The aging kidney and the nephrotoxic effects of mercury.

Owing to advances in modern medicine, life expectancies are lengthening and leading to an increase in the population of older individuals. The aging process leads to significant alterations in many organ systems, with the kidney being particularly susceptible to age-related changes. Within the kidney, aging leads to ultrastructural changes such as glomerular and tubular hypertrophy, glomerulosclerosis, and tubulointerstitial fibrosis, which may compromise renal plasma flow (RPF) and glomerular filtration rate (GFR). These alterations may reduce the functional reserve of the kidneys, making them more susceptible to pathological events when challenged or stressed, such as following exposure to nephrotoxicants. An important and prevalent environmental toxicant that induces nephrotoxic effects is mercury (Hg). Since exposure of normal kidneys to mercuric ions might induce glomerular and tubular injury, aged kidneys, which may not be functioning at full capacity, may be more sensitive to the effects of Hg than normal kidneys. Age-related renal changes and the effects of Hg in the kidney have been characterized separately. However, little is known regarding the influence of nephrotoxicants, such as Hg, on aged kidneys. The purpose of this review was to summarize known findings related to exposure of aged and diseased kidneys to the environmentally relevant nephrotoxicant Hg.

Mechanisms involved in the transport of mercuric ions in target tissues.

Mercury exists in the environment in various forms, all of which pose a risk to human health. Despite guidelines regulating the industrial release of mercury into the environment, humans continue to be exposed regularly to various forms of this metal via inhalation or ingestion. Following exposure, mercuric ions are taken up by and accumulate in numerous organs, including brain, intestine, kidney, liver, and placenta. In order to understand the toxicological effects of exposure to mercury, a thorough understanding of the mechanisms that facilitate entry of mercuric ions into target cells must first be obtained. A number of mechanisms for the transport of mercuric ions into target cells and organs have been proposed in recent years. However, the ability of these mechanisms to transport mercuric ions and the regulatory features of these carriers have not been characterized completely. The purpose of this review is to summarize the current findings related to the mechanisms that may be involved in the transport of inorganic and organic forms of mercury in target tissues and organs. This review will describe mechanisms known to be involved in the transport of mercury and will also propose additional mechanisms that may potentially be involved in the transport of mercuric ions into target cells.

Organic and inorganic mercurials have distinct effects on cellular thiols, metal homeostasis, and Fe-binding proteins in Escherichia coli.

The protean chemical properties of the toxic metal mercury (Hg) have made it attractive in diverse applications since antiquity. However, growing public concern has led to an international agreement to decrease its impact on health and the environment. During a recent proteomics study of acute Hg exposure in E. coli, we also examined the effects of inorganic and organic Hg compounds on thiol and metal homeostases. On brief exposure, lower concentrations of divalent inorganic mercury Hg(II) blocked bulk cellular thiols and protein-associated thiols more completely than higher concentrations of monovalent organomercurials, phenylmercuric acetate (PMA) and merthiolate (MT). Cells bound Hg(II) and PMA in excess of their available thiol ligands; X-ray absorption spectroscopy indicated nitrogens as likely additional ligands. The mercurials released protein-bound iron (Fe) more effectively than common organic oxidants and all disturbed the Na(+)/K(+) electrolyte balance, but none provoked efflux of six essential transition metals including Fe. PMA and MT made stable cysteine monothiol adducts in many Fe-binding proteins, but stable Hg(II) adducts were only seen in CysXxx(n)Cys peptides. We conclude that on acute exposure: (a) the distinct effects of mercurials on thiol and Fe homeostases reflected their different uptake and valences; (b) their similar effects on essential metal and electrolyte homeostases reflected the energy dependence of these processes; and (c) peptide phenylmercury-adducts were more stable or detectable in mass spectrometry than Hg(II)-adducts. These first in vivo observations in a well-defined model organism reveal differences upon acute exposure to inorganic and organic mercurials that may underlie their distinct toxicology.

[Bibliographical study of the toxicity of organic mercury compounds].

OBJECTIVES: The aim of this study is to correct the misunderstanding that the toxicity of organic mercury compounds is unknown at the time of the outbreak of Minamata disease (May 1, 1956). RESULTS AND DISCUSSION: Two case reports of organic mercury (methylmercury) intoxication were published already in 1865 and 1866. The conversion of inorganic mercury added in acetoaldehyde synthesis was already pointed out in 1921. In 1930 several cases of organic mercury poisoning among workers engaged in acetoaldehyde production were reported. Many reports on not only in occupational exposure but a oral exposure via the ingestion of flour made from grains treated with organic mercurials were available at the time of the outbreak of Minamata disease (May 1, 1956). These reports pointed out the toxic effects of organic mercury on the central nervous system, and indicated cleary that the causal substance of Minamata disease must be the organic mercury compounds (methylmercury) from the Chisso plant. The identification of methylmercury as the causal substance by the authority was presented in 1968 when acetoaldehyde production in the Chisso plant was closed. Most of these reports except that of (Hunter et al.) were not referred to in the study of Minamata disease . Inadequate referencing should be pointed out. CONCLUSION: Several reports indicated that the causal substance of Minamata disease must be methylmercury from the Chisso Plant. However, most of these reports were not referred to during the study of Minamata disease. Inadequate referencing of literatures should be pointed out.

The Irrawaddy dolphin, Orcaella brevirostris from the Mekong river Cambodia: Preliminary health and toxicological investigations.

The subpopulation of the Irrawaddy dolphin (Orcaella brevirostris) living in the Mekong River, Cambodia, is considered to be critically endangered. The aim of the investigation was to gain information about the genetic variation, health status and exposure to toxic compounds of these dolphins. Tissue samples from 27 Irrawaddy river dolphins found dead along the Mekong River between 2004 and 2009 were analysed with regards to genetics, pathology and ecotoxicology. Genetic maternal lineage detection, based on polymorphisms of the mitochondrial d-loop sequences, was performed. Data indicate a genetic separation of the Mekong dolphins from both the coastal population and the Mahakam dolphins. Pathological investigations revealed acute moderate multifocal suppurative bronchopneumonia, moderate periportal hepatic lipidosis, moderate diffuse hepatic atrophy and acute severe diffuse suppurative leptomeningitis. Residue levels of organochlorines and polybrominated diphenyl ethers in Irrawaddy dolphins from the Mekong River were lower than the concentrations reported for other cetaceans in the coastal and riverine waters of Asia, except for Dichlorodiphenyltrichloroethane. A high percentage of organic mercury compared to the immuno-toxic methylmercury was observed. Due to numerous confounding factors, it is not possible to relate levels of pollutants to observed morphological lesions. However, it is likely that chemical contaminants do adversely impact on the health of the Irrawaddy dolphins at present, and have also affected previous generations.

Scopoli's work in the field of mercurialism in light of today's knowledge: past and present perspectives.

The Idrija Mercury Mine (1490-1994) appointed its first physician, Joannes Antonius Scopoli, in 1754. Most of his descriptions of mercurialism are still relevant today. This study highlights Scopoli's observations on the interaction between elemental mercury (Hg degrees ) and alcohol, on the appearance of lung impairment, insomnia, and depressive mood in mercurialism. This presentation is based on Scopoli's experiences presented in his book, De Hydrargyro Idriensi Tentamina (1761), current knowledge, and our own experience acquired through health monitoring of occupational Hg degrees exposure. Some studies have confirmed Scopoli's observation that alcohol enhances mercurialism and his hypothesis that exposure to high Hg degrees concentrations causes serious lung impairment. Neurobiological studies have highlighted the influence of Hg degrees on sleep disorder and depressive mood observed by Scopoli. Although today's knowledge provides new perspectives of Scopoli's work on mercurialism, his work is still very important and can be considered a part of occupational medicine heritage.

Revision of reciprocal action of mercury and selenium.

Diverse forms of mercury (Hg) have various effects on animals and humans because of a variety of routes of administration. Inorganic mercury (iHg) binds to thiol groups of proteins and enzymes in one's body or is methylated by microorganisms. Organic form of Hg, contrary to the iHg, is more stable but may be demethylated to Hg2+ in the tissue of intestinal flora. Selenium (Se) also occurs in a variety of chemical forms in one's body but both of these elements behave very differently from one another. Mercury binding to selenide or Se-containing ligands is a primary molecular mechanism that reduces toxicity of Hg. Complexes formed in such a way are irreversible, and thus, biologically inactive. Se deficiency in a human body may impair normal synthesis of selenoproteins and its expression because expression of mRNA may be potentially regulated by the Se status. This paper provides a comprehensive review concerning Hg-Se reciprocal action as a potential mechanism of protective action of Se against Hg toxicity as well as a potential detoxification mechanism. Although interactions between Hg-Se have been presented in numerous studies concerning animals and humans, we have focused mainly on animal models so as to understand molecular mechanisms responsible for antagonism better. The review also investigates what conclusions have been drawn by researchers with respect to the chemical species of Se and Hg (and their relationship) in biological systems as well as genetic variations and expression and/or activity of selenoproteins related to the thioredoxin (thioredoxin Trx/TrxR) system and glutathione metabolism. Int J Occup Med Environ Health 2018;31(5):575-592.

Versatile mercury-resistant cloning and expression vectors.

Cloning vectors have been constructed employing two diverse replicons, IncQ and P15A. Both vectors confer resistance to kanamycin (Km) and mercuric ions (Hg2+). One of these vectors, pDG105, is a broad-host-range, nonconjugative, oligocopy IncQ plasmid, which is capable of transforming Escherichia coli, Acinetobacter calcoaceticus, and Pseudomonas putida. The second vector, pDG106, is a narrow-host-range, multicopy cloning vector compatible with pBR322. Both vectors contain unique cloning sites in the Km-resistance gene for HindIII, SmaI, and XhoI, as well as unique EcoRI and ScaI sites in the mer operon. Cloning into the EcoRI site in the mer operon results in the mercury "supersensitive" phenotype, easily detectable by replica plating. Insertion of the galK gene into the EcoRI site in the mer operon results in Hg2+-inducible galactokinase activity, demonstrating the application of these plasmids as regulated expression vectors.

Physical and genetic map of the organomercury resistance (Omr) and inorganic mercury resistance (Hgr) loci of the IncM plasmid R831b.

Tn7 insertion mutagenesis has been used to facilitate the generation of a physical (restriction endonuclease) and genetic map of the IncM plasmid, R831b. The only selectable phenotypes carried by this 90-kb conjugative plasmid are resistances to inorganic mercury [Hg(II)] and to organomercury compounds. Mutants in the Hgr locus of R831b complemented previously described mutants in the mer operon of the IncFII plasmid R100, indicating functional homology of the locus in each of these different plasmids. However, the R831b Hgr locus is not notably similar in restriction site pattern to either the mer operon of R100 or the mercury resistance transposon, Tn501. Although the enzymes they encode are co-ordinately regulated, the Omr locus of R831b maps approx. 13.5 kb away from the Hgr locus. Three insertions which affect neither phenotype lie between the Hgr and Omr loci; thus, the loci are separated both physically and genetically. One mutant was obtained which tentatively identifies the position of the Tra locus of R831b as adjacent to the Hgr locus.

Chemical induction of nondisjunction in drosophila.

Tests for chemically induced nondisjunction and loss of the sex chromosomes in Drosophila were performed. Of 31 compounds tested four gave rise only to an increase of XO exceptions, indicating the induction of chromosome loss. Six compounds, all known spindle inhibitors (colchicine, organic mercury, lead, and tin compounds) gave rise to an increase both of XXY and XO or of only XXY. The effect by metalloorganic compounds of which methylmercury was studied particularly closely, follows a peculiar pattern. In females with structurally normal X chromosomes only an increase of XX gametes is obtained, while with X chromosomes heterozygous for long inversions only O gametes are increased. The data indicates that the effect of the metal compounds occurs at first meiosis and that the process is connected with a meiotic drive, giving rise to a preferential segregation of the two X chromosomes to the functioning pole. The increase only of O gametes with structurally heterozygous X chromosomes can tentatively be explained by a loss due to crossing over within the inversion. An increase of the effect of methyl mercury was obtained where the normal pairing of the X chromosomes was interfered with by means of autosomal inversions. Likewise a synergistic increase of nondisjunction was obtained when a temperature chock of 10 degrees C was applied together with treatment with methylmercury. It is concluded that chemical induction of nondisjunction can be studied in Drosophila, but the sensitivity of the test is rather low and large amount of material is required.

Toxicity of mercury.

A ruling by the European Union heralds the demise of those useful clinical instruments, the mercury thermometer and the mercury sphygmomanometer. The new laws have been passed because of worries about mercury poisoning. Yet you can drink metallic mercury and come to no harm. What does it all mean? There are three forms of mercury from a toxicological point of view: inorganic mercury salts; organic mercury compounds; and metallic mercury. Inorganic mercury salts are water soluble, irritate the gut, and cause severe kidney damage. Organic mercury compounds, which are fat soluble, can cross the blood brain barrier and cause neurological damage. Mercury metal poses two dangers. It can be vaporised: the vapour pressure at room temperature is about 100 times the safe amount, so poisoning can occur if mercury metal is spilled into crevices or cracks in the floorboards. Dentists are occasionally poisoned this way. Mercury easily crosses into the brain, and causes tremor, depression, and behavioural disturbances. A second danger from metallic mercury is that it is biotransformed into organic mercury, by bacteria at the bottom of lakes. This can be passed along the food chain and eventually to man. It was this process that led to the Japanese tragedy at Minimata Bay in the late 1950s when over 800 people were poisoned. It is the need to reduce mercury contamination of the environment which should encourage us to cut the usage of metallic mercury. However, much more metallic mercury is spilled as waste by the chemical industry than is dropped on the floor in the clinic.

Organomercury(II) complexes of kojic acid and maltol: synthesis, characterization, and biological studies.

A number of organomercury(II) complexes of kojic acid (HL1, I) and maltol (HL2, II) of the type p-XC6H4HgL1 (III) and p-XC6H4HgL2 (IV) [X = Me, MeO, NO2] have been synthesized and characterized. [formula: see text] Conductance measurements indicate the nonelectrolyte behavior of the complexes. From IR and UV studies, the bonding modes of the ligands to the organomercury(II) moieties have been elucidated. The 1H and 13C NMR spectra support the stoichiometry of the complexes. The fragmentation pattern has been analyzed on the basis of mass spectra. From thermal studies (TG and DTA), various kinetic and thermodynamic parameters for thermal degradation have been enumerated. The complexes have been screened against some pathogenic bacterial strains. The bactericidal activity has been correlated with the thermal data.

In vitro cyto- and genotoxicity of organomercurials to cells in culture.

The sequence of cytotoxic effects for a series of mercury compounds to the BG/F epithelioid cells derived from fin tissue of bluegill sunfish was phenyl mercuric chloride greater than methyl mercuric chloride greater than ethyl mercuric chloride much greater than mercuric chloride. This sequence of in vitro cytotoxicity was similar to that observed in a 48-h LC50 in vivo acute toxicity assay with rainbow trout. Using induction of micronuclei as an indicator of genetic damage, the organomercurials, but not mercuric chloride, were noted to be clastogenic to the BG/F cells.

Mutagenicity and teratogenicity of mercury compounds.

Agriculture, consumption of fossil fuels and, to a lesser extent, industry, are the main sources of pollution by mercury which is discharged into the environment as metallic mercury, as inorganic mercury compounds, or as organic compounds. Once in the environment, mercury compounds are capable of a variety of transformations. Some professional or accidental mercury poisonings have been reported in human populations, but they can easily be minimized by appropriate preventive measures. Production of C-mitosis in plant material is the most noticeable genetic effect of mercury compounds. No positive report that mercury could be carcinogenic in man has appeared up to now and animal experiments have also provided negative results. Although placenta may represent a certain barrier to mercury, embryotoxicity and teratogenicity of organic mercury compounds have been observed in numerous systems such as fish, birds and mammals.

Potentiating effects of organomercuries on clastogen-induced chromosome aberrations in cultured Chinese hamster cells.

Mercury compounds are among the most serious environmental pollutants. In this communication, the potentiating effects of organic and inorganic mercuries on clastogen-induced chromosome aberrations were studied in Chinese hamster CHO K1 cells. Post-treatment with monoalkylated mercuries--methyl mercuric chloride (MeHgCl) and ethyl mercuric chloride (EtHgCl)--increased the number of breakage- and exchange-type aberrations induced by 4-nitroquinoline 1-oxide (4NQO) and methyl methanesulfonate. With the DNA crosslinking agents mitomycin C (MMC) and cisplatin, MeHgCl enhanced both types of aberrations while EtHgCl enhanced breakage-type aberrations only. Since these monoalkylated mercuries did not show clastogenic effects by themselves under the present experimental conditions, the increases in chromosome aberrations were not additive. Dialkylated mercuries (dimethyl mercury and diethyl mercury) and inorganic mercuries (HgCl and HgCl2) did not show any potentiating effects. When MMC- or 4NQO-treated cells were post-treated with MeHgCl during the G1 phase, both breakage- and exchange-type aberrations were enhanced. Treatment with EtHgCl during the G1 phase also enhanced both types of aberrations induced by 4NQO. With MMC, however, G1 treatment with EtHgCl did not show any potentiating effect. MeHgCl and EtHgCl treatments during the G2 phase enhanced breakage-type aberrations only. Based on these results, the following possible mechanisms for potentiation of clastogenicity by monoalkylated mercuries were suggested; (1) they interfere with repair of base lesions induced by 4NQO and MMS during the pre-replicational stage, thereby increasing unrepaired DNA lesions which convert into DNA double-strand breaks in S phase, (2) MeHgCl (but not EtHgCl) also inhibits repair of crosslinking lesions during the pre-replicational stage, and (3) their G2 effects enhance breakage-type aberrations only.

Simultaneous experimental study of direct and direct plus trophic contamination of the crayfish Astacus astacus by inorganic mercury and methylmercury.

An experimental study was carried out to investigate direct and direct plus trophic contamination routes of the crayfish Astacus astacus by inorganic mercury (Hg(II)) or methylmercury (MeHg). Direct exposure was based on low contamination conditions, 300 and 30 ng/L in the dissolved phase, respectively, during 30 d at 20 degrees C. Trophic exposure was based on daily consumption of the Asiatic clam Corbicula fluminea, previously contaminated during 40 d with similar exposure conditions. The Hg concentrations in the bivalves were very similar: 1,451 +/- 287 ng/g for Hg(II) and 1,346 +/- 143 ng/g for MeHg. In the crustaceans, Hg bioaccumulation was analyzed at the whole-organism level and in eight organs (gills, stomach, intestine, hepatopancreas, tail muscle, green gland, carapace, and hemolymph), after 15 and 30 d of exposure. Analysis of the results showed marked differences between Hg(II) and MeHg accumulation in favor of MeHg: for the direct route, the ratio between metal concentrations was close to 8; for the trophic route, no significant increase in Hg accumulation was observed for Hg(II) even when the ratio between Hg concentration in the direct plus trophic contamination route and Hg concentration in the direct contamination route was 1.6 for MeHg, with an estimated trophic transfer rate close to 20%. Mercury organotropism was also specifically connected to the exposure conditions, especially at the biological barrier level according to the route of exposure: gills and carapace for the direct route and digestive tract including hepatopancreas for the trophic route.

Inverse relationship between bioconcentration factor and exposure concentration for metals: implications for hazard assessment of metals in the aquatic environment.

The bioconcentration factor (BCF) and bioaccumulation factor (BAF) are used as the criteria for bioaccumulation in the context of identifying and classifying substances that are hazardous to the aquatic environment. The BCF/BAF criteria, while developed as surrogates for chronic toxicity and/or biomagnification of anthropogenic organic substances, are applied to all substances including metals. This work examines the theoretical and experimental basis for the use of BCF/BAF in the hazard assessment of Zn, Cd, Cu, Pb, Ni, and Ag. As well, BCF/BAFs for Hg (methyl and inorganic forms) and hexachlorobenzene (HCB) were evaluated. The BCF/BAF data for Zn, Cd, Cu, Pb, Ni, and Ag were characterized by extreme variability in mean BCF/BAF values and a clear inverse relationship between BCF/BAF and aqueous exposure. The high variability persisted when even when data were limited to an exposure range where chronic toxicity would be expected. Mean BCF/BAF values for Hg were also variable, but the inverse relationship was equivocal, in contrast with HCB, which conformed to the BCF model. This study illustrates that the BCF/BAF criteria, as currently applied, are inappropriate for the hazard identification and classification of metals. Furthermore, using BCF and BAF data leads to conclusions that are inconsistent with the toxicological data, as values are highest (indicating hazard) at low exposure concentrations and are lowest (indicating no hazard) at high exposure concentrations, where impacts are likely. Bioconcentration and bioaccumulation factors do not distinguish between essential mineral nutrient, normal background metal bioaccumulation, the adaptive capabilities of animals to vary uptake and elimination within the spectrum of exposure regimes, nor the specific ability to sequester, detoxify, and store internalized metal from metal uptake that results in adverse effect. An alternative to BCF, the accumulation factor (ACF), for metals was assessed and, while providing an improvement, it did not provide a complete solution. A bioaccumulation criterion for the hazard identification of metals is required, and work directed at linking chronic toxicity and bioaccumulation may provide some solutions.

The neurotoxicology and pathology of organomercury, organolead, and organotin.

The toxicities of many metals, such as mercury and lead, are known to man since the dawn of civilization. Organic compounds of some heavy metals are known to have a particular toxic impact on the central nervous system. Organomercury, particularly alkyl-mercuric compounds (e.g. methylmercury), has a selective effect on the granule cells of the cerebellum, the nerve cells of the calcarine cortex, and the sensory neurons in the dorsal root ganglia. The well known Minamata Bay disease is the result of a massive epidemic episode of human exposure to alkylmercury contaminated food sources. Mental retardation and other developmental defects are also known to be a consequence of exposure to this toxic metal. Organic lead compounds have been employed as gasoline additives and in other industrial purposes. Unlike its inorganic counterpart, organolead compounds have a more prominent impact on the central nervous system. Pathological changes of the brain stem neurons have been described. Organotin compounds have been used in plastic industries and as agricultural chemicals. Both trimethyl and triethyl tin compounds are found to be extremely neurotoxic. Despite the similarity of their chemical structures, trimethyl and triethyl tins have a diversely different toxic property and effects. While triethyl tin is myelinotoxic, producing edematous and vacuolar changes in the central myelin, trimethyl tin is neurotoxic, producing prominent toxic changes in the neurons of the limbic system (hippocampus, entorhinal cortex, etc.). The factors which determine the specificity and selectivity of the neurotoxic impacts by various organometals are still unknown. In view that most of the organometals are still widely employed by many countries for industrial and for agricultural purposes, caution must be made for their proper handling and disposure to avoid undesirable exposures to workers and environmental contamination of water sources and food-chain for the common public. Since organometals are difficult to eliminate from the central nervous system, injuries usually lead to permanent neurological deficits, such tragedies are frequently long lasting and create not only a medical problem, but also a social economical problem for the society.

[History of ignorance of methylmercury toxicity and intoxication in Japan in relation to Minamata disease].

The first reports of methylmercury intoxication appeared in 1865 and 1866. These reports had sensational effects in European countries, and were introduced not only in journals but also in newspapers. These two reports were referable in Japan at the latest in 1927. The formation of organic mercury in the production of acetoaldehyde was also referable in 1906 in Japan. In 1931 (one year before the start of acetoaldehyde production in Minamata) these important reports cited above were referable in Kumamoto University, and there were warnings about the toxicity of organic mercury and environmental pollution prior to the start of acetoaldehyde production. However, not only the plant, authorities (Ministry of Welfare), and Kumamoto Prefectural Office, but also the scientists completely ignored these reports. Waste was dumped into the environment without any treatment. Serious pollution of the environment by organic mercury started, which resulted in the outbreak of Minamata disease (=methylmercury intoxication).

Risks associated with the transfer of toxic organo-metallic mercury from soils into the terrestrial feed chain.

Although the transfer of organo-metallic mercury (OrgHg) in aquatic food webs has long been studied, it has only been recently recognized that there is also accumulation in terrestrial systems. There is still however little information about the exposure of grazing animals to OrgHg from soils and feed as well as on risks of exposure to animal and humans. In this study we collected 78 soil samples and 40 plant samples (Lolium perenne and Brassica juncea) from agricultural fields near a contaminated industrial area and evaluated the soil-to-plant transfer of Hg as well as subsequent trophic transfer. Inorganic Hg (IHg) concentrations ranged from 0.080 to 210mgkg(-1) d.w. in soils, from 0.010 to 84mgkg(-1) d.w. in roots and from 0.020 to 6.9mgkg(-1) d.w. in shoots. OrgHg concentrations in soils varied between 0.20 and 130µgkg(-1) d.w. representing on average 0.13% of the total Hg (THg). In root and shoot samples OrgHg comprised on average 0.58% (roots) and 0.66% (shoots) of THg. Average bioaccumulation factors (BAFs) for OrgHg in relation to soil concentrations were 3.3 (for roots) and 1.5 (for shoots). The daily intake (DI) of THg in 33 sampling sites exceeded the acceptable daily intake (ADI) of THg of both cows (ADI=1.4mgd(-1)) and sheep (ADI=0.28mgd(-1)), in view of food safety associated with THg in animal kidneys. Estimated DI of OrgHg for grazing animals were up to 220µgd(-1) (for cows) and up to 33µgd(-1) (for sheep). This study suggested that solely monitoring the levels of THg in soils and feed may not allow to adequately taking into account accumulation of OrgHg in feed crops and properly address risks associated with OrgHg exposure for animals and humans. Hence, the inclusion of limits for OrgHg in feed quality and food safety legislation is advised.