu exposure was, respectively, approximately 1.3- and 1.6-fold higher than with CH3HgCl exposure. A composite of the CH3Hg(II) concentrations in the visceral organs (gill, liver, and intestine) highlighted the effect of the organic compounds, where concentrations in all mercury-thiolate treatments were significantly higher than CH3HgCl alone after 72 h. The most dramatic changes in the different tissues measured were observed in the liver, where the CH3Hg(II) concentrations in the sulfur treatments were significantly higher than the CH3HgCl treatment after 72 h. The results of this study suggest that the CH3Hg-thiolate complexes were bioavailable to sheepshead minnows and effectively induced CH3Hg(II) uptake in tissues at environmentally realistic CH3HgCl concentrations.

Animals↗
PubMed1997

The toxicology of mercury.

The major physical forms of mercury to which humans are exposed are mercury vapor, Hg0, and methylmercury compounds, Ch3HgX. Mercury vapor emitted from both natural and anthropogenic sources is globally distributed in the atmosphere. It is returned as a water-soluble form in precipitation and finds its way into bodies of fresh and ocean water. Land run-off also accounts for further input into lakes and oceans. Inorganic mercury, present in water sediments, is subject to bacterial conversion to methylmercury compounds that are bioaccumulated in the aquatic food chain to reach the highest concentration in predatory fish. Human exposure to mercury vapor is from dental amalgam and industries using mercury. Methylmercury compounds are found exclusively in seafood and freshwater fish. The health effects of mercury vapor have been known since ancient times. Severe exposure results in a triad of symptoms, erethism, tremor, and gingivitis. Today, we are concerned with more subtle effects such as preclinical changes in kidney function and behavioral and cognitive changes associated with effects on the central nervous system. Methylmercury is a neurological poison affecting primarily brain tissue. In adults, brain damage is focal affecting the function of such areas as the cerebellum (ataxia) and the visual cortex (constricted visual fields). Methylmercury also at high doses can cause severe damage to the developing brain. Today the chief concern is with the more subtle effects arising from prenatal exposure such as delayed development and cognitive changes in children.

Administration, Inhalation↗
PubMed1985

Preparation of CH3 203HgCl of high specific activity.

In order to have a methylmercury compound of much higher specific activity than was obtainable from commercial suppliers of the compound, a procedure for the methylation of radioactive mercuric chloride with no addition of non-radioactive mercury has been developed. Methylation is accomplished by reacting the mercuric chloride with tetramethyl tin. Extractions into and out of benzene twice produces a methylmercury compound which is finally dissolved in a dilute sodium carbonate solution suitable for biological experiments. The entire procedure to produce a batch of the compound may be accomplished within a single day.

Indicators and Reagents↗
PubMed1978

Change in permeability of liposomes caused by methylmercury and inorganic mercury.

The effects of two mercurial compounds, methylmercury and inorganic mercury, on lipids were examined by measuring permeability change of lipid bilayer, liposome. Both decrease in the cholesterol content and increase in the content of unsaturated fatty acid moieties in the lipid bilayers, augmented to susceptibility of the liposomes to the mercurial compounds. Inorganic mercury and methylmercury disrupted the lipid membrane to essentially the same extent. The influence on the permeability seems to be specific for mercury compounds. The significant increase in the permeability of some liposomal preparation noted even at the mercurial concentration of 10(-7) M strongly suggests that lipid in biomembrane could be one of the primary targets of these toxic substances.

Animals↗
PubMed1997

Lymphocyte proliferative response and tissue distribution of methylmercury sulfide and chloride in exposed rats.

The immunotoxic effects and tissue distribution of different forms of methylmercury compounds were studied in rats. Methylmercury sulfide or methylmercury chloride was fed to rats at concentrations of 5 or 500 microg/L in drinking water for 8 wk. T-cell lymphocyte proliferative response to phytohemagglutinin (PHA) and determination of tissue distribution of mercury by gas chromatography using electron capture were assayed. Four different forms of mercury compounds were employed: MeHgS-, (MeHg)2S, (MeHg)3S+, and MeHgCl. Results indicated that exposure to methylmercury significantly enhanced lymphocyte responsiveness in most of the exposed groups at the low concentration of 5 microg/L, with the highest proliferative response (fourfold increase) in the MeHgCl group. At 500 microg/L, a significant decrease in the lymphocyte proliferative response was observed in the (MeHg)3S+ and MeHgCl groups; conversely, the MeHgS(-)- and (MeHg)2S-exposed animals had a modest increase of the lymphocyte proliferative response. The largest concentrations of all four mercury forms were detected in the kidney and spleen. The levels of mercury found in kidney, spleen, liver, brain, and testis were lower in the MeHgCl group than in those exposed to (MeHg)2S and (MeHg)3S+. These data indicate that the organ distribution of mercury and immune alteration may vary according to the chemical structure of the compound. This observation may have important implications in humans potentially exposed to low levels of methylmercury present in the environment, since the immune system plays an important regulatory role in the host-defense mechanisms.

Administration, Oral↗
PubMed2000

Occupational and environmental toxicology of mercury and its compounds.

Mercury exists in various chemical forms. The important forms from a toxicological viewpoint are the metallic form, also called the elemental form, the divalent inorganic forms and methylmercury compounds. Elemental (Hg0) mercury has a high vapor pressure and the vapor causes a number of cases of poisoning via inhalation. Classical mercury poisoning is characterized by a triad of signs, namely tremors, erethism and gingivitis. Mercurial erethism, which is characterized by behavioral and personality changes such as extreme shyness, excitability, loss of memory, and insomnia are also observed. Recently, the effects of mercury exposure at levels around 0.05 mg/m3 or lower have been of concern and may include minor renal tubular damage, increased complaints of tiredness, memory disturbance and other symptoms, subclinical finger tremor, abnormal EEG by computerized analysis and impaired performance in neurobehavioral or neuropsychological tests. Abnormal gait, dysarthria, ataxia, deafness and constriction of the visual field are typical of the symptoms of methylmercury poisoning observed in Minamata and Iraqi outbreaks, as well as in occupational methylmercury poisoning cases. Furthermore, an infant born to a mother with excessive methylmercury consumption showed various neurological disturbances and delayed development. Since several populations are believed to be still exposed to methylmercury through the consumption of fish and sea mammals, neurobehavioral deviations in children of these populations have recently been investigated.

Ataxia↗
PubMed1976

Mercury toxicity in the pregnant woman, fetus, and newborn infant. A review.

This paper reviews the reported cases of mercury poisoning in pregnancy and the data based on sources of contamination, maternal uptake, and distribution. It analyzes current knowledge of placental transfer of various mercury compounds, fetal uptake, and distribution. It identifies the embryopathic and fetal toxic effects of mercury in general while emphasizing the greater toxicity of methylmercury compounds. Since maternal exposure to methylmercury is primarily through fish consumption, it recommends that women of childbearing age should not consume more than 350 Gm. of fish per week. In addition, they should not be occupationally exposed to air concentrations of mercury vapor greater than 0.01 mg. per cubic meter, of inorganic and phenylmercuric compounds greater than 0.02 mg. per cubic meter, or any detectable concentration of methylmercury.

Abnormalities, Drug-Induced↗
PubMed1980

The cumulation of methylmercury in fish (Poecilia reticulata).

Methylmercury labelled with mercury-203 was used for the investigation of the uptake and the release of methylmercury in fish. It has been found that methylmercury compounds adsorbed on fish food remain completely in fish and that they are released with the biological half-time of 110 +/- 20 days. The cumulation of methylmercury from water is very rapid: the cumulation constant is 237 +/- 67 days-1. Equations for the calculation of the concentration of methylmercury in fish were derived and compared with the uptake of phenylmercury and inorganic mercury.

Animal Feed↗
PubMed1993

Mercury: major issues in environmental health.

In the past, methylmercury compounds were manufactured as fungicides or appeared as unwanted byproducts of the chemical industry, but today the methylation of inorganic mercury in aquatic sediments and soils is the predominant if not the sole source of methylmercury. This form of mercury is bioaccumulated to a high degree in aquatic food chains to attain its highest concentrations in edible tissues in long-lived predatory fish living in both fresh and ocean waters. It is well absorbed from the diet and distributes within a few days to all tissues in the body. It crosses without hindrance the blood-brain and placental barriers to reach its principal target tissue, the brain. It is eliminated chiefly in the feces after conversion to inorganic mercury. The biological half-time of methylmercury in human tissues is about 50 days, but there is wide individual variation. Adult poisoning is characterized by focal damage to discrete anatomical areas of the brain such as the visual cortex and granule layer of the cerebellum. A latent period of weeks or months may ensue before the appearance of signs and symptoms of poisoning. The latter manifest themselves as paresthesia, ataxia, constriction of the visual fields, and hearing loss. The prenatal period is the most sensitive stage of the life cycle to methylmercury. Prenatally poisoned infants exhibit a range of effects from severe cerebral palsy to subtle developmental delays. Methylmercury is believed to inhibit those processes in the brain specially involved in development and growth such as neuronal cell division and migration.

Dose-Response Relationship, Drug↗
PubMed1991

[Investigation of the effect of polluted water in Song-hua River on the chromosome aberrations and SCE of inhabitants].

This investigation indicated that the chromosome aberration of lymphocytes in inhabitants influenced by mercury- or methylmercury-polluted water was higher than that in control persons although the difference was not significant; but the SCE of them was significantly higher than the control. Both endpoints had a tendency of decreasing with the distance away from the polluted river water. Smoking and age did not have any effect. It was suggested that the polluted river water by mercury or methylmercury compounds could have some cytogenetic effects, although other factors cannot be excluded.

Adolescent↗
PubMed1975

The methylation of mercuric chloride by human intestinal bacteria.

Most strains of staphylococci, streptococci, yeasts and E. coli isolated from human faeces, could synthesize methylmercury compounds. In contrast, few strains of obligate anaerobes could do so. Up to 6 ng methylmercury/ml were formed in 44 h from 2 mug mercuric chloride.

Actinomycetaceae↗
PubMed1982

Reversible effects of monothiol (D-penicillamine) and dithiol (dimercaptosuccinic acid) chelating compounds on methylmercury-inhibited choline acetyltransferase activity and high affinity choline uptake.

The effects of thiol compounds on methylmercury chloride (MMC)-inhibited choline acetyltransferase (ChAT) activity and MMC-inhibited high affinity choline uptake of rat brain tissue were studied in vitro. D-penicillamine (D-Pc) and dimercaptosuccinic acid (DMS) reversed the MMC-inhibited ChAT activity dose-dependently. Equilibrium dialysis of MMC-inhibited ChAT against the buffer containing 10(-3) M D-Pc reversed the ChAT activity almost completely. The reversal effect of D-Pc (monothiol compound) on MMC-inhibited ChAT was significantly more potent than that of DMS (dithiol compound). D-Pc and DMS almost equally reversed the MMC-inhibited high affinity choline uptake by synaptosomes in a dose dependent fashion. Washing with a solution containing D-Pc or DMS equally reversed the MMC-inhibited high affinity choline uptake in a dose-dependent fashion. Neither D-Pc nor DMS could reverse the hemicholinium-3-inhibited high affinity choline uptake.

Absorption↗
PubMed1988

Mechanisms of neurotoxicity related to selective disruption of microtubules and intermediate filaments.

The neuronal response to several neurotoxic chemicals includes disruption of the cytoskeleton such as interactions with microtubules and altered distribution of neurofilaments. Methylmercury (microtubule disrupting) and acrylamide and 2,5-hexanedione (neurofilament disrupting) have been used in a cell culture (PtK2) system to distinguish the cytoskeletal targets of these compounds. Methylmercury caused disassembly of microtubules with secondary collapse of vimentin filaments (epithelial cell equivalent of neurofilaments) at higher concentrations; actin filaments were unaltered. This confirms that disruption of actin does not contribute to methylmercury-induced interference with mitosis. In contrast, both acrylamide and 2,5-hexanedione caused a perinuclear redistribution of vimentin filaments with sparing of microtubules. Biochemical studies revealed that 2,5-hexanedione treatment resulted in high molecular weight vimentin-immunoreactive species, presumably by cross-linking of proteins. Selective action of both acrylamide and 2,5-hexanedione on vimentin filaments and the similarity of effects suggest that a common mechanism of damage may occur whereby these compounds act directly on both vimentin and neurofilaments.

Acrylamide↗
PubMed1997

Mercury compounds and the immune system: a review.

This article reviews the literature data concerning the immunologic monitoring of animals and cell cultures exposed to mercury compounds. Mercury is present in nature as metallic mercury, mono- and bivalent inorganic compounds, and organic alkyl, aryl and alloxy-alkyl compounds. Methylmercury is most important in terms of environmental exposure while metallic mercury is the most common form to which workers are exposed. The database on immune function disturbances in human induced by mercury compounds is limited. Immunotoxicity assessment in animals, mainly in rodents, with subsequent extrapolation to man, is the basis of human risk assessment. The strength of in vitro immunotoxicity testing lies in studies aimed at unravelling mechanisms of immunotoxicity. These experimental investigations show clearly that mercury compounds can have immunomodulating activity. Mercuric chloride and methylmercury inhibit most of animal and human lymphocyte functions including proliferation, expression of cell activation markers on cell surface and cytokine production. These cells exhibit a greater sensitivity to the immunotoxic effects of methylmercury than to mercuric chloride. Repeated administration of mercuric chloride to rats, mice and rabbits can induce autoimmune response and a membranous nephropathy. In contrast, Lewis rats injected with mercuric chloride do not develop autoimmunity but exhibit immunosuppression. The immunosuppressive effects associated with exposure to chemical substances are often accompanied by increased susceptibility to challenge with infectious agents or tumour cells. Only few reports are available on animal studies of increased mortality connected with exposure to mercury compounds and challenge with infectious agents. It is difficult to establish a relationship between the observed immunomodulatory properties of mercury compounds and their possible carcinogenicity. In fact, the epidemiological studies performed so far failed to bring any conclusive evidence of carcinogenicity of mercury in animal experiments. The induction of renal tumours in male rodents by methylmercury was observed only.

Animals↗
PubMed2002

Determination of methylmercury and butyltin compounds in marine biota and sediments using microwave-assisted acid extraction, solid-phase microextraction, and gas chromatography with microwave-induced plasma atomic emission spectrometric detection.

A method is described for the determination of methylmercury and butyltin compounds in marine sediment and tissue using microwave-assisted acid extraction or digestion and solid-phase microextraction (SPME) followed by analysis using gas chromatography with microwave-induced plasma atomic emission spectrometric detection (GC-MIP-AES). Using the SPME-GC-MIP-AES method, enrichment factors for methylmercury and butyltin compounds of 50-100 were achieved, as compared to the typical hexane extraction, and measurements in marine tissue and sediment matrixes were possible at 1-2 microg/kg (methylmercury) and 10-100 ng/kg (butyltins). The SPME-GC-MIP-AES method was validated using several marine sediment and tissue matrix certified reference materials (CRMs) with certified values for methylmercury and butyltin compounds. The SPME-GC-MIP-AES method was used to measure methylmercury in four marine tissue CRMs ranging from oyster tissue at 13.0 +/- 1.0 microg/kg to fish tissue at 397 +/- 13 microg/kg (as Hg dry mass). Results from the SPME-GC-MIP-AES method were used in conjunction with results from other techniques to assign certified values for methylmercury in oyster, mussel, and fish tissue CRMs. Mono-, di-, and tributyltin were measured in three sediment CRMs at concentration levels of (0.08 +/- 0.03)-(0.35 +/- 0.05) mg/kg (as Sn dry mass).

Animals↗