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This review covers the toxicology of mercury and its compounds. Special attention is paid to those forms of mercury of current public health concern. Human exposure to the vapor of metallic mercury dates back to antiquity but continues today in occupational settings and from dental amalgam. Health risks from methylmercury in edible tissues of fish have been the subject of several large epidemiological investigations and continue to be the subject of intense debate. Ethylmercury in the form of a preservative, thimerosal, added to certain vaccines, is the most recent form of mercury that has become a public health concern. The review leads to general discussion of evolutionary aspects of mercury, protective and toxic mechanisms, and ends on a note that mercury is still an \"element of mystery.\"

Whales accumulate mercury (Hg), but do not seem to show immediate evidence of toxic effects. Analysis of different tissues (liver, kidney, muscle) and biofluids (blood, milk) from a pod of stranded long-finned pilot whales ( Globicephala melas ) showed accumulation of Hg as a function of age, with a significant decrease in the MeHg fraction. Isotopic analysis revealed remarkable differences between juvenile and adult whales. During the first period of life, Hg in the liver became isotopically lighter (δ 202 Hg decreased) with a strongly decreasing methylmercury (MeHg) fraction. We suggest this is due to preferential demethylation of MeHg with the lighter Hg isotopes and transport of MeHg to less sensitive organs, such as the muscles. Also changes in diet, with high MeHg intake in utero and during lactation, followed by increasing consumption of solid food contribute to this behavior. Interestingly, this trend in δ 202 Hg is reversed for livers of adult whales (increasing δ 202 Hg value), accompanied by a progressive decrease of δ 202 Hg in muscle at older ages. These total Hg (THg) isotopic trends suggest changes in the Hg metabolism of the long-finned pilot whales, development of (a) detoxification mechanism(s) ( e.g ., though the formation of HgSe particles), and Hg redistribution across the different organs.

Acute toxicity of inorganic mercury [Hg(II)] and methylmercury (MeHg) to Daphnia magna was characterized using a 48-h static, non-renewal acute toxicity test, in which we compared the toxicity of Hg(II) and MeHg in the absence (water-only) and presence of diet [green alga ( Raphidocelis subcapitata ), yeast, Cerophyll, and trout chow (YCT), or both]. Overall, Hg(II) is more toxic to D. magna than MeHg, with 48-h median lethal concentrations (LC50s) being 4.3 µg/L (95% confidence interval: 4.1–4.5 µg/L) for Hg(II) and 14.3 µg/L (13.2–15.3 µg/L) for MeHg. For Hg(II), the addition of any diet would significantly increase its 48-h LC50, but the 48-h LC50 for MeHg decreased significantly to 7.1 µg/L (6.4–7.8 µg/L) with the algal addition. We also show that the addition of diets significantly influenced the levels and speciation (dissolved vs. particulate) of both Hg forms in the test solution. The bioaccumulation of Hg(II) and MeHg was impacted by the dietary addition, and it appears that the body residue level triggering mortality varied widely among treatments. The results suggest that standard short-term toxicity tests (water-only) should be supplemented with extra tests with dietary addition to provide a more environmentally relevant estimation of short-term toxicity of chemical compounds.

Bacterial resistance to inorganic and organic mercury compounds (HgR) is one of the most widely observed phenotypes in eubacteria. Loci conferring HgR in Gram-positive or Gram-negative bacteria typically have at minimum a mercuric reductase enzyme (MerA) that reduces reactive ionic Hg(II) to volatile, relatively inert, monoatomic Hg(0) vapor and a membrane-bound protein (MerT) for uptake of Hg(II) arranged in an operon under control of MerR, a novel metal-responsive regulator. Many HgR loci encode an additional enzyme, MerB, that degrades organomercurials by protonolysis, and one or more additional proteins apparently involved in transport. Genes conferring HgR occur on chromosomes, plasmids, and transposons and their operon arrangements can be quite diverse, frequently involving duplications of the above noted structural genes, several of which are modular themselves. How this very mobile and plastic suite of proteins protects host cells from this pervasive toxic metal, what roles it has in the biogeochemical cycling of Hg, and how it has been employed in ameliorating environmental contamination are the subjects of this review.

Mercury pollution has emerged as a major problem in industrialized zones and presents a serious threat to environment and health of local communities. Effectiveness and wide distribution of mer operon by horizontal and vertical gene transfer in its various forms among large community of microbe reflect importance and compatibility of this mechanism in nature. This review specifically describes mer operon and its generic molecular mechanism with reference to the central role played by merA gene and its related gene products. The combinatorial action of merA and merB together maintains broad spectrum mercury detoxification system for substantial detoxification of mercurial compounds. Feasibility of mer operon to coexist with antibiotic resistance gene ( amp r , kan r , tet r ) clusters enables extensive adaptation of bacterial species to adverse environment. Flexibility of the mer genes to exist as intricate part of chromosome, plasmids, transposons, and integrons enables high distribution of these genes in wider microbial gene pool. Unique ability of this system to manipulate oligodynamic property of mercurial compounds for volatilization of mercuric ions (Hg 2+ ) makes it possible for a wide range of microbes to tolerate mercury-mediated toxicity.

Hyperammonemia is a metabolic condition characterized by elevated levels of ammonia and a common event in acute liver injury/failure and chronic liver disease. Even though hepatic ammonia levels are potential predictive factors of patient outcome, easy and inexpensive methods aiming at the detection of liver ammonia accumulation in the clinical setting remain unavailable. Thus, herein we have developed a morphological method, based on the utilization of Nessler´s reagent, to accurately and precisely detect the accumulation of ammonia in biological tissue. We have validated our method against a commercially available kit in mouse tissue samples and, by using this modified method, we have confirmed the hepatic accumulation of ammonia in clinical and animal models of acute and chronic advanced liver injury as well as in the progression of fatty liver disease. Overall, we propose a morphological method for ammonia detection in liver that correlates well with the degree of liver disease severity and therefore can be potentially used to predict patient outcome.

We evaluated associations between total mercury (Hg) concentrations in blood and skin and endocrine, hepatic, renal, and hematological parameters in free-ranging bottlenose dolphins ( Tursiops truncatus ). Dolphins in Indian River Lagoon, FL had higher concentrations of Hg in blood (0.67 μg/l wet wt) and skin (7.24 μg/g dry wt) compared with those from Charleston Harbor, SC (0.15 μg/l wet wt, 1.68 μg/g dry wt). An inverse relationship was observed between blood and skin Hg concentrations and total thyroxine, triiodothyronine, absolute numbers of lymphocytes, eosinophils, and platelets. Adrenocorticotropic hormone (ACTH), blood urea nitrogen, and gamma-glutamyl transferase increased with increasing concentrations of Hg in blood and skin; lactate dehydrogenase and neutrophils increased with concentrations in skin only. Hemoglobin and mean corpuscular hemoglobin increased with increasing concentrations of Hg in blood. Selenium was negatively associated with free T4, progesterone, and absolute numbers of monocytes, and positively correlated with absolute numbers of eosinophils and lymphocytes, and mean corpuscular volume. The results suggest the potential for a deleterious effect of Hg in highly exposed dolphins.

Kynurenic acid (KYNA) is one of the metabolites of evolutionary conserved tryptophan (Trp)/kynurenine (Kyn) metabolic pathway. Elevation of KYNA contributes to development of psychosis in schizophrenia but attenuates neurodegeneration in Drosophila model of Huntington’s disease. We have reported that KYNA increased lethality of pupae of wild-type flies, but not of vermilion ( v ) mutants with impaired formation of Kyn from Trp, suggesting that KYNA toxicity depends on its interaction with downstream Kyn metabolites [i.e., 3-hydroxykynurenine (3-HK) and/or xanthurenic acid (XA)]. The present study aimed to further explore the mechanisms of KYNA-induced lethality by the assessment of KYNA effect on pupae of two Drosophila mutants: cinnabar ( cn ), characterized by higher KYNA and lower 3-HK production, and cardinal ( cd ), characterized by higher 3-HK and XA levels compared to wild-type flies. Our microarray datamining revealed that the gene expression pattern of enzymes forming Trp/Kyn pathway stands in line with previously reported developmental changes in KYNA, 3-HK, and XA concentrations in wild-type and mutant flies. Administration of KYNA increased pupae lethality in cd , but not in cn mutants. Present data suggest that toxic effect of exogenous KYNA depends on the presence of 3-HK and/or XA. This is further supported by our finding that early stages of Drosophila development are associated with a positive expression pattern of genes encoding sulfotransferases, enzymes that are inhibited by KYNA and are involved in detoxification of XA. Alternatively, the toxic effect of KYNA might depend on anti-proliferative effects of KYNA.

A eukaryotic microalga, Chlorella sp. DT, was transformed with the Bacillus megaterium strain MB1 merA gene, encoding mercuric reductase (MerA), which mediates the reduction of Hg2+ to volatile elemental Hg0. The transformed Chlorella cells were selected first by hygromycin B and then by HgCl2. The existence of merA gene in the genomic DNA of transgenic strains was shown by polymerase chain reaction amplification, while the stable integration of merA into genomic DNA of transgenic strains was confirmed by Southern blot analysis. The ability to remove Hg2+ in merA transgenic strains was higher than that in the wild type. The merA transgenic strains showed higher growth rate and photosynthetic activity than the wild type did in the presence of a toxic concentration of Hg2+. Cultured with Hg2+, the expression level of superoxide dismutase in transgenic strains was lower than that in the wild type, suggesting that the transgenic strains faced a lower level of oxidative stress. All the results indicated that merA gene was successfully integrated into the genome of transgenic strains and functionally expressed to promote the removal of Hg2+.

The aim of this study was to determine the concentration of mercury (Hg) in liver (L), kidney (K), breast muscle [BM ( musculus pectoralis major )], breast feathers (BF), and stomach contents (SC) of mallard ( Anas platyrhynchos L. 1758). Among the edible parts of mallard, the greatest concentrations of Hg were observed in K and L, although they did not exceed 1.5 mg/kg dry weight (dw). Average concentrations in K, L, and BM were 0.27, 0.25, and 0.13 mg/kg dw, respectively. Significant correlations were observed between Hg concentrations in BM and K and in BM and L ( r s  = 0.92) as well as between Hg concentrations in these tissues and BF. In addition, we found significant correlations between Hg concentrations in SC and BM ( r s  = 0.72) and in L and K ( r s  = 0.55). In conclusion, mallard exhibits a measurable response to environmental Hg pollution and meets the requirements of a bioindicator.