Burden of Mild Mental Retardation attributed to prenatal methylmercury exposure in Amazon: local and regional estimates / Carga de Retardo Mental Leve atribuída à exposição pré-natal ao metilmercúrio na Amazônia: estimativas local e regional

Abstract 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.

Resumo A corrida pelo ouro na Amazônia elevou os níveis de mercúrio (Hg) no ambiente e, consequentemente, aumentou a exposição humana. Uma vez liberado em sistemas aquáticos, o Hg pode gerar metilmercúrio (MeHg), um composto tóxico que se acumula ao longo de cadeias tróficas. Vários estudos têm gerado evidências sobre a sensibilidade do cérebro ao MeHg, bem como sobre a vulnerabilidade do feto durante a gravidez. O principal objetivo deste trabalho foi estimar a carga de Retardo Mental Leve (RML) em populações amazônicas, causada pela exposição pré-natal ao MeHg, utilizando a metodologia proposta por Poulin (2008). As estimativas de RML, atribuída à exposição ao MeHg pré-natal, foram baseadas no cálculo dos Anos de Vida Ajustados por Incapacidade (DALY), que foi desenvolvido a partir de taxa de incidência RML nas populações estudadas. Em nível local, o cálculo da taxa de incidência RML baseou-se em dados primários sobre a exposição ao MeHg em mulheres ribeirinhas em idade fértil. A taxa de incidência RML foi igual a 5,96/1.000 nascidos, o que resulta na perda de 2,0 pontos de QI em 34,31% dos nascidos. A estimativa de DALY/1.000 nascidos foi igual a 71,2, enquanto o DALY foi de 576. Para as estimativas regionais, foram criados diferentes cenários de exposição. Os DALYs calculados variaram de 3.256 a 65.952 por ano.

Developmental neurotoxicity: methylmercury and prenatal exposure protection in the context of the Minamata Convention / Neurotoxicidad durante el desarrollo: metilmercurio y protección frente a la exposición prenatal a este contaminante en el contexto del Convenio de Minamata

Mercury is a global pollutant of public environmental health concern due to its long-range atmospheric distribution, environmental distribution, and neurotoxic effects. Following biological methylation, methylmercury (MeHg) can be un-evenly bioaccumulated within aquatic food chains. Fish consumption can be a significant route of human exposure to MeHg. MeHg exposure in the prenatal stage, at relatively low levels, has recently been established as harmful during neurological development, potentially leading to intellectual disability. The Minamata Convention on Mercury is a global agreement, currently under ratification, to protect human health and the environment from anthropogenic emissions and releases of mercury and mercury compounds. The resolution regarding the role of the World Health Organization and ministries of health in the implementation of the Convention includes protection of human health from critical exposures to MeHg. Riverside populations living in areas with artisanal small-scale gold mining, and relying heavily on fish consumption, have been identified as the most vulnerable population in terms of MeHg exposure and developmental neurotoxicity. This article focuses on the proper design and dissemination of fish advisories within the context of implementation of the Convention.

El mercurio es un contaminante global motivo de preocupación en materia de salud pública ambiental como consecuencia de su amplia distribución atmosférica, su distribución ambiental y sus efectos neurotóxicos. Tras su metilación biológica, el metilmercurio (MeHg) se puede bioacumular de manera desigual en las cadenas alimentarias acuáticas. El consumo de pescado puede ser una ruta significativa de exposición humana al MeHg. Recientemente, se ha establecido que la exposición a niveles relativamente bajos de MeHg en la etapa prenatal es perjudicial para el neurodesarrollo, pudiendo ocasionar discapacidad intelectual. El Convenio de Minamata sobre el Mercurio es un acuerdo a escala mundial, actualmente en fase de ratificación, cuyo objeto es proteger la salud humana y el medio ambiente de las emisiones antropogénicas y los vertidos de mercurio y sus compuestos. La resolución referente a la función de la Organización Mundial de la Salud y los ministerios de salud en la aplicación del Convenio incluye la protección de la salud humana de exposiciones importantes al MeHg. Se ha establecido que las poblaciones ribereñas que residen en zonas de extracción artesanal de oro a pequeña escala, y que dependen en gran medida del consumo de pescado, son las más vulnerables en términos de exposición al MeHg y neurotoxicidad durante el desarrollo. Este artículo se centra en el diseño y la difusión adecuados de las recomendaciones relativas al consumo de pescado en el contexto de la aplicación del Convenio.

Methylmercury inhibits prolactin release in a cell line of pituitary origin

Heavy metals, such as methylmercury, are key environmental pollutants that easily reach human beings by bioaccumulation through the food chain. Several reports have demonstrated that endocrine organs, and especially the pituitary gland, are potential targets for mercury accumulation; however, the effects on the regulation of hormonal release are unclear. It has been suggested that serum prolactin could represent a biomarker of heavy metal exposure. The aim of this study was to evaluate the effect of methylmercury on prolactin release and the role of the nitrergic system using prolactin secretory cells (the mammosomatotroph cell line, GH3B6). Exposure to methylmercury (0-100 μM) was cytotoxic in a time- and concentration-dependent manner, with an LC50 higher than described for cells of neuronal origin, suggesting GH3B6 cells have a relative resistance. Methylmercury (at exposures as low as 1 μM for 2 h) also decreased prolactin release. Interestingly, inhibition of nitric oxide synthase by N-nitro-L-arginine completely prevented the decrease in prolactin release without acute neurotoxic effects of methylmercury. These data indicate that the decrease in prolactin production occurs via activation of the nitrergic system and is an early effect of methylmercury in cells of pituitary origin.

Environmental Mercury and Its Toxic Effects / 예방의학회지

Mercury exists naturally and as a man-made contaminant. The release of processed mercury can lead to a progressive increase in the amount of atmospheric mercury, which enters the atmospheric-soil-water distribution cycles where it can remain in circulation for years. Mercury poisoning is the result of exposure to mercury or mercury compounds resulting in various toxic effects depend on its chemical form and route of exposure. The major route of human exposure to methylmercury (MeHg) is largely through eating contaminated fish, seafood, and wildlife which have been exposed to mercury through ingestion of contaminated lower organisms. MeHg toxicity is associated with nervous system damage in adults and impaired neurological development in infants and children. Ingested mercury may undergo bioaccumulation leading to progressive increases in body burdens. This review addresses the systemic pathophysiology of individual organ systems associated with mercury poisoning. Mercury has profound cellular, cardiovascular, hematological, pulmonary, renal, immunological, neurological, endocrine, reproductive, and embryonic toxicological effects.

Toxic effects of methylmercury, arsanilic acid and danofloxacin on the differentiation of mouse embryonic stem cells into neural cells

This study was performed to assess the neurotoxic effects of methylmercury, arsanilic acid and danofloxacin by quantification of neural-specific proteins in vitro. Quantitation of the protein markers during 14 days of differentiation indicated that the mouse ESCs were completely differentiated into neural cells by Day 8. The cells were treated with non-cytotoxic concentrations of three chemicals during differentiation. Low levels of exposure to methylmercury decreased the expression of GABAA-R and Nestin during the differentiating stage, and Nestin during the differentiated stage. In contrast, GFAP, Tuj1, and MAP2 expression was affected only by relatively high doses during both stages. Arsanilic acid affected the levels of GABA(A)-R and GFAP during the differentiated stage while the changes of Nestin and Tuj1 were greater during the differentiating stage. For the neural markers (except Nestin) expressed during both stages, danofloxacin affected protein levels at lower concentrations in the differentiated stage than the differentiating stage. Acetylcholinesterase activity was inhibited by relatively low concentrations of methylmercury and arsanilic acid during the differentiating stage while this activity was inhibited only by more than 40 microM of danofloxacin in the differentiated stage. Our results provide useful information about the different toxicities of chemicals and the impact on neural development.

Protective effects of organoselenium compounds against methylmercury-induced oxidative stress in mouse brain mitochondrial-enriched fractions

We evaluated the potential neuroprotective effect of 1-100 µM of four organoselenium compounds: diphenyl diselenide, 3’3-ditri-fluoromethyldiphenyl diselenide, p-methoxy-diphenyl diselenide, and p-chloro-diphenyl diselenide, against methylmercury-induced mitochondrial dysfunction and oxidative stress in mitochondrial-enriched fractions from adult Swiss mouse brain. Methylmercury (10-100 µM) significantly decreased mitochondrial activity, assessed by MTT reduction assay, in a dose-dependent manner, which occurred in parallel with increased glutathione oxidation, hydroperoxide formation (xylenol orange assay) and lipid peroxidation end-products (thiobarbituric acid reactive substances, TBARS). The co-incubation with diphenyl diselenide (100 µM) completely prevented the disruption of mitochondrial activity as well as the increase in TBARS levels caused by methylmercury. The compound 3’3-ditrifluoromethyldiphenyl diselenide provided a partial but significant protection against methylmercury-induced mitochondrial dysfunction (45.4 ± 5.8 percent inhibition of the methylmercury effect). Diphenyl diselenide showed a higher thiol peroxidase activity compared to the other three compounds. Catalase blocked methylmercury-induced TBARS, pointing to hydrogen peroxide as a vector during methylmercury toxicity in this model. This result also suggests that thiol peroxidase activity of organoselenium compounds accounts for their protective actions against methylmercury-induced oxidative stress. Our results show that diphenyl diselenide and potentially other organoselenium compounds may represent important molecules in the search for an improved therapy against the deleterious effects of methylmercury as well as other mercury compounds.

Studies of micronuclei and other nuclear abnormalities in red blood cells of Colossoma macropomum exposed to methylmercury

The frequencies of micronuclei (MN) and morphological nuclear abnormalities (NA) in erythrocytes in the peripheral blood of tambaqui (Colossoma macropomum), treated with 2 mg.L-1 methylmercury (MeHg), were analyzed. Two groups (nine specimens in each) were exposed to MeHg for different periods (group A - 24 h; group B - 120 h). A third group served as negative control (group C, untreated; n = 9). Although, when compared to the control group there were no significant differences in MN frequency in the treated groups, for NA, the differences between the frequencies of group B (treated for 120 h) and the control group were extremely significant (p < 0.02), thus demonstrating the potentially adverse effects of MeHg on C. macropomum erythrocytes after prolonged exposure.

Methylmercury neurotoxicity & antioxidant defenses.

Neurotoxicity induced by methylmercury (MeHg) increases the formation of reactive radicals and accelerates free radical reactions. This review summarizes recent findings in the MeHg-induced formation of free radicals and the role of oxidative stress in its neurotoxicity. Oxidative stress on CNS can produce damage by several interacting mechanisms, including mitochondrial damage with increase in intracellular free Ca(2+), activation and inhibition of enzymes, release of excitatory amino acids, metallothioneins expression, and microtubule disassembly. The nature of antioxidants is discussed and it is suggested that antioxidant enzymes and others antioxidants molecules may protect the central nervous system against neurotoxicity caused by MeHg.

Human mercury exposure and adverse health effects in the Amazon: a review / Exposição humana ao mercúrio e efeitos adversos à saúde na Amazônia: uma revisão

This paper examines issues of human mercury (Hg) exposure and adverse health effects throughout the Amazon region. An extensive review was conducted using bibliographic indexes as well as secondary sources. There are several sources of Hg (mining, deforestation, reservoirs), and exposure takes place through inhalation or from fish consumption. There is a wide range of exposure, with mean hair-Hg levels above 15µg/g in several Amazonian communities, placing them among the highest reported levels in the world today. Dietary Hg intake has been estimated in the vicinity of 1-2µg/kg/day, considerably higher than the USEPA RfD of 0.1µg/kg/day or the World Health Organization recommendation of 0.23µg/kg/day. Neurobehavioral deficits and, in some cases, clinical signs have been reported both for adults and children in relation to Hg exposure in several Amazonian countries. There is also some evidence of cytogenetic damage, immune alterations, and cardiovascular toxicity. Since fish provide a highly nutritious food source, there is an urgent need to find realistic and feasible solutions that will reduce exposure and toxic risk, while maintaining healthy traditional dietary habits and preserving this unique biodiversity.

Este artigo examina questões sobre exposição humana ao mercúrio (Hg) e seus efeitos adversos à saúde na Amazônia, com base em extensa revisão da literatura. Diferentes bioindicadores revelam uma ampla faixa de exposição, com teores médios de Hg em cabelo acima de 15µg/g em diversas comunidades amazônicas, situando-as dentre as mais expostas no mundo atualmente. Taxas de ingestão diária de Hg foram estimadas em alguns estudos e situam-se entre 1-2µg/kg/dia, consideravelmente acima das doses de referência estabelecidas pela USEPA (0,1µg/kg/dia) ou pela OMS (0,23µg/kg/dia). Déficits neurocomportamentais e, em alguns casos, sinais clínicos relacionados à exposição mercurial têm sido relatados tanto em adultos quanto em crianças de diversos países amazônicos. Há também evidências de dano citogenético, mudanças imunológicas e toxicidade cardiovascular. Visto que peixe é altamente nutritivo e há diversas fontes de Hg nesta região, existe uma necessidade urgente de encontrar soluções realistas e viáveis capazes de reduzir os níveis de exposição e de risco tóxico, ao mesmo tempo mantendo os hábitos alimentares tradicionais, preservando a biodiversidade píscea e frutífera e melhorando a saúde das populações desfavorecidas e afetadas.

Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicity

This review addresses the mechanisms of methylmercury (MeHg)-induced neurotoxicity, specifically examining the role of oxidative stress in mediating neuronal damage. A number of critical findings point to a central role for astrocytes in mediating MeHg-induced neurotoxicity as evidenced by the following observations: a) MeHg preferentially accumulates in astrocytes; b) MeHg specifically inhibits glutamate uptake in astrocytes; c) neuronal dysfunction is secondary to disturbances in astrocytes. The generation of reactive oxygen species (ROS) by MeHg has been observed in various experimental paradigms. For example, MeHg enhances ROS formation both in vivo (rodent cerebellum) and in vitro (isolated rat brain synaptosomes), as well as in neuronal and mixed reaggregating cell cultures. Antioxidants, including selenocompounds, can rescue astrocytes from MeHg-induced cytotoxicity by reducing ROS formation. We emphasize that oxidative stress plays a significant role in mediating MeHg-induced neurotoxic damage with active involvement of the mitochondria in this process. Furthermore, we provide a mechanistic overview on oxidative stress induced by MeHg that is triggered by a series of molecular events such as activation of various kinases, stress proteins and other immediate early genes culminating in cell damage.

Effects of mercury intoxication on the response of horizontal cells of the retina of thraira fish (Hoplias malabaricus)

Methyl mercury (MeHg) is highly neurotoxic, affecting visual function in addition to other central nervous system functions. The effect of mercury intoxication on the amplitude of horizontal cell responses to light was studied in the retina of the fish Hoplias malabaricus. Intracellular responses were recorded from horizontal cells of fish previously intoxicated with MeHg by intraperitoneal injection (IP group) or by trophic exposure (T group). Only one retina per fish was used. The doses of MeHg chloride administered to the IP group were 0.01, 0.05, 0.1, 1.0, 2.0, and 6.0 mg/kg. The amplitudes of the horizontal cell responses were lower than control in individuals exposed to 0.01 (N = 4 retinas), 0.05 (N = 2 retinas) and 0.1 mg/kg (N = 1 retina), whereas no responses were recorded in the 1.0, 2.0, and 6.0 mg/kg groups. T group individuals were fed young specimens of Astyanax sp previously injected with MeHg corresponding to 0.75 (N = 1 retina), 0.075 (N = 8 retinas) or 0.0075 (N = 4 retinas) mg/kg fish body weight. After 14 doses, one every 5 days, the amplitude of the horizontal cell response was higher than control in individuals exposed to 0.075 and 0.0075 mg/kg, and lower in individuals exposed to 0.75 mg/kg. We conclude that intoxication with MeHg affects the electrophysiological response of the horizontal cells in the retina, either reducing or increasing its amplitude compared to control, and that these effects are related to the dose and/or to the mode of administration.

Losses of immunoreactive parvalbumin amacrine and immunoreactive alphaprotein kinase C bipolar cells caused by methylmercury chloride intoxication in the retina of the tropical fish Hoplias malabaricus

To quantify the effects of methylmercury (MeHg) on amacrine and on ON-bipolar cells in the retina, experiments were performed in MeHg-exposed groups of adult trahiras (Hoplias malabaricus) at two dose levels (2 and 6 µg/g, ip). The retinas of test and control groups were processed by mouse anti-parvalbumin and rabbit anti-alphaprotein kinase C (alphaPKC) immunocytochemistry. Morphology and soma location in the inner nuclear layer were used to identify immunoreactive parvalbumin (PV-IR) and alphaPKC (alphaPKC-IR) in wholemount preparations. Cell density, topography and isodensity maps were estimated using confocal images. PV-IR was detected in amacrine cells in the inner nuclear layer and in displaced amacrine cells from the ganglion cell layer, and alphaPKC-IR was detected in ON-bipolar cells. The MeHg-treated group (6 µg/g) showed significant reduction of the ON-bipolar alphaPKC-IR cell density (mean density = 1306 ± 393 cells/mm²) compared to control (1886 ± 892 cells/mm²; P < 0.001). The mean densities found for amacrine PV-IR cells in MeHg-treated retinas were 1040 ± 56 cells/mm² (2 µg/g) and 845 ± 82 cells/mm² (6 µg/g), also lower than control (1312 ± 31 cells/mm²; P < 0.05), differently from the data observed in displaced PV-IR amacrine cells. These results show that MeHg changed the PV-IR amacrine cell density in a dose-dependent way, and reduced the density of alphaKC-IR bipolar cells at the dose of 6 µg/g. Further studies are needed to identify the physiological impact of these findings on visual function.

Methylmercury intoxication activates nitric oxide synthase in chick retinal cell culture

The visual system is a potential target for methylmercury (MeHg) intoxication. Nevertheless, there are few studies about the cellular mechanisms of toxicity induced by MeHg in retinal cells. Various reports have indicated a critical role for nitric oxide synthase (NOS) activation in modulating MeHg neurotoxicity in cerebellar and cortical regions. The aim of the present study is to describe the effects of MeHg on cell viability and NOS activation in chick retinal cell cultures. For this purpose, primary cultures were prepared from 7-day-old chick embryos: retinas were aseptically dissected and dissociated and cells were grown at 37°C for 7-8 days. Cultures were exposed to MeHg (10 µM, 100 µM, and 1 mM) for 2, 4, and 6 h. Cell viability was measured by MTT method and NOS activity by monitoring the conversion of L-[H³]-arginine to L-[H³]-citrulline. The incubation of cultured retina cells with 10 and 100 µM MeHg promoted an increase of NOS activity compared to control (P < 0.05). Maximum values (P < 0.05) were reached after 4 h of MeHg incubation: increases of 81.6 ± 5.3 and 91.3 ± 3.7 percent, respectively (data are reported as mean ± SEM for 4 replicates). MeHg also promoted a concentration- and time-dependent decrease in cell viability, with the highest toxicity (a reduction of about 80 percent in cell viability) being observed at the concentration of 1 mM and after 4-6 h of incubation. The present study demonstrates for the first time the modulation of MeHg neurotoxicity in retinal cells by the nitrergic system.

Cytotoxicity and genotoxicity of low doses of mercury chloride and methylmercury chloride on human lymphocytes in vitro

Mercury is a xenobiotic metal that is a highly deleterious environmental pollutant. The biotransformation of mercury chloride (HgCl2) into methylmercury chloride (CH3HgCl) in aquatic environments is well-known and humans are exposed by consumption of contaminated fish, shellfish and algae. The objective of the present study was to determine the changes induced in vitro by two mercury compounds (HgCl2 and CH3HgCl) in cultured human lymphocytes. Short-term human leukocyte cultures from 10 healthy donors (5 females and 5 males) were set-up by adding drops of whole blood in complete medium. Cultures were separately and simultaneously treated with low doses (0.1 to 1000 æg/l) of HgCl2 and CH3HgCl and incubated at 37°C for 48 h. Genotoxicity was assessed by chromosome aberrations and polyploid cells. Mitotic index was used as a measure of cytotoxicity. A significant increase (P < 0.05) in the relative frequency of chromosome aberrations was observed for all concentrations of CH3HgCl when compared to control, whether alone or in an evident sinergistic combination with HgCl2. The frequency of polyploid cells was also significantly increased (P < 0.05) when compared to control after exposure to all concentrations of CH3HgCl alone or in combination with HgCl2. CH3HgCl significantly decreased (P < 0.05) the mitotic index at 100 and 1000 æg/l alone, and at 1, 10, 100, and 1000 æg/l when combined with HgCl2, showing a synergistic cytotoxic effect. Our data showed that low concentrations of CH3HgCl might be cytotoxic/genotoxic. Such effects may indicate early cellular changes with possible biological consequences and should be considered in the preliminary evaluation of the risks of populations exposed in vivo to low doses of mercury.

Avaliaçäo da exposiçäo ao metil-mercúrio na população ribeirinha da baixada cuiabana, no Pantanal Mato-Grossense - Brasil / Evaluation of methylmercury exposure in riverine population from Baixada Cuiabana, Pantanal Region of Brazil

A população ribeirinha na região do Pantanal, Brasil, é dependente do peixe, como principal fonte de alimentos e proteínas. Naquela região, o resultado de décadas de mineração de ouro, em pequena escala, foi a contaminação de muitos sistemas aquáticos com mercúrio. Conseqüentemente, muitas espécies de peixes possuem níveis de MeHg relativamente altos. O objetivo deste trabalho foi avaliar o nível de exposição ao MeHg entre a população ribeirinha do Pantanal. No primeiro artigo, apresentam-se os resultados de validação do método recordatório de 24 horas auto-referido, utilizando-se como padrão ouro, o método da pesagem, tendo-se verificado que há aproximadamente um erro de 30 por cento ao estimar a quantidade de peixe consumido por aquela população. Um erro de 30 por cento na estimativa do consumo de peixe pode nao ter muita influencia na avaliaçao da ingestão de mercúrio, se se considerarem os peixes das espécies herbívoras. Porém, este erro pode ser importante em se tratando do consumo de peixes carnívoros, os quais apresentam altos teores de mercúrio. No segundo artigo, ao analisar a associação entre o status neurocognitivo e a concentração de mercúrio no cabelo da população acima, os resultados indicaram que adultos expostos ao metil-mercúrio, através do consumo de peixe, podem ter déficits importantes nas medidas do desempenho neurocomportamental, sem alterações detectáveis no humor ou afetividade. Os efeitos mais importantes do mercúrio, entre os indivíduos analisados, foram detectados nos testes de velocidade e destreza da coordenação motora fina, na inibição da resposta na busca visual, e em tarefas de atenção. Estes resultados são consistentes com outros estudos, que sugeriram que o mercúrio causa alterações no cerebelo. A possibilidade de efeitos adversos, em adultos expostos a níveis mais baixos de mercúrio, foi também levantada por outros estudos no Brasil, que abordaram o consumo de peixe pelas populações ribeirinhas. No terceiro artigo ... calculou-se a dose marcadora (BMD) e o limite inferior do intervalo de confiança do BMD (BMDL)...

Protective effects of garlic juice against embryotoxicity of methylmercuric chloride administered to pregnant Fischer 344 rats

In order to investigate the beneficial effects of 0.5 or 1.0 g/kg Korean garlic juice against the embryotoxicity of 20 mg/kg methylmercury chloride (MMC, CH3HgCl), pregnant Fisher 344 rats were simultaneously orally administered on day 7 of gestation. On day 20 of gestation the dams were laparotomized under ether anesthesia, and the fetuses were removed and examined for toxicity of methylmercury. Garlic juice depressed the toxicity in terms of some parameters. In the case of simultaneous treatment with 0.1 g/kg garlic juice and MMC, rates of increase were 17.5% in maternal body weight, 13.2% and 41.9% in fetal and litters' weight respectively, and 37.0% in fetal survival rate. Decreasing rates were 10.0% in maternal death rate, and 6.9% and 31.3% in pre- and post-implantation loss respectively. Decreasing rates of mercury levels in dams were 67.2% in liver, 57.6% in brain, 47.2% in kidney, 42.1% in spleen and 40.9% in blood. As well, decreasing rates of mercury level in fetuses were 54.9% in all body burden, 55.9% in liver, 46.7% in kidney and 37% in brain, respectively. The number of fetal ossification centers were reduced by 23.8% to 58.0% following simultaneous treatment with 1.0 g/kg garlic juice. These findings indicated that garlic juice effectively inhibited the embryotoxicity of methylmercury in pregnant Fischer 344 rats.

Methylmercury induced biochemical and histochemical alterations in rat testis.

The methylmercurry chloride (MMC) administered at doses of 5 and 10 micrograms/kg over a period of 90 days to male rats caused enzymatic impairments in testicular tissue. The study at intervals of 15, 30, 60 and 90 days showed gradual diminution of testicular weight and gradual decrements in testicular protein and inhibition in testicular succinic dehydrogenase activity. Histochemical and biochemical studies revealed that testicular acid phosphatase activity was also inhibited at both the doses of MMC treatment. The inhibition of enzyme activity in testicular tissues after MMC treatment caused the impairment of both spermatogenesis and steroidogenesis in rats.

Algumas bases bioquímicas da Toxodinâmica do mercúrio / Some biochemical bases of toxicological dynamics of mercury

Num pequeno artigo de revisäo colecionam-se muitas das possíveis explicaçöes para a toxicodinâmica do mercúrio encontradas na literatura específica. Enfase especial é dada à ligaçäo do mercúrio com o grupo sulfidrila e às consequentes alteraçöes da atividade de várias enzimas. O papel genotóxico do mércúrio e seus compostos é levantado. Uma série advertência com relaçäo ao intenso uso do mercúrio metálico no garimpo do ouro no Brasil é feita