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Navegando por Assunto "Compostos de metilmercúrio"

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    Análise transcriptômica das linhagens celulares B103 e C6 expostas à ação do metilmercúrio
    (Universidade Federal do Pará, 2023-04) BONFIM, Laís Teixeira; FERREIRA, Wallax Augusto Silva Ferreira; OLIVEIRA, Edivaldo Herculano Correa de; http://lattes.cnpq.br/009400771470765; https://orcid.org/0000-0001-6315-3352
    The intensification of anthropogenic activities produces a high rate of environmental pollution, mainly in water bodies, where the contamination by metals has become an object of great interest, due to their inability to support such load. Mercury (Hg) is a naturally occurring metal that can be used in the manufacture of home products such as fluorescent lamps, fungicides, and germicides. The entry of Hg into the food chain occurs through the methylation of Hg2+ ions into MeHg. After methylation, Hg is considered highly toxic to humans, and among the main target organs of this intoxication we can mention the brain, since MeHg easily crosses the blood-brain barrier and can accumulate in different brain areas. It is known that, once in the CNS, MeHg can cause extensive cellular damage, such as DNA damage, oxidative stress, neuroinflammation and cell death in both neurons and glial cells. Thus, the objective of this study was to analyze the transcriptomic alterations of cell lines B103 and C6, derived from neuroblastoma and glioma of Rattus norvegicus, exposed to the action of methylmercury. For this, the expression microarray technique was used to evaluate the global profile of gene expression after 24h of MeHg exposure. Our results demonstrate that MeHg induces significant alterations in gene expression of the two cell lines evaluated. The alterations were more prominent in the C6 cell line, in which a greater amount of differentially expressed genes was observed. Among the genes differentially expressed of the B103 cells we can highlight the genes Cdc42se2 (log2 FC -4.055713), Dcx (log2 FC 3.618981) and 4930449C09Rik (log2 FC 3.5129156) at a concentration of 0.1 μM. As for the exposure of 2.8 μM, the genes with the highest FC were Crem (log2 FC -4.027875), Otoa (log2 FC 3.501512) and Dcx (log2 FC 3.423433). In addition to the abovementioned genes, the genes Trim14, Gm14169, Gm30871, Otoa and Dcx were shared between the two exposed groups. As for the C6 lineage, ten transcripts with FC above 3 (Aldh1l2, Dac1, Rps4l, Zbtb46, 6430573p05Rik, Tcf12, Awat2, Muc3, Dclre1b, Slc38a6) are highlighted. In the 6.3 μM treatment, only three genes were altered more than 3 times (Rps4l, Ankdr44 and 2610318N02Rik). It is also noteworthy that three genes were shared between treatments (Rps4l, Lamb 3 and Gm 41386).
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    Avaliação do efeito protetor da Euterpe oleracea (açaí) na resposta eletrofisiológica da retina de ratos expostos ao metilmercúrio
    (Universidade Federal do Pará, 2013-03-19) COSTA, Alódia Brasil; ROCHA, Fernando Allan de Farias; http://lattes.cnpq.br/3882851981484245; HERCULANO, Anderson Manoel; http://lattes.cnpq.br/8407177208423247
    Methylmercury (MeHg) is organic form most toxic of mercury. The MeHg exposure generates oxidative stress may affect the retina, because it has a high vulnerability due to their high content of polyunsaturated fatty acids and oxygen consumption. In this context, administration of exogenous antioxidants obtained from the diet, such as those present in Euterpe oleracea (açaí), could be a way to prevent this imbalance and its consequences. Therefore, the objective of this study was to evaluate the possible protective effect of Euterpe oleracea in electrophysiological changes caused by MeHg in the retina. For this was performed gavage with MeHgCl (5mg/kg) or saline (NaCl 0.9%) for 7 days and pretreatment with açaí (10%) per 28 days. Was used Wistar rats were divided into 4 groups: Group MeHg (received standard diet and MeHgCl); MeHg + Acai (enriched diet with acai and MeHgCl); Acai (enriched diet with açai and NaCl); Vehicle (standard diet and NaCl). One day after the last gavage animals were subjected to full-field electroretinography (ffERG) to obtain the scotopic responses (rods, mixed 1 and mixed 2) and photopic responses (cone and flicker at 12, 18, 24 and 30Hz). The next day to the ffERG was applied open field test to evaluate the animals locomotor activity. Subsequently, measurement of the lipid peroxidation by the method TBARS in retinal tissue. Statistical analysis was done by one-way ANOVA with Tukey post-test, considering significant p<0.05. The open field and body weight results showed no difference between groups. The MeHg reduced the amplitude of the following responses: b-wave in rod response (Vehicle: 114.6 ± 23.6 μV and MeHg: 41.2 ± 9.6 μV); a-wave (Vehicle: 8.4 μV and MeHg ± 1.4: 3.4 ± 0.3 μV) and b-wave (Vehicle: 176.7 ± 17.8 μV and MeHg: 69.5 ± 12.0 μV) in mixed 1 responses; a-wave (Vehicle: 103.1 ± 23.3 μV and MeHg: 40.2 ± 9.6 μV) and b-wave (Vehicle: 281 ±, 38.3 μV and MeHg: 138.6 ± 14μV) in mixed 2 response; a-wave (Vehicle: 27.2 ± 3.6 μV and MeHg: 7.5 ± 1.8 μV) and b-wave (Vehicle: 139.3 ± 16.1 μV and MeHg: 54.4 ± 10μV) of cones response; b-wave in frequencies 12 Hz (Vehicle: 67.7 ± 10μV and MeHg: 28.6 ± 6.9 μV), 18Hz (Vehicle: 31.3 ± 3.4 μV and MeHg : 14.2 ± 2.3 μV), 24Hz (Vehicle: 21.0 ± 1.8 μV and MeHg: 11.0 ± 1.1 μV) and 30Hz (Vehicle: 10.9 ± 0.6 μV and MeHg: 6.0 ± 1.1 μV). While the implicit time of the waves was not altered. The pretreatment with Euterpe oleracea prevented the decrease of amplitude of both waves in mixed 1 (a-wave: 8.3 ± 0.6 μV; b-wave: 144.1 ± 7,1 μV) and mixed 2 responses (a-wave: 106.4 ± 13.6 μV; b-wave: 275,2±27,6 μV), b-wave of cone response (104.5 ± 5.9 μV) and photopic flicker at 12 Hz (67.2 ± 9.1 μV), 18 Hz (29.5 ± 4.8 μV) and 24 Hz (21.9 ± 2.4 μV). Lipid peroxidation in retinal tissue of MeHg group (294.9 ± 205.8%) was higher than that of the Vehicle (100 ± 25.1%) and açaí protected against this oxidative damage (MeHg + Acai = 111.2 ± 26.1%). Our results demonstrate diffuse alteration in the electrophysiological response and increase in lipid peroxidation of the retina induced by MeHg and protection exerted by Euterpe oleracea in these two parameters. Thus, Euterpe oleracea could be used as an important alternative to attenuate the changes in the retina caused by MeHg.
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    Avaliação dos marcadores de injúria miocárdica induzida pela exposição ao metilmercúrio em modelos experimentais de primatas do novo mundo (Cebus Apella)
    (Universidade Federal do Pará, 2009-07-10) MAGNO, Ismaelino Mauro Nunes; QUARESMA, Juarez Antônio Simões; http://lattes.cnpq.br/3350166863853054
    This study aimed to examine effects of the mechanisms of injury producing cellular damage in the heart of the monkey Cebus apella exposed for 120 consecutive days, with daily dose of 1.5 methyl Hg, by changes detected in biochemical markers of myocardial injury CK - MB, the histopathological findings as well as the technique of immunolabeling of apoptotic cells. For that, we related to the serum profiles of CK-MB, total CK, AST, ALT, urea, creatinine and total bilirubin with the histopathological and immunohistochemical findings in the involvement of the heart muscle during exposure to methyl Hg, and compared with a control group. The method used for determination and analysis of the serum and the determination of mercury in blood was the kinetic ultraviolet; atomic absorption spectroscopy, respectively; for histopathological analysis used the technique of Hematoxylin and Eosin; and for detection of apoptotic profiles the method APOPTAG. Was obtained information that correlate the biochemical changes, histopathologic profiles and apoptotic mechanism of cardiac involvement in three animals exposed to methyl Hg, when compared with control group. Among all substances of biochemical analysis were found that there was only marked increase of serum CK-MB enzyme, whereas, the histopathologic analysis showed reversible cell damage by accumulation of water in the three organs examined (heart, liver and kidney). It is also the observation of a clear labeling of apoptotic cells in heart, liver and kidney tissues of exposed animals, showing a higher number of positive cells in cells of renal tubules. Emphasizing that there was no inflammatory infiltrate around these tissues described and analyzed, and was there absence of such lesions in tissues of three control animals. It was concluded that the enzyme CK-MB, the hydropic degeneration and the mechanism of apoptosis may be indicators of myocardial injury in acute exposure to methyl Hg whose pathogenesis could be related to mitochondrial decompensation because massive commitment of the Na + / K + and Ca + + pumps. Requiring a greater intake of experimental studies that can clarify the exact pathogenesis, the mechanism of cellular injury and aggression in individuals exposed to toxic doses of methyl Hg.
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    Efeitos protetores da prolactina em cultivo glial de córtex de ratos expostos ao metilmercúrio
    (Universidade Federal do Pará, 2008-04-04) SANTOS, Andréa Cristina Monteiro dos; DINIZ, Domingos Luiz Wanderley Picanço; http://lattes.cnpq.br/9601463988942971
    Methylmercury (MeHg) is a compound highly neurotoxic and its degenerative mechanisms are not very clear yet. In Central Nervous System, MeHg is mostly uptake by astrocytes, decreasing neuronal exposition. Studies demonstrated that prolactin (PRL) has mitogenic effects on astrocytes and it can regulate pro-inflammatories cytokines expression. The aim of this work was to verify the protective effects of PRL on disturbs provoked by MeHg on cellular viability, morphology, GFAP (glial fibrillary acidic protein) expression, mitogenesis and release of interleukin-1β in glia primary culture of cerebral cortex of newborn rats, with astrocytes in focus. Glia primary culture were exposed to differents concentrations of MeHg (0,1, 1, 5 e 10 μM) in differents time intervals (2, 4, 6, 18 e 24 h) in medium with fetal bovine serum 10%. Results demonstrated progressive decreasing of 20% e 62% on cellular viability after exposed to 5 e 10 μM MeHg for 24 h, respectively, by MTT [3- (4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay and disturbs in the GFAP expression and distribution. Differents concentrations of PRL (0.1, 1 e 10 nM) were added in free serum medium to evaluate it proliferative action. This was confirmed by mitogenesis induction around 4.5x in 18h at 10 mM PRL. In this conditions (free serum) were evaluated the effects of co-treatment of 1 nM PRL + 5 μM MeHg on cellular viability, morphology, GFAP expression, mitotic index and release of IL-1β. PRL attenuated disturbs caused by MeHg, increasing viability in 33%, GFAP expression, cellular proliferation (4x), and attenuating morphologic alterations like nuclear picnosis and lisis. These findings prove that PRL can act like a cytoprotective agent in primary culture of glia, particularly in astrocytes, in addition to its mitogenic effects.
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    Investigação dos efeitos protetores do selenito de sódio sobre a neurotoxicidade do metilmercúrio em diferentes períodos de desenvolvimento de ratos wistar
    (Universidade Federal do Pará, 2011-12-28) SANTOS, Nilton Barreto dos; COSTA, Edmar Tavares da; http://lattes.cnpq.br/6776869402973569; YAMADA, Elizabeth Sumi; http://lattes.cnpq.br/7240314827308306
    Exposure to mercury compounds results in oxidative damages, seriously affecting the central nervous system both in humans and in experimental models. We used Wistar rats at different stages of neuro-development in order to investigate potential protective effects of selenium (sodium selenite) in an in vivo model of exposure to methylmercury (MeHg). Subjects (age groups P1 and P21) were given lactational and orally, respectively: vehicle, Selenium (5ppm), MeHg (10 ppm) or selenium (5 ppm) plus MeHg (10 ppm) for 20 and 10 days respectively (n = 8 per group). After treatment, the rats were submitted to the following behavioral tests: open field and Morris water maze to examine motor deficits and memory/learning, respectively. After intracardiac perfusion we performed immunohistochemistry for Neu-N. In order to evaluate possible deleterious effects in neuronal populations, we counted neurons in the hippocampus (polymorphic layer). As a result, we found significant reduction in locomotor activity of neonates (P1) when exposed to MeHg. Besides, groups exposed to MeHg (alone or in association with selenium) showed learning/memory deficits. P21 animals treated with MeHg showed increase in locomotor activity, effect abolished by concomitant administration of selenium. When submitted to water maze, only subjects in the control and selenium groups showed reduction of the time latency. As assessed by stereological counting, we noticed reduction in the number of hippocampal neurons only in P21 animals exposed to MeHg. Combined, our results showed that MeHg exposure produces age-dependent behavioral effects. Also, despite other findings in the literature, under our experimental conditions administration of selenium was only able to interfere with motor deficits in older animals, besides not being able to interfere with memory/learning deficits nor the MeHg-induced neuronal death. Possible mechanisms associated with these partial protective properties of selenium in the later stages of neural development have yet to be elucidated.
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    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
    (2006-03) BONCI, Daniela Maria Oliveira; LIMA, Silene Maria Araújo de; GRÖTZNER, Sonia Regina; RIBEIRO, Ciro Alberto de Oliveira; HAMASSAKI, Dânia Emi; VENTURA, Dora Selma Fix
    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-aprotein kinase C (aPKC) immunocytochemistry. Morphology and soma location in the inner nuclear layer were used to identify immunoreactive parvalbumin (PV-IR) and aPKC (aPKC-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 aPKC-IR was detected in ON-bipolar cells. The MeHg-treated group (6 µg/g) showed significant reduction of the ON-bipolar aPKC-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 aKC-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.
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    Potencial neuroprotetor da atividade física em populações ribeirinhas da Amazônia expostas ao mercúrio
    (Universidade Federal do Pará, 2025-05) NAZARÉ, Caio Gustavo Leal de; OLIVEIRA, Marcus Augusto de; http://lattes.cnpq.br/6036530007649294; HTTPS://ORCID.ORG/0000-0002-4772-9929; LOPEZ, Maria Elena Crespo; http://lattes.cnpq.br/9900144256348265; https://orcid.org/0000-0002-1335-6853
    Mercury is a highly toxic metal and is among the three substances with the greatest potential threat to human health. Its organic form, methylmercury, is particularly dangerous to human health due to its ability to easily cross biological barriers. The brain is a critical target for methylmercury, where it can cause neurological disorders, including motor, visual, auditory, behavioral, and cognitive deficits. Glial cells are closely involved in the mechanisms mediating such disorders and can either protect or damage the central nervous system (CNS), depending on the context. Moreover, no pharmacological treatment has proven effective against mercury intoxication to date, and literature has shown that both physical exercise and physical activity are capable of modulating glial aspects involved in the pathophysiology common to various neurological conditions and methylmercury intoxication. Thus, a potentially therapeutic and non-pharmacological approach, such as physical exercise – and even physical activity – would be particularly suitable for vulnerable populations who are economically, socially, and geographically disadvantaged, such as the riverine communities of the Amazon, who are chronically exposed to methylmercury through the consumption of contaminated fish. This study aims to assess whether physical activity profiles can influence the symptomatology of methylmercury intoxication in riverside residents of the Tucuruí Lake region. Interviews were conducted to obtain a profile of physical activity and self-reported neurological symptoms, and total mercury was measured from hair samples. Our results point to a possible and complex relationship between hair mercury levels and physical activity, suggesting that physical exercise may be a viable alternative to be included in daily life.
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