Antifungal chemosensitization through induction of oxidative stress: A model for control of candidiasis based on the Lippia origanoides essential oil.

In this work, evaluated the antifungal chemosensitizing effect of the Lippia origanoides essential oil (EO) through the induction of oxidative stress. The EO was obtained by hydrodistillation and analyzed by GC-MS. To evaluate the antifungal chemosensitizing effect through induction of oxidative stress, cultures of the model yeast Saccharomyces cerevisiae ∆ycf1 were exposed to sub-inhibitory concentrations of the EO, and the expression of genes known, due be overexpressed in response to oxidative and mutagenic stress was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR) method. Carvacrol and thymol were identified as the main components. The EO was effective in preventing or reducing the growth of the microorganisms tested. The gene expression profiles showed that EO promoted changes in the patterns of expression of genes involved in oxidative and mutagenic stress resistance. The combined use of the L. origanoides EO with fluconazole has been tested on Candida yeasts and the strategy resulted in a synergistic enhancement of the antifungal action of the azolic chemical product. Indeed, in association with EO, the fluconazole MICs dropped. Thus, the combinatorial use of L. origanoides EO as a chemosensitizer agent should contribute to enhancing the efficiency of conventional antifungal drugs, reducing their negative side effects.

Toxicity of the herbicides used on herbicide-tolerant crops, and societal consequences of their use in France.

In France, the implementation of mutant herbicide-tolerant crops and the use of the related herbicides - sulfonylureas and imidazolinones - have triggered a strong societal reaction illustrated by the intervening actions of environmentalist groups illegally mowing such crops. Trials are in progress, and therefore should be addressed the questions of the environmental risks and the toxicity of these herbicides for the animals and humans consuming the products derived from these plants. Regulatory authorities have allowed these mutant and herbicide-tolerant plants arguing that the herbicides against which they resist only target an enzyme found in 'weeds' (the acetolactate synthase, ALS), and that therefore all organisms lacking this enzyme would be endowed with immunity to these herbicides. The toxicological literature does not match with this argument: 1) Even in organisms displaying the enzyme ALS, these herbicides impact other molecular targets than ALS; 2) These herbicides are toxic for animals, organisms that do not possess the enzyme ALS, and especially invertebrates, amphibians and fish. In humans, epidemiological studies have shown that the use and handling of these toxins are associated with a significantly increased risk of colon and bladder cancers, and miscarriages. In agricultural soils, these herbicides have a persistence of up to several months, and water samples have concentrations of some of these herbicides above the limit value in drinking water.

Acute Toxicity of Divalent Mercury to Bacteria Explained by the Formation of Dicysteinate and Tetracysteinate Complexes Bound to Proteins in Escherichia coli and Bacillus subtilis.

Bacteria are the most abundant organisms on Earth and also the major life form affected by mercury (Hg) poisoning in aquatic and terrestrial food webs. In this study, we applied high energy-resolution X-ray absorption near edge structure (HR-XANES) spectroscopy to bacteria with intracellular concentrations of Hg as low as 0.7 ng/mg (ppm) for identifying the intracellular molecular forms and trafficking pathways of Hg in bacteria at environmentally relevant concentrations. Gram-positive Bacillus subtilis and Gram-negative Escherichia coli were exposed to three Hg species: HgCl2, Hg-dicysteinate (Hg(Cys)2), and Hg-dithioglycolate (Hg(TGA)2). In all cases, Hg was transformed into new two- and four-coordinate cysteinate complexes, interpreted to be bound, respectively, to the consensus metal-binding CXXC motif and zinc finger domains of proteins, with glutathione acting as a transfer ligand. Replacement of zinc cofactors essential to gene regulatory proteins with Hg would inhibit vital functions such as DNA transcription and repair and is suggested to be a main cause of Hg genotoxicity.

Demethylation of Methylmercury in Bird, Fish, and Earthworm.

Toxicity of methylmercury (MeHg) to wildlife and humans results from its binding to cysteine residues of proteins, forming MeHg-cysteinate (MeHgCys) complexes that hinder biological functions. MeHgCys complexes can be detoxified in vivo, yet how this occurs is unknown. We report that MeHgCys complexes are transformed into selenocysteinate [Hg(Sec)4] complexes in multiple animals from two phyla (a waterbird, freshwater fish, and earthworms) sampled in different geographical areas and contaminated by different Hg sources. In addition, high energy-resolution X-ray absorption spectroscopy (HR-XANES) and chromatography-inductively coupled plasma mass spectrometry of the waterbird liver support the binding of Hg(Sec)4 to selenoprotein P and biomineralization of Hg(Sec)4 to chemically inert nanoparticulate mercury selenide (HgSe). The results provide a foundation for understanding mercury detoxification in higher organisms and suggest that the identified MeHgCys to Hg(Sec)4 demethylation pathway is common in nature.

Gold and silver nanoparticles effects to the earthworm Eisenia fetida - the importance of tissue over soil concentrations.

To address and to compare the respective impact of gold and silver nanoparticles (Au and Ag NPs) in soil invertebrate, the earthworm Eisenia fetida was exposed to soil containing 2, 10, and 50 mg/kg of Au and Ag in both nanoparticulate and ionic forms for 10 days. Both metal NPs were 2-15 times less bioavailable than their ionic forms, and displayed similar transfer coefficients from soil to earthworm tissues. Both metal NPs triggered the onset of an oxidative stress as illustrated by increased glutathione S-transferase levels, decreased catalase levels, and increased malondialdehyde concentrations. Protein carbonylation distinguished the nanoparticular from the ionic forms as its increase was observed only after exposure to the highest concentration of both metal NPs. Au and Ag NPs triggered DNA modifications even at the lowest concentration, and both repressed the expression of genes involved in the general defense and stress response at high concentrations as did their ionic counterparts. Despite the fact that both metal NPs were less bioavailable than their ionic forms, at equivalent concentrations accumulated within earthworms tissues they exerted equal or higher toxic potential than their ionic counterparts.Capsule: At equivalent concentrations accumulated within earthworm tissues Au and Ag NPs exert equal or higher toxic potential than their ionic forms.

Mercury(II) Binding to Metallothionein in Mytilus edulis revealed by High Energy-Resolution XANES Spectroscopy.

Of all divalent metals, mercury (HgII ) has the highest affinity for metallothioneins. HgII is considered to be enclosed in the α and ß domains as tetrahedral α-type Hg4 Cys11-12 and ß-type Hg3 Cys9 clusters similar to CdII and ZnII . However, neither the four-fold coordination of Hg nor the existence of Hg-Hg atomic pairs have ever been demonstrated, and the HgII partitioning among the two protein domains is unknown. Using high energy-resolution XANES spectroscopy, MP2 geometry optimization, and biochemical analysis, evidence for the coexistence of two-coordinate Hg-thiolate complex and four-coordinate Hg-thiolate cluster with a metacinnabar-type (ß-HgS) structure in the α domain of separate metallothionein molecules from blue mussel under in vivo exposure is provided. The findings suggest that the CXXC claw setting of thiolate donors, which only exists in the α domain, acts as a nucleation center for the polynuclear complex and that the five CXC motifs from this domain serve as the cluster-forming motifs. Oligomerization is driven by metallophilic Hg⋅⋅⋅Hg interactions. Our results provide clues as to why Hg has higher affinity for the α than the ß domain. More generally, this work provides a foundation for understanding how metallothioneins mediate mercury detoxification in the cell under in vivo conditions.

Divalent Mercury in Dissolved Organic Matter Is Bioavailable to Fish and Accumulates as Dithiolate and Tetrathiolate Complexes.

The freshwater cyprinid Tanichthys albonubes was used to assess the bioavailability of divalent mercury (Hg(II)) complexed in dissolved organic matter (DOM) to fish. The fish acquired 0.3 to 2.2 µg Hg/g dry weight after 8 weeks in aquaria containing DOM from a Carex peat with complexed mercury at initial concentrations of 14 nM to 724 nM. Changes in the relative proportions of dithiolate Hg(SR)2 and nanoparticulate ß-HgS in the DOM, as quantified by high energy-resolution XANES (HR-XANES) spectroscopy, indicate that Hg(SR)2 complexes either produced by microbially induced dissolution of nanoparticulate ß-HgS in the DOM or present in the original DOM were the forms of mercury that entered the fish. In the fish with 2.2 µg Hg/g, 84 ± 8% of Hg(II) was bonded to two axial thiolate ligands and one or two equatorial N/O electron donors (Hg[(SR)2+(N/O)1-2] coordination), and 16% had a Hg(SR)4 coordination, as determined by HR-XANES. For comparison, fish exposed to Hg2+ from 40 nM HgCl2 contained 10.4 µg Hg/g in the forms of dithiolate (20 ± 10%) and tetrathiolate (23 ± 10%) complexes, and also Hg xS y clusters (57 ± 15%) having a ß-HgS-type local structure and a dimension that exceeded the size of metallothionein clusters. There was no evidence of methylmercury in the fish or DOM within the 10% uncertainty of the HR-XANES. Together, the results indicate that inorganic Hg(II) bound to DOM is a source of mercury to biota with dithiolate Hg(SR)2 complexes as the immediate species bioavailable to fish, and that these complexes transform in response to cellular processes.

Emerging human pathogen Acinetobacter baumannii in the natural aquatic environment: a public health risk?

Bacterium Acinetobacter baumannii is an emerging human pathogen whose presence in the aquatic environment raises the issue of public health risk. Fish colonization represents the potential route of pathogen transmission to humans. The aim was to examine the colonization of A. baumannii to freshwater fish Poecilia reticulata. An extensively drug-resistant A. baumannii was tested at three concentrations in natural spring water. Additionally, 70 fish from the Sava River (Croatia) were screened for the presence of A. baumannii, which was not found in gill swabs or analysed gut. The colonization potential of A. baumannii in freshwater fish is dependent upon its concentration in surrounding water. The low concentration of A. baumannii in natural waters represents low colonization potential of freshwater fish. The risk for public health exists in closed water bodies where there is constant inflow of water polluted by A. baumannii in concentrations above 3 log CFU mL-1.

Chemical Forms of Mercury in Human Hair Reveal Sources of Exposure.

Humans are contaminated by mercury in different forms from different sources. In practice, contamination by methylmercury from fish consumption is assessed by measuring hair mercury concentration, whereas exposure to elemental and inorganic mercury from other sources is tested by analysis of blood or urine. Here, we show that diverse sources of hair mercury at concentrations as low as 0.5 ppm can be individually identified by specific coordination to C, N, and S ligands with high energy-resolution X-ray absorption spectroscopy. Methylmercury from seafood, ethylmercury used as a bactericide, inorganic mercury from dental amalgams, and exogenously derived atmospheric mercury bind in distinctive intermolecular configurations to hair proteins, as supported by molecular modeling. A mercury spike located by X-ray nanofluorescence on one hair strand could even be dated to removal of a single dental amalgam. Chemical forms of other known or putative toxic metals in human tissues could be identified by this approach with potential broader applications to forensic, energy, and materials science.

Danio rerio ABC transporter genes abcb3 and abcb7 play a protecting role against metal contamination.

ATP-binding cassette (ABC) proteins are efflux transporters and some of them are involved in xenobiotic detoxification. The involvement of four zebrafish ABC transporters in cadmium, zinc and mercury detoxification was characterized in a metal hypersensitive mutant of Escherichia coli. The E. coli tolC mutant expressing ABCB3 or ABCB7 transporters exhibited higher survival ratios and lower metal accumulation under a metal exposure condition than the controls. For instance, in the presence of 8 and 10 µM of HgCl2 , the survival ratios of bacteria expressing ABCB3 were four and six-times higher than the control whereas the mercury concentrations were 2.5 and 2-times lower than in the control. This work provides new data on the function of zebrafish ABCB3 and ABCB7 transporters and highlights their significance in metal detoxification. Copyright © 2016 John Wiley & Sons, Ltd.

Transcriptomic, Biochemical, and Histopathological Responses of the Clam Ruditapes decussatus from a Metal-Contaminated Tunis Lagoon.

This study was designed to investigate the molecular (transcriptional expression), biochemical (oxidative stress and neurotoxicity), and histopathological effects of metal contamination in the gill of clams (Ruditapes decussatus) sampled from the Tunis lagoon. The concentrations of five heavy metals (Cd, Pb, Hg, Cu, and Zn) in surface sediments and their accumulation in soft tissues of R. decussatus were evaluated in three sites (Z1, Z2, and Z3). A metal contamination state of Tunis lagoon sediments was noted with spatial variations with relatively high levels at Z2. Biomarker analyses showed an increase in glutathione S-transferase and catalase activities and lipid peroxidation levels and a decrease in acetylcholinesterase activity in the studied sites. Molecular investigation showed a significant overexpression of: cytochrome c oxidase subunit I, ribosomal RNA 16S, Cu/Zn superoxide dismutase, heat shock protein 70, and metallothioneins in the three sampling sites. Moreover, our data were correlated to severe and diverse histopathological alterations in the clam gills. The principal component analysis showed that the Z2 region is more affected by metal contamination than Z1 and Z3 regions. Current field results suggest the use of several combined biomarkers at different cell levels instead of individual ones in monitoring programs.

Genomic and gene expression responses to genotoxic stress in PAC2 zebrafish embryonic cell line.

PAC2 cell line is, along most of the developed zebrafish cell lines, poorly characterized concerning its response to genotoxicants. To define the PAC2 cell line response to different forms of genotoxic stress, we exposed the cells to model genotoxic agents (benzo[a]pyrene, B[a]P, and ethyl methanesulfonate) and subsequently monitored DNA damage and alterations by using the battery of tests, including the Comet assay, quantitative random-amplified polymorphic DNA and amplified fragment length polymorphism. The expression of several DNA repair (xpc, xpd, hr23b, rad51, msh2) and oxidative stress response (sod (Cu/Zn)) genes was monitored as well. To obtain an indication of the PAC2 cell line metabolizing capacity, the expression of genes belonging to cyp1, cyp2 and cyp3 families was assessed upon exposure to B[a]P. Genotoxic responses were observed in all the used methods, and quantitative random-amplified polymorphic DNA and amplified fragment length polymorphism proved to be more sensitive by revealing DNA alterations even when the Comet assay indicated lack of significant damage. The PAC2 cell line demonstrated basal and B[a]P-induced expression of several cyp genes, suggesting its ability to metabolize indirect acting xenobiotics to a certain point. Based on these results, PAC2 cells seem to be sensitive zebrafish in vitro model in the genotoxicity assessment of the direct acting genotoxicant; however, they are less sensitive toward the indirect acting genotoxicant due to their limited metabolizing properties.

Zebrafish genome instability after exposure to model genotoxicants.

Sublethal exposure to environmental genotoxicants may impact genome integrity in affected organisms. It is therefore necessary to develop tools to measure the extent and longevity of genotoxicant-induced DNA damage, and choose appropriate model organisms for biomonitoring. To this end, markers of DNA damage were measured in zebrafish larvae and adults following exposure to model genotoxicants (benzo[a]pyrene and ethyl methanesulfonate). Specifically, we assessed primary DNA damage and the existence of potentially persistent genomic alterations through application of the comet assay, quantitative random amplified polymorphic DNA (qRAPD) and amplified fragment length polymorphism (AFLP) assays. Furthermore, expression of genes involved in DNA repair, oxidative stress response and xenobiotic metabolism was evaluated as well. Additionally, the AFLP method was applied to adult specimens 1 year after larval exposure to the genotoxicants to evaluate the longevity of the observed DNA alterations. Large numbers of DNA alterations were detected in larval DNA using the comet assay, qRAPD and AFLP, demonstrating that zebrafish larvae are a sensitive model for revealing genotoxic effects. Furthermore, some of these genomic alterations persisted into adulthood, indicating the formation of stable genomic modifications. qRAPD and AFLP methods proved to be highly sensitive to genotoxic effects, even in cases when the comet assay indicated a lack of significant damage. These results thus support the use of zebrafish larvae as a sensitive model for monitoring the impact of genotoxic insult and give evidence of the longevity of genomic modifications induced by genotoxic agents.

DNA alterations triggered by environmentally relevant polymetallic concentrations in marine clams Ruditapes philippinarum and polychaete worms Hediste diversicolor.

We exposed marine clams (Ruditapes philippinarum) and aquatic worms (Hediste diversicolor) to environmentally relevant concentrations of two metal mixtures each containing three divalent metals [(C1 in µg/L) cadmium (Cd) 1, mercury (Hg) 0.1, and lead (Pb) 4] and [C2 in µg/L) Cd 17, Hg 1.1, and Pb 55]. Animals collected in the Arcachon Bay were exposed for 8 days in microcosms made up of a mixed biotope consisting of a water column and natural marine sediment both taken up from the Arcachon Bay. Bioaccumulation analysis showed a significant increase of Cd, Hg, and Pb in clams, particularly at C2 concentration in the water column reaching, in soft body, 2.3 ± 0.3 µg Cd/g, 0.7 ± 0.2 µg Hg/g, and 45 µg Pb/g dry weight (dw). DNA alterations and upregulation of the cox1 mitochondrial gene were also observed in clam gill after exposure to the metal blend. For worms exposed to the C2 metal blend, DNA alterations and significant increase of Cd and Hg concentrations were observed reaching 0.5 ± 0.1 µg Cd/g and 2 ± 0.6 µg Hg/g dw.

Genotoxic effects of exposure to waterborne uranium, dietary methylmercury and hyperoxia in zebrafish assessed by the quantitative RAPD-PCR method.

Release of chemicals and fluctuation in oxygen content in the aquatic environment represent hazards for fish health. The present study aims at assessing the genotoxic impact of low concentration exposures to waterborne uranium (U), dietary methyl mercury (MeHg) and hyperoxia in zebrafish by using the RAPD-PCR quantitative method. A significant increase of the number hybridization sites was observed in fish exposed to 30µgU/L and 100µgU/L and hyperoxia. In fish exposed to MeHg (13.5µg Hg/g, dry weight) no change in the number of hybridization sites were found, however, the frequency of PCR products showed significant variation. The mechanisms of toxicity leading to DNA damage in fish exposed to waterborne uranium, mercury and hyperoxia are discussed and the results from the literature given by the comet assay, micronucleus test and RAPD-PCR method compared. The study provides new data regarding the genotoxic effects of MeHg, hyperoxia and low U concentrations (30µgU/L) in fish. The present work highlights the use of the RAPD-PCR as a sensitive method in the assessment of chemically-induced DNA damage in animals.

Mutagenic effects of a commercial glyphosate-based herbicide formulation on the soil filamentous fungus Aspergillus nidulans depending on the mode of exposure.

Glyphosate-based herbicides (GBH) are the most used pesticides worldwide. This widespread dissemination raises the question of non-target effects on a wide range of organisms, including soil micro-organisms. Despite a large body of scientific studies reporting the harmful effects of GBHs, the health and environmental safety of glyphosate and its commercial formulations remains controversial. In particular, contradictory results have been obtained on the possible genotoxicity of these herbicides depending on the organisms or biological systems tested, the modes and durations of exposure and the sensitivity of the detection technique used. We previously showed that the well-characterized soil filamentous fungus Aspergillus nidulans was highly affected by a commercial GBH formulation containing 450 g/L of glyphosate (R450), even when used at doses far below the agricultural application rate. In the present study, we analysed the possible mutagenicity of R450 in A. nidulans by screening for specific mutants after different modes of exposure to the herbicide. R450 was found to exert a mutagenic effect only after repeated exposure during growth on agar-medium, and depending on the metabolic status of the tested strain. The nature of some mutants and their ability to tolerate the herbicide better than did the wild-type strain suggested that their emergence may reflect an adaptive response of the fungus to offset the herbicide effects. The use of a non-selective molecular approach, the quantitative random amplified polymorphic DNA (RAPD-qPCR), showed that R450 could also exert a mutagenic effect after a one-shot overnight exposure during growth in liquid culture. However, this effect was subtle and no longer detectable when the fungus had previously been repeatedly exposed to the herbicide on a solid medium. This indicated an elevation of the sensitivity threshold of A. nidulans to the R450 mutagenicity, and thus confirmed the adaptive capacity of the fungus to the herbicide.

Dietary mercury exposure resulted in behavioral differences in mice contaminated with fish-associated methylmercury compared to methylmercury chloride added to diet.

Methylmercury (MeHg) is a potent neurotoxin, and humans are mainly exposed to this pollutant through fish consumption. However, in classical toxicological studies, pure methylmercury chloride (MeHgCl) is injected, given to drink or incorporated within feed assuming that its effects are identical to those of MeHg naturally associated to fish. In the present study, we wanted to address the question whether a diet containing MeHg associated to fish could result in observable adverse effects in mice as compared to a diet containing the same concentration of MeHg added pure to the diet and whether beneficial nutriments from fish were able to counterbalance the deleterious effects of fish-associated mercury, if any. After two months of feeding, the fish-containing diet resulted in significant observable effects as compared to the control and MeHg-containing diets, encompassing altered behavioral performances as monitored in a Y-shaped maze and an open field, and an increased dopamine metabolic turnover in hippocampus, despite the fact that the fish-containing diet was enriched in polyunsaturated fatty acids and selenium compared to the fish-devoid diets.

Effects of dietary methylmercury on the zebrafish brain: histological, mitochondrial, and gene transcription analyses.

The neurotoxic compound methylmercury (MeHg) is a commonly encountered pollutant in the environment, and constitutes a hazard for wildlife and human health through fish consumption. To study the neurotoxic impact of MeHg on piscivorous fish, we contaminated the model fish species Danio rerio for 25 and 50 days with food containing 13.5 µg/g dry weight (dw) of MeHg (0.6 µg MeHg/fish/day), an environmentally relevant dose leading to brain mercury concentrations of 30 ± 4 µg of Hg g(-1) (dw) after 25 days of exposure and 46 ± 7 µg of Hg g(-1) (dw) after 50 days. Brain mitochondrial respiration was not modified by exposure to MeHg, contrary to what happens in skeletal muscles. A 6-fold increase in the expression of the sdh gene encoding the succinate dehydrogenase Fe/S protein subunit was detected in the contaminated brain after 50 days of exposure. An up regulation of 3 genes, atp2b3a, atp2b3b, and slc8a2b, encoding for calcium transporters was noticed after 25 days of exposure but the atp2b3a and atp2b3b were repressed and the slc8a2b gene expression returned to its basal level after 50 days, suggesting a perturbation of calcium homeostasis. After 50 days, we detected the up regulation of glial fibrillary acidic protein and glutathione S-transferase genes (gfap and gst), along with a repression of the glutathione peroxidase gene gpx1. These results match well with a MeHg-induced onset of oxidative stress and inflammation. A transmission electron microscopic observation confirmed an impairment of the optical tectum integrity, with a decrease of the nucleal area in contaminated granular cells compared to control cells, and a lower density of cells in the contaminated tissue. A potential functional significance of such changes observed in optical tectum when considering wild fish contaminated in their natural habitat might be an impaired vision and therefore a lowered adaptability to their environment.

Effects of methylmercury contained in a diet mimicking the Wayana Amerindians contamination through fish consumption: mercury accumulation, metallothionein induction, gene expression variations, and role of the chemokine CCL2.

Methylmercury (MeHg) is a potent neurotoxin, and human beings are mainly exposed to this pollutant through fish consumption. We addressed the question of whether a diet mimicking the fish consumption of Wayanas Amerindians from French Guiana could result in observable adverse effects in mice. Wayanas adult men are subjected to a mean mercurial dose of 7 g Hg/week/kg of body weight. We decided to supplement a vegetarian-based mice diet with 0.1% of lyophilized Hoplias aimara fish, which Wayanas are fond of and equivalent to the same dose as that afflicting the Wayanas Amerindians. Total mercury contents were 1.4 ± 0.2 and 5.4 ± 0.5 ng Hg/g of food pellets for the control and aimara diets, respectively. After 14 months of exposure, the body parts and tissues displaying the highest mercury concentration on a dry weight (dw) basis were hair (733 ng/g) and kidney (511 ng/g), followed by the liver (77 ng/g). Surprisingly, despite the fact that MeHg is a neurotoxic compound, the brain accumulated low levels of mercury (35 ng/g in the cortex). The metallothionein (MT) protein concentration only increased in those tissues (kidney, muscles) in which MeHg demethylation had occurred. This can be taken as a molecular sign of divalent mercurial contamination since only Hg(2+) has been reported yet to induce MT accumulation in contaminated tissues. The suppression of the synthesis of the chemokine CCL2 in the corresponding knockout (KO) mice resulted in important changes in gene expression patterns in the liver and brain. After three months of exposure to an aimara-containing diet, eight of 10 genes selected (Sdhb, Cytb, Cox1, Sod1, Sod2, Mt2, Mdr1a and Bax) were repressed in wild-type mice liver whereas none presented a differential expression in KO Ccl2(-/-) mice. In the wild-type mice brain, six of 12 genes selected (Cytb, Cox1, Sod1, Sod2, Mdr1a and Bax) presented a stimulated expression, whereas all remained at the basal level of expression in KO Ccl2(-/-) mice. In the liver of aimara-fed mice, histological alterations were observed for an accumulated mercury concentration as low as 32 ng/g, dw, and metal deposits were observed within the cytoplasm of hepatic cells.

Mercury contamination in humans in Upper Maroni, French Guiana between 2004 and 2009.

We measured hair mercury concentration in Amerindians between 2004 and 2009 in Upper Maroni, French Guiana. Hair samples were collected from 387 residents (males: 153, females: 234). Average hair mercury concentration was high (males: 9.4 ppm, females: 9.9 ppm). We examined fish consumption by 37 residents. There was a significant correlation between hair mercury concentration and fish consumption. We also measured mercury concentration in polluted fish in upper reaches of the Maroni River. Muscle mercury concentrations were high in the fish. These results indicate that current high hair mercury concentrations in Amerindians remain linked to fish consumption.