Methylmercury Exposure Research Articles

Mercury Concentration in Nestling Feathers Better Predicts Individual Reproductive Success than Egg or Nestling Blood in a Piscivorous Bird.

Piscivorous birds are at high risk of mercury exposure in aquatic food webs, and their reproductive success is sensitive to methylmercury exposure. Although effects are convincingly shown in a handful of lab studies, sublethal effects at environmentally relevant concentrations in the field, where there is a range of other natural stressors, are not well delineated. Part of that uncertainty arises because mercury concentration (hereafter, [Hg]) in adult tissues used to assess Hg risk can be influenced by Hg values in wintering grounds or other nonrelated areas. Several studies have used nestling tissues under the assumption that they better represent local risk to breeding since nestlings consume locally derived food. However, the correlation between [Hg] in nestling tissues and local breeding success remains unassessed. We analyzed great egret ( Ardea alba) breeding parameters collected over 3 years (2015-2017) in the Everglades (Florida, USA). The Everglades is a large contiguous wetland with geographically dispersed wading bird breeding sites exposed to variable and biologically relevant ranges of mercury concentrations. We examined mercury concentrations in albumen and nestling blood and feathers as predictors of 6 measures of reproductive success at individual nests. Albumen [Hg] did not correlate with reproductive end points, and correlations with blood [Hg] were weak. Feather [Hg] correlated negatively with all of the posthatching endpoints and explained 8.3% of the variance in the probability of a laid egg resulting in a fledged chick. However, most of the observed failures were hatching failures, which were not explained by albumen [Hg], and other nestling tissues could therefore not be evaluated. While our results support the use of nestling feathers as indicators of site-specific mercury exposure, we discuss both advantages and possible limitations of using nestling feathers as indicators of local mercury exposure.

Comparative effects of mercury chloride and methylmercury exposure on early neurodevelopment in zebrafish larvae

Mercury (Hg) is a ubiquitous environmental toxicant with important public health implications. Hg causes neurotoxicity through astrocytes, Ca2+, neurotransmitters, mitochondrial damage, elevations of reactive oxygen species and post-translational modifications. However, the similarities and differences between the neurotoxic mechanisms caused by different chemical forms of Hg remain unclear. Zebrafish embryos were exposed to methylmercury (MeHgCl) or mercury chloride (HgCl2) (0, 4, 40, 400 nM) up for 96 h. HgCl2 exposure could significantly decrease survival rate, body length and eye size, delay the hatching period, induce tail bending and reduce the locomotor activity, and these effects were aggravated in the MeHgCl group. The compounds could increase the number of apoptotic cells in the brain and downregulate the expression of Shha, Ngn1 and Nrd, which contribute to early nervous development. The underlying mechanisms were investigated by metabolomics data. Galactose metabolism, tyrosine metabolism and starch and sucrose metabolism pathways were disturbed after HgCl2 or MeHgCl exposure. In addition, the levels of three neurotransmitters including tyrosine, dopamine and tryptophan were reduced after HgCl2 or MeHgCl exposure. Oxidative stress is related to metabolite changes, such as changes in the putrescine, niacinamide and uric acid contents in the HgCl2 group, and squalene in the MeHgCl group. These data indicated that downregulation of these genes and abnormal metabolic profile and pathways contribute to the neurotoxicity of HgCl2 and MeHgCl.

Health Risk Assessment of Inorganic Mercury and Methylmercury via Rice Consumption in the Urban City of Guiyang, Southwest China.

Rice consumption is the main methylmercury (MeHg) exposure route for residents in mercury (Hg) mining areas. However, there is limited studies on mercury in commercial rice, which has high liquidity and can be directly consumed by urban residents. This study measured the total Hg (THg) and MeHg concentrations in 146 rice samples purchased from the markets in Guiyang city, southwest China, and both the inorganic Hg (IHg) and MeHg estimated daily intakes (EDIs) and hazard quotients (HQs) were calculated according to rice consumption. The THg concentrations in all rice samples (range: 0.97 to 13.10 μg·kg−1; mean: 3.88 μg·kg−1) were lower than the Chinese national standard (20 μg·kg−1). The average MeHg concentration in rice was 1.16 μg·kg−1. The total HQs (THQs) ranged from 0.0106 to 0.1048, with a mean of 0.0462, which was far lower than 1. This result suggests that there were low Hg exposure levels through consumption of commercial rice in residents of Guiyang.

Gene expression profiles in the dorsal root ganglia of methylmercury-exposed rats.

Methylmercury (MeHg) exposure is known to induce neurodegeneration in both the central nervous system (CNS) and peripheral nervous system (PNS). Molecular mechanisms of MeHg-induced neurotoxicity have been well investigated in the CNS, however, it remains unclear in the PNS. In the present study, comprehensive gene expression analysis was performed by analyzing MeHg-exposed adult rat dorsal root ganglion (DRG) by DNA microarray. Methylmercuric chloride (6.7 mg/kg/day) was administered to nine-week-old male Wistar rats for five days, followed by two days without administration; this cycle was repeated once. Rats were anesthetized at 7 or 14 days after commencement of MeHg exposure, and their DRGs were removed and homogenized to make total RNA samples. DNA microarray data from Day 7 samples identified 100 out of 18,513 detected genes as annotated genes with more than two-fold upregulated or downregulated expression compared with controls. Database for Annotation, Visualization, and Integrated Discovery (DAVID) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses suggested strong involvement of immune activation and inflammation pathways in rat DRG exposed to MeHg, and some genes overlapped with previously reported genes affected by MeHg exposure in the cerebellum. The present results suggest that MeHg-induced neurotoxicity is associated with immune activation and inflammatory responses in rat DRG.

Environmentally relevant methylmercury exposure reduces the metabolic scope of a model songbird

For most birds, energy efficiency and conservation are paramount to balancing the competing demands of self-maintenance, reproduction, and other demanding life history stages. Yet the ability to maximize energy output for behaviors like predator escape and migration is often also critical. Environmental perturbations that affect energy metabolism may therefore have important consequences for fitness and survival. Methylmercury (MeHg) is a global pollutant that has wide-ranging impacts on physiological systems, but its effects on the metabolism of birds and other vertebrates are poorly understood. We investigated dose-dependent effects of dietary MeHg on the body composition, basal and peak metabolic rates (BMR, PMR), and respiratory quotients (RQ) of zebra finches (Taeniopygia guttata). Dietary exposure levels (0.0, 0.1, or 0.6 ppm wet weight) were intended to reflect a range of mercury concentrations found in invertebrate prey of songbirds in areas contaminated by atmospheric deposition or point-source pollution. We found adiposity increased with MeHg exposure. BMR also increased with exposure while PMR decreased, together resulting in reduced metabolic scope in both MeHg-exposed treatments. There were differences in RQ among treatments that suggested a compromised ability of exposed birds to rapidly metabolize carbohydrates during exercise in a hop-hover wheel. The elevated BMR of exposed birds may have been due to energetic costs of depurating MeHg, whereas the reduced PMR could have been due to reduced oxygen carrying capacity and/or reduced glycolytic capacity. Our results suggest that environmentally relevant mercury exposure is capable of compromising the ability of songbirds to both budget and rapidly exert energy.

Mercury contamination in resident and migrant songbirds and potential effects on body condition

Methlymercury is a significant risk to environmental health globally. We examined the ecological drivers of methylmercury bioaccumulation in songbirds and its effect on body condition while experimentally removing the potentially confounding and predominant effects of site and habitat. We measured blood and feather mercury concentrations and body condition in nearly 1200 individuals representing resident or migrant songbirds of 52 species and 5 foraging guilds. Songbird mercury concentrations differed among species, foraging guilds, residency status, dates, and ages, but not sexes. Blood mercury concentrations 1) ranged from 0.003 in house finch to 0.85 μg/g ww in American robin, 2) were 125 times greater in insectivores than granivores and 3.6 times greater in insectivores than omnivores, 3) were 3.3 times greater in summer residents than in migrating songbirds, 4) increased by 25% throughout spring and summer, and 5) were 45% higher in adults than juveniles. Songbird mercury concentrations were negatively correlated with body condition, with blood mercury concentrations decreasing by 44% and 34% over the range of standardized body masses and fat scores, respectively. Our results highlight the importance of foraging and migration ecology in determining methylmercury contamination in birds, and the potential for reduced body condition with methylmercury exposure in songbirds.

Genetic Predisposition to Prenatal Methylmercury Toxicity and Child Cognitive Development at Age 8 Years

Background: The association of childhood cognitive function and prenatal exposure to methylmercury was previously found to be modified by genetic variation. We further explored the potential genetic predisposition in an extended study of children from the Avon Longitudinal Study of Parents and Children (Bristol, UK) (ALSPAC). Methods: A subgroup (n = 1 127 from the pilot study and 1 045 from the present study) of the ALSPAC cohort was identified based on the availability of the mercury (Hg) concentration of umbilical cord tissue as a measure of prenatal methylmercury exposure, data on 247 single-nucleotide polymorphisms (SNPs) within relevant genes, as well as scores on the Wechsler Intelligence Scale for Children Intelligence Quotient (IQ) at age 8 years. Multivariable regression models were used to assess the associations between methylmercury exposure and IQ as a cognitive development measure and to determine possible gene-environment interactions. Inclusion of covariate variables reduced the total sample size from 2 172 to 1 723 complete cases; inverse probability weighting was applied in final models. Findings: At the low exposure level in this population, the log10-transformed mercury concentration was positively associated with IQ, but adjustment for nutritional and sociodemographic cofactors attenuated this association. Inclusion of selenium and vitamin D measured in pregnancy blood samples did not affect these findings. Enhanced interaction with methylmercury neurotoxicity was replicated in the new study for the minor allele of rs1042838 (progesterone receptor) (Beta; 95% Confidence Interval) = (-11.8; -23.0 to -0.7) (P-for-interaction = 0.004) and less clearly for rs662 (paraoxonase 1) (-3.6; -11.5 to 4.2) (P = 0.115). In the joint sample, new potential interacting SNPs were discovered in relation to superoxide dismutase 2, ATP binding cassette subfamily A member 1 and metallothionein 1M genes. Interpretation: Low-level prenatal exposure to methylmercury was weakly, though positively, associated with child cognitive development 8 years later. However, for PGR rs1042838, the presence of the minor allele revealed a clear negative association of mercury exposure with IQ. These findings emphasize that understanding of methylmercury neurotoxicity can be enhanced by integrating genetic data into the analysis. Funding Statement: Spanish Institute of Health Carlos III. Declaration of Interests: The authors have no conflicts of interest to declare. All the authors have no financial relationships relevant to this article to disclose. Ethics Approval Statement: Ethical approval for the study was obtained from the ALSPAC Ethics and Law Committee and the Local Research Ethics Committees.

Burden of Mild Mental Retardation attributed to prenatal methylmercury exposure in Amazon: local and regional estimates.

The gold rush in the Amazon Region caused an increase of mercury (Hg) levels in the environment, and, consequently, raised human exposure. Once released into aquatic systems, Hg could generate methylmercury (MeHg), an extremely toxic compound, which is accumulated through trophic chains. Several studies have provided evidences of the brain sensitivity to MeHg, as well as, of the fetus vulnerability during pregnancy. The main objective of this study was to estimate the Mild Mental Retardation (MMR) in Amazonian populations, caused by prenatal exposure to MeHg, using the methodology proposed by Poulin (2008), which quantifies the environmental burden of disease. The estimates of the MMR burden, attributed to prenatal MeHg exposure, were based on the calculation of Disability-Adjusted Life Years (DALY), which were obtained from MMR incidence rate in the studied populations. At the local level, the MMR incidence rate calculations were based on primary data of MeHg exposure of riverine women at childbearing age. The MMR incidence rate was equal to 5.96/1,000 infants, which would result in 2.0 IQ points loss in 34.31% of the newborns. The estimated DALY/1,000 infants was equal to 71.2, while the DALY was 576. For the regional estimates, different exposure scenarios were created. The calculated DALY varied from 3,256 to 65,952 per year.

Adolescent methylmercury exposure: Behavioral mechanisms and effects of sodium butyrate in mice

Methylmercury (MeHg), an environmental neurotoxicant primarily found in fish, produces neurobehavioral impairment when exposure occurs during gestation. Whether other developmental periods, such as adolescence, display enhanced vulnerability to the behavioral effects of MeHg exposure is only beginning to be explored. Further, little is known about the effects of repeated administration of lysine deacetylase inhibitors, such as sodium butyrate (NaB), on operant behavior. In Experiment 1, male C57BL6/n mice were exposed to 0, 0.3, and 3.0 ppm MeHg (n = 12 each) via drinking water from postnatal days 21 to 60 (murine adolescence). As adults, mice were trained to lever press under an ascending series of fixed-ratio schedules of milk reinforcement selected to enable the analysis of three important parameters of operant behavior using the framework provided by Mathematical Principles of Reinforcement. Adolescent MeHg exposure dose-dependently increased saturation rate, a measure of the retroactive reach of a reinforcer, and decreased minimum response time relative to controls. In Experiment 2, the behavioral effects of repeated NaB administration both alone and following adolescent MeHg exposure were examined. Male C57BL6/n mice were given either 0 or 3.0 ppm MeHg during adolescence and, before behavioral testing, two weeks of once daily i.p. injections of saline or 0.6 g/kg NaB (n = 12 in each cell). Adolescent MeHg exposure again increased saturation rate but did not significantly alter minimum response time. NaB also increased saturation rate in both MeHg exposure groups. These data suggest that the behavioral mechanisms of adolescent MeHg exposure and NaB may be related to the impact of reinforcement on prior responses. Specifically, MeHg and NaB concentrated the effects of reinforcers onto the most recent responses.

Neurobehavioral and oxidative stress alterations following methylmercury and retinyl palmitate co-administration in pregnant and lactating rats and their offspring

Fish consumption and ubiquitous methylmercury (MeHg) exposure represent a public health problem globally. Micronutrients presented in fish affects MeHg uptake/distribution. Vitamin A (VitA), another fish micronutrient is used in nutritional supplementation, especially during pregnancy. However, there is no information about the health effects arising from their combined exposure. The present study aimed to examine the effects of both MeHg and retinyl palmitate administered to pregnant and lactating rats. Thirty Wistar female rats were orally supplemented with MeHg (0,5 mg/Kg/day) and retinyl palmitate (7500 μg RAE111μg RAE = micrograms of retinol activity equivalents (3,33 international units or IU)/Kg/day), either individually or in combination from the gestational day 0 to weaning. In dams, maternal behavior was scored. In neonatal and infant offspring, associative learning and neurodevelopment were evaluated. Further periadolescent male and female pups were assessed for open field, habituation and object recognition using episodic-like memory paradigm. Maternal and offspring redox parameters were evaluated. Our results showed no effects of MeHg-VitA co-administration in the quality of maternal care but showed subtle alterations in the pro-oxidant response of the hippocampus. In offspring, MeHg-VitA co-exposure affected early associative learning in neonatal pups, with no further modifications in neurodevelopment, and no locomotor or exploratory alterations in later developmental stages. Habituation was altered in a sex-dependent manner, but no overall memory disturbances were encountered. Finally, MeHg-VitA co-administration reduced lipoperoxidation in male offspring hippocampus. In conclusion, VitA co-administration in dams, under our exposure protocol, can counteract the deleterious neurodevelopmental effects solely attributed to low-dose MeHg in a tissue-specific mechanism, suggesting a protective effect of VitA against MeHg-induced oxidative damage in the central nervous system, especially in the offspring. Further work is needed to confirm our findings and elucidate the molecular mechanisms of MeHg-VitA modulation. Pre-clinical assays are necessary to demonstrate the potential therapeutical use of VitA in populations directly or indirectly exposed to MeHg.

Responses of Antioxidant Defense and Immune Gene Expression in Early Life Stages of Large Yellow Croaker (Pseudosciaena crocea) Under Methyl Mercury Exposure.

Early life stages of marine organisms are the most sensitive stages to environment stressors including pollutants. In order to understand the toxicological effects induced by MeHg exposure on juveniles of large yellow croaker (Pseudosciaena crocea), a toxicity test was performed wherein fish were exposed to sub-lethal concentrations of MeHg under laboratory conditions (18 ± 1°C; 26 ± 1 in salinity). After 30 days of 0–4.0 μg L-1 MeHg exposure, SOD activity was significantly decreased in the 0.25, 1.0, and 4.0 μg L-1 treatments; while CAT activity was significantly increased in the 4.0 μg L-1 treatments; GSH level, GPx activity were significantly elevated in the 4.0 μg L-1 treatments, respectively. Meanwhile, malondialdehyde content was also significantly increased in the 1.0 and 4.0 μg L-1 treatments with respect to the control. Acetylcholinesterase activity was significantly decreased by 18.3, 25.2, and 21.7% in the 0.25, 1.0, and 4.0 μg L-1 treatments, respectively. The expression of TCTP, GST3, Hsp70, Hsp27 mRNA were all up-regulated in juveniles with a dose-dependent manner exposed to MeHg. These results suggest that large yellow croaker juveniles have the potential to regulate the levels of antioxidant enzymes and initiate immune response in order to protect fish to some extent from oxidative stress induced by MeHg.

Sub-Micromolar Methylmercury Exposure Promotes Premature Differentiation of Murine Embryonic Neural Precursor at the Expense of Their Proliferation.

Methylmercury (MeHg) is a ubiquitous environmental pollutant that is known to be neurotoxic, particularly during fetal development. However, the mechanisms responsible for MeHg-induced changes in adult neuronal function, when their exposure occurred primarily during fetal development, are not yet understood. We hypothesized that fetal MeHg exposure could affect neural precursor development leading to long-term neurotoxic effects. Primary cortical precursor cultures obtained from embryonic day 12 were exposed to 0 µM, 0.25 µM, 0.5 µM, 2.5 µM, and 5 µM MeHg for 48 or 72 h. All of the concentrations tested in the study did not affect cell viability. Intriguingly, we observed that cortical precursor exposed to 0.25 µM MeHg showed increased neuronal differentiation, while its proliferation was inhibited. Reduced neuronal differentiation, however, was observed in the higher dose groups. Our results suggest that micromolar MeHg exposure may deplete the pool of neural precursors by increasing premature neuronal differentiation, which can lead to long-term neurological effects in adulthood as opposed to the higher MeHg doses that cause more immediate toxicity during infant development.

Maternal Methylmercury Exposure through Rice Ingestion and Offspring Neurodevelopment in Rural China: A Prospective Cohort Study

Background: Dietary methylmercury intake can occur not only through fish ingestion but also through rice ingestion; however, rice does not contain the same beneficial nutrients as fish. In rural China, where rice is a staple food, associations between prenatal methylmercury exposure and offspring neurodevelopment were investigated.Methods: 398 mothers living in Daxin, China were recruited at parturition, and had a hair sample collected. Hair total mercury concentrations were measured as a proxy for methylmercury exposure. Mothers completed a semi-quantitative food frequency questionnaire, including rice and fish ingestion. Children were assessed at 12 months (n=270, 68%) and 36 months (n=197, 49%) using the Bayley Scales of Infant Development-II, yielding age-adjusted scores for the Mental Developmental Index (MDI) and Psychomotor Developmental Index (PDI). Multivariable regression was used to model log-transformed hair mercury with outcomes, adjusting for potential confounders, including fish and rice intake. Results: Among 398 mothers, 86% ingested rice daily, 43% never ate fish, and 11% ingested fish >twice/week. Maternal hair mercury averaged 0.48 mcg/g (median: 0.40 mcg/g). At 12 months, in adjusted models, a doubling in hair mercury corresponded to a 1.5-point decrease in the MDI (95% CI: -2.9, -0.03), while a doubling in hair mercury was associated with a 0.82-point decrease in the PDI (95% CI: -2.5, 0.86). At 36 months, in adjusted models, confidence intervals were wide for both MDI and PDI. A doubling in hair mercury corresponded to a 0.32-point decrease in the MDI (95% CI: -2.1, 1.5), and a 1.0-point decrease in the PDI (95% CI: -3.3, 1.3). Conclusions: For 12-month old children from rural China, prenatal methylmercury exposure was associated with statistically significant decrements in cognition; however, this association attenuated over time and was diminished and no longer statistically significant at 36 months. Funding: NIEHS R15ES022409 R21ES026412

Prenatal Exposure to Polychlorinated Biphenyls and Mercury Are Associated with Insulin-Like Growth Factor 1 and Thyroid-Stimulating Hormone in Cord Plasma

Impact on maternal endocrine system during pregnancy may also affect growth and development of a fetus. Certain toxic elements and polychlorinated biphenyls (PCBs) are known to disturbe human endocrine system. In our previous study, we showed that birth weight were affected by prenatal PCBs and methylmercury exposure. In this study, we used the data from the Tohoku Study of Child Development in Japan. The objective of the study was to evaluate the effect of prenatal exposure to methylmercury, arsenic, cadmium, lead, and PCBs on insulin-like growth factor 1 (IGF-1) and thyroid related hormones (TSH, T3, freeT3, T4 and freeT4) in cord blood. Those factros are considered to be associated with fetal growth. Elements except for mercury were analyzed by an inductivity coupled plasma mass spectrometry. Mercury levels were measured using a cold vapor atomic absorption spectrometer. IGF-1 and insulin-like growth factor binding protein 1 (IGFBP1) were detemined by an enzyme-linked immunosorbent assay (ELISA). Thyroid related hormones were assessed by an electrochemiluminescence immunoassay. The data were examined by Pearson’s correlation and multiple regression analyses. The IGF-1 in cord plasma was negatively associated with PCB concentrations in cord blood, especially with tri-, tetra-, penta-, hexa- and hepta-chlorobiphenyls. Cord plasma free T4 was negatively associated with mercury concentrations in cord blood. This study indicated PCBs and mercury could affect birth weight through altering the IGF1 and T4 mechanism. Further studies are necessary to investigate the effect of decrease in IGF-1 and thyroid hormones on birth weight.

The Role of the Gut Microbiome on Mercury Toxicology: Protein-Rich Diet Alters Gut Microbiota Composition and Increases Methylmercury Demethylation

Methylmercury (MeHg) exposure is a global health concern particularly among coastal populations that rely on fish and marine mammals for sustenance. It has been shown that diet can modulate the MeH...

Method Development and Validation of Dried Blood Spots as a Tool for Mercury Exposure Assessment

Dried blood spots (DBS) provide a minimally invasive collection method with potential to be used as a field-based research tool for exposure to environmental contaminants such as mercury (Hg). Even though previous studies provided novel techniques to measure Total Mercury (THg) and Methylmercury (MeHg) in residual DBS from newborn screening programs, a range of limitations remains including challenges with detection limit, lack of mercury speciation, and validation with paired DBS-Blood samples collected under laboratory conditions. This study follows our previous work on the matter and specifically evaluates the suitability of DBS to assess methylmercury (MeHg) and THg exposure in human and fish blood samples. It focuses on paired DBS-blood samples from venous and capillary sources of 49 human volunteers, and 10 fish (Artic Char) samples. Paired DBS-blood, reference material and venous blood from one volunteer, was used to develop the analytical method. We used a GC-CVAFS to analyze MeHg and a Dual-Stage Gold Preconcentration for THg. Method development results based on EPA1630 guidelines, wet spikes and the use of blood reference materials showed that the measurement of MeHg in whole blood and DBS was both accurate (95-107%) and precise (2-11%). Initial results showed a high correlation for DBS-blood (r2=0.83) for MeHg (average 0.96 ± 0.73 µg/L) for human samples, as well as for DBS-blood fish samples MeHg (r2=0.94), (average 919.46 ± 492.97µg/L). When coupled with other recent work in this area, there is growing confidence in the use of DBS samples to measure MeHg exposure.

Associations of maternal immune response with MeHg exposure at 28 weeks' gestation in the Seychelles Child Development Study.

ProblemMaternal methylmercury (MeHg) exposure may be associated with immune response during pregnancy.Method of studyIn the high fish‐eating Seychelles Child Development Study Nutrition Cohort 2, we examined the association between maternal MeHg, polyunsaturated fatty acids (PUFA), and immune markers (Th1:Th2; TNF‐α, IL‐1β, IFN‐γ, IL‐2, IL‐4, IL‐5, IL‐10, MCP‐1, TARC, sFlt‐1, VEGF‐D, CRP and IL‐6) at 28 weeks’ gestation. Linear regression examined associations between MeHg exposure and immune markers with and without adjustment for PUFA.ResultsIn all models, as MeHg concentrations increased, the Th1:Th2 ratio, total Th1 and individual Th1 (IL‐1β, IL‐2, TNF‐α) concentrations decreased. MeHg was not associated with total Th2 cytokines but was associated with a decrease in IL‐4 and IL‐10. MeHg was positively associated with TARC and VEGF‐D and negatively associated with CRP. There was a significant interaction between MeHg and the n‐6:n‐3 ratio, with MeHg associated with a larger decrease in Th1:Th2 at higher n‐6:n‐3 PUFA ratios. The n‐3 PUFA were associated with lower CRP, IL‐4 and higher IFN‐γ. The n‐6 PUFA were associated with higher IL‐1β, IL‐2, TNF‐α, IL‐4, IL‐10, CRP and IL‐6.ConclusionMaternal MeHg was associated with markers of immune function at 28 weeks’ gestation. A significant interaction between MeHg and the n‐6:n‐3 ratio on the Th1:Th2 ratio suggests that the n‐3 PUFA may mitigate any immunosuppressive associations of MeHg. The n‐3 and n‐6 PUFA were associated with suppressive and stimulatory immune responses, respectively. Overall, the associations were of small magnitude, and further research is required to determine the clinical significance.

Low doses of methylmercury exposure during adulthood in rats display oxidative stress, neurodegeneration in the motor cortex and lead to impairment of motor skills

Despite the vast distribution among tissues, the central nervous system (CNS) represents the main target of methylmercury (MeHg) toxicity. However, few studies have evaluated the effects of MeHg exposure on the CNS at equivalent doses to human environmental exposure. In our study, we evaluated the motor cortex, an important area of motor control, in adult rats chronically exposed to MeHg in a concentration equivalent to those found in fish-eating populations exposed to mercury (Hg). The parameters evaluated were total Hg accumulation, oxidative stress, tissue damage, and behavioral assessment in functional actions that involved this cortical region. Our results show in exposed animals a significantly greater level of Hg in the motor cortex; increase of nitrite levels and lipid peroxidation, associated with decreased antioxidant capacity against peroxyl radicals; reduction of neuronal and astrocyte density; and poor coordination and motor learning impairment. Our data showed that chronic exposure at low doses to MeHg is capable of promoting damages to the motor cortex of adult animals, with changes in oxidative biochemistry misbalance, neurodegeneration, and motor function impairment.

Methylmercury exposure develops atherosclerotic risk factors in the aorta and programmed cell death in the cerebellum: ameliorative action of Celastrus paniculatus ethanolic extract in male Wistar rats.

Methylmercury (MeHg) is a bioaccumulative global environmental contaminant present in fishes and seafood. MeHg is the methylated form of mercury emitted from diverse anthropogenic and natural sources. MeHg is accumulated in the aquatic environment and eventually reaches human system via food chain by biomagnification. We have reported previously that the neurotoxic effect of MeHg in rat cerebellum is mitigated by the administration of an ayurvedic medicinal plant, Celastrus paniculatus ethanolic extract. The present study has focussed to further explore the mechanism of action of Celastrus paniculatus against MeHg-induced neurotoxicity in the cerebellum. We have also inspected the effect of Celastrus paniculatus (CP) against MeHg-induced atherosclerotic risk factors like alterations in antioxidant levels, aortic lipid profile, and aortic histology by MeHg in the largest vasculature, aorta, which are the initiating factors of cardiovascular diseases. Male Wistar rats were divided as (i) control, (ii) MeHg (5mg/kg b.w.), (iii) MeHg + CP (200mg/kg b.w.), and (iv) CP alone (200mg/kg b.w.). All were given orally for 21days. In cerebellum Celastrus paniculatus, there were increased mitochondrial electron transport chain (p < 0.05) activity, reduced cytochrome c release (p < 0.05), and caspase 3 mRNA expression (p < 0.05). In the aorta, MeHg-induced oxidative stress, lipid profile changes, and endothelial denudation were ameliorated by Celastrus paniculatus. Hence, we conclude that Celastrus paniculatus protects against MeHg toxicity by inhibiting mitochondrial cytochrome c/caspase 3 apoptotic pathway in the cerebellum and reducing the development of atherosclerotic risk factors in the aorta.

Methylmercury Exposure and Developmental Outcomes in Tohoku Study of Child Development at 18 Months of Age.

Seafood is an important component in a healthy diet and may contain methylmercury or other contaminants. It is important to recognize the risks and benefits of consuming seafood. A longitudinal prospective birth cohort study has been conducted to clarify the effects of neurotoxicants on child development—the Tohoku Study of Child Development (TSCD) in Japan. TSCD comprises two cohorts; a polychlorinated biphenyls (PCB) cohort (urban area) and a methylmercury cohort (coastal area). Our previous results from the coastal area showed prenatal methylmercury exposure affected psychomotor development in 18-month-olds, and boys appear to be more vulnerable to the exposure than girls. In this report, we have added the urban area cohort and we reanalyzed the impact of prenatal exposure to methylmercury, which gave the same results as before. These findings suggest prenatal exposure to low levels methylmercury may have adverse effects on child development, especially in boys.