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Mercury Exposure (mercury + exposure)

Distribution by Scientific Domains

Chemistry	27%

Selected Abstracts

Detoxification and antioxidant effects of curcumin in rats experimentally exposed to mercury

JOURNAL OF APPLIED TOXICOLOGY, Issue 5 2010
Rakhi Agarwal
Abstract Curcumin, a safe nutritional component and a highly promising natural antioxidant with a wide spectrum of biological functions, has been examined in several metal toxicity studies, but its role in protection against mercury toxicity has not been investigated. Therefore, the detoxification and antioxidant effects of curcumin were examined to determine its prophylactic/therapeutic role in rats experimentally exposed to mercury (in the from of mercuric chloride-HgCl2, 12,µmol,kg,1 b.w. single intraperitoneal injection). Curcumin treatment (80,mg,kg,1 b.w. daily for 3 days, orally) was found to have a protective effect on mercury-induced oxidative stress parameters, namely, lipid peroxidation and glutathione levels and superoxide dismutase, glutathione peroxidase and catalase activities in the liver, kidney and brain. Curcumin treatment was also effective for reversing mercury-induced serum biochemical changes, which are the markers of liver and kidney injury. Mercury concentration in the tissues was also decreased by the pre/post-treatment with curcumin. However, histopathological alterations in the liver and kidney were not reversed by curcumin treatment. Mercury exposure resulted in the induction of metallothionein (MT) mRNA expressions in the liver and kidney. Metallothionein mRNA expression levels were found to decrease after the pre-treatment with curcumin, whereas post-treatment with curcumin further increased MT mRNA expression levels. Our findings suggest that curcumin pretreatment has a protective effect and that curcumin can be used as a therapeutic agent in mercury intoxication. The study indicates that curcumin, an effective antioxidant, may have a protective effect through its routine dietary intake against mercury exposure. [source]

Mercury-induced reproductive impairment in fish,,

ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 5 2009
Kate L. Crump
Abstract Mercury is a potent neurotoxin, and increasing levels have led to concern for human and wildlife health in many regions of the world. During the past three decades, studies in fish have examined the effects of sublethal mercury exposure on a range of endpoints within the reproductive axis. Mercury studies have varied from highly concentrated aqueous exposures to ecologically relevant dietary exposures using levels comparable to those currently found in the environment. This review summarizes data from both laboratory and field studies supporting the hypothesis that mercury in the aquatic environment impacts the reproductive health of fish. The evidence presented suggests that the inhibitory effects of mercury on reproduction occur at multiple sites within the reproductive axis, including the hypothalamus, pituitary, and gonads. Accumulation of mercury in the fish brain has resulted in reduced neurosecretory material, hypothalamic neuron degeneration, and alterations in parameters of monoaminergic neurotransmission. At the level of the pituitary, mercury exposure has reduced and/or inactivated gonadotropin-secreting cells. Finally, studies have examined the effects of mercury on the reproductive organs and demonstrated a range of effects, including reductions in gonad size, circulating reproductive steroids, gamete production, and spawning success. Despite some variation between studies, there appears to be sufficient evidence from laboratory studies to link exposure to mercury with reproductive impairment in many fish species. Currently, the mechanisms underlying these effects are unknown; however, several physiological and cellular mechanisms are proposed within this review. [source]

Genetic and demographic responses of mercury-exposed mosquitofish (Gambusia holbrooki) populations: Temporal stability and reproductive components of fitness

ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 10 2002
Christopher Paul Tatara
Abstract Two previous mesocosm studies showed changes in glucosephosphate isomerase-2 (Gpi-2) allele frequencies in mosquitofish populations exposed to mercury for 111 d or two years. A previous selection component analysis of single-generation populations exposed for 111 d to 18 ,/L Hg suggested that female sexual selection and fecundity selection could contribute to changes in Gpi-2 allele frequencies. The present multigeneration study was conducted to determine the stability of Gpi-2 allele frequencies over four years of mercury exposure, measure the reproductive fitness of Gpi-2 genotypes inhabiting control and mercury-contaminated mesocosms to determine a mechanism explaining changes in Gpi-2 allele frequencies, investigate differences in the demographic characteristics of mercury-exposed and control populations, and investigate the water quality of the mesocosms to determine if variables other than mercury show concordant patterns among mesocosms. Differences in Gpi-2 allele frequencies between control and mercury-exposed populations were stable over four years (, eight generations) of mercury exposure. Mercury-exposed female mosquitofish had a lower probability of being gravid than control females (p = 0.001). Mercury-exposed females also had lower fecundity (total number of eggs and embryos) than control females (p = 0.036). Unlike the results of the more intense mercury exposures in the single generation study, no strong evidence was found that Gpi-2 genotype influenced fecundity or the probability of being gravid in both control and mercury-exposed females. The quantification of fitness components is difficult but has the potential to enhance our understanding of how toxicants alter allele frequencies in exposed populations. [source]

Effect of mercury and Gpi-2 genotype on standard metabolic rate of eastern mosquitofish (Gambusia holbrooki),

ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 4 2001
Christopher Paul Tatara
Abstract Previous studies demonstrated differential mortality among mosquitofish of different Gpi-2 genotypes during acute mercury and arsenate exposures. Mercury-exposed mosquitofish also had Gpi-2 genotype-specific differences in glycolytic and Krebs cycle metabolite pools. The mortality and metabolite data suggested that mosquitofish bearing specific Gpi-2 genotypes might differ in metabolic efficiency, with less efficient Gpi-2 genotypes having higher standard metabolic rates (SMRs) and shorter times to death during acute mercury exposure. Effect of Gpi-2 genotype on SMR was assessed with a factorial arrangement of six Gpi-2 genotypes and two exposure sequences (Control , Control; Control , 100 ,g/L Hg). The SMRs were estimated by measuring oxygen consumption using an indirect, closed-circuit, computer-controlled respirometer. A 48-h exposure to 100 ,g/L of mercury resulted in a 16.7% elevation of SMR above control levels (p = 0.001). The Gpi-2 genotype and the number of heterozygous loci per individual had no significant effect on SMR in mercury-exposed mosquitofish. The experimental results do not support the hypothesis that Gpi-2 genotype-specific differences in glycolytic and Krebs cycle metabolite pools and mortality in mosquitofish exposed to mercury are associated with differences in SMR. [source]

Statistical methods for the evaluation of health effects of prenatal mercury exposure

ENVIRONMETRICS, Issue 2 2003
Esben Budtz-Jørgensen
Abstract Environmental risk assessment based on epidemiological data puts stringent demands on the statistical procedures. First, convincing evidence has to be established that there is a risk at all. In practice this endeavor requires prudent use of the observational epidemiological information with delicate balancing between utilizing the information optimally but not over-interpreting it. If a case for an environmental risk has been made, the second challenge is to provide useful input that regulatory authorities can use to set standards. This article surveys some of these issues in the concrete case of neurobehavioral effects in Faroese children prenatally exposed to methylmercury. A selection of modern, appropriate methods has been applied in the analysis of this material that may be considered typical of environmental epidemiology today. In particular we emphasize the potential of structural equation models for improving standard multiple regression analysis of complex environmental epidemiology data. Copyright © 2003 John Wiley & Sons, Ltd. [source]

Detoxification and antioxidant effects of curcumin in rats experimentally exposed to mercury

Diphenyl diselenide protects against hematological and immunological alterations induced by mercury in mice

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 5 2008
Ricardo Brandão
Abstract Mercury is a heavy metal that can cause a variety of toxic effects on the organism, such as hematological and immunological alterations. In the present investigation, deleterious effects of mercury-intoxication in mice and a possible protective effect of diphenyl diselenide (PhSe)2 were studied. Male adult Swiss albino mice received daily a pretreatment with (PhSe)2 (15.6 mg/kg, orally) for 1 week. After this week, mice received daily mercuric chloride (1 mg/kg, subcutaneously) for 2 weeks. A number of hematological (erythrocytes, leukocytes, platelets, hemoglobin, hematocrit, reticulocytes, and leukocytes differential) and immunological (immunoglobulin G and M plasma concentration) parameters were evaluated. Another biomarker of tissue damage, lactate dehydrogenase (LDH), was also determined. The results demonstrated that mercury exposure caused a reduction in the erythrocyte, hematocrit, hemoglobin, leukocyte, and platelet counts and an increase in the reticulocyte percentages. (PhSe)2 was effective in protecting against the reduction in hematocrit, hemoglobin, and leukocyte levels. (PhSe)2 ameliorated reticulocyte percentages increased by mercury. However, (PhSe)2 was partially effective in preventing against the decrease in erythrocyte and platelet counts. Immunoglobulin G and M concentrations and LDH activity were increased by mercury exposure, and (PhSe)2 was effective in protecting against these effects. In conclusion, (PhSe)2 was effective in protecting against hematological and immunological alterations induced by mercury in mice. © 2008 Wiley Periodicals, Inc. J Biochem Mol Toxicol 22:311,319, 2008; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20242 [source]

Inheritance of mercury tolerance in the aquatic oligochaete Tubifex tubifex

ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 9 2003
Dora Elva Vidal
Abstract Resistance to contaminants is an important yet unmeasured factor in sediment toxicity tests. The rate at which mercury resistance develops and its genetic persistence in the oligochaete worm Tubifex tubifex were studied under laboratory conditions. Worms were raised for four generations under two different sediment treatments, one reference clean sediment, the other contaminated with mercury. Worms raised in mercury-contaminated sediment developed mercury tolerance that persisted even when the worms were raised for three subsequent generations in clean sediment. Mercury tolerance was determined by comparative water-only toxicity tests with mercury as the only stressor. Control worms had a mean lethal concentration (LC50) of 0.18 mg/L,1. Worms exposed to high levels of mercury in sediment had high mercury tolerance with a mean LC50 of 1.40 mg/L,1. When mercury-tolerant and control mercury-intolerant worms were crossed, their descendants also demonstrated mercury tolerance during lethal toxicity tests. The LC50 for worm descendants resulting from this cross was 1.39 mg/L,1. Adaptation to mercury exposures occurred rapidly in this group of worms and appears to be due to both phenotypic and genotypic mechanisms. Development of contaminant resistance and adaptation may be common phenomena in aquatic benthic invertebrates, which should be considered during the design and interpretation of toxicity tests. [source]

Genetic and demographic responses of mercury-exposed mosquitofish (Gambusia holbrooki) populations: Temporal stability and reproductive components of fitness

Maximum limits of organic and inorganic mercury in fish feed

AQUACULTURE NUTRITION, Issue 2 2004
M.H.G. Berntssen
Abstract The relatively high levels of mercury found in fish feeds might form a fish health and food safety risk. The present study aims to establish sublethal toxic threshold levels in fish and assess feed-fillet transfer of dietary mercury. Atlantic salmon (Salmo salar L.) parr were fed for 4 months on fish meal-based diets supplemented with mercuric chloride (0, 0.1, 1, 10 or 100 mg Hg kg,1 dry weight (DW)) or methylmercuric chloride (0, 0.1, 0.5, 5 or 10 mg MeHg kg,1 DW). At the end of the experiment, dietary inorganic mercury mainly accumulated in intestine (80% of body burden) and assimilation was low (6%). In contrast, methylmercury readily accumulated in internal organs and muscle (80% of body burden) and had a relatively high assimilation (23%). Highest accumulation of dietary inorganic mercury was observed in the gut and kidney. Fish fed 10 mg Hg kg,1 had an early (after 2 months) significant increase in renal metallothionein (MT) level and intestinal cell proliferation, followed by intestinal pathological conditions after 4 months of exposure. At 100 mg Hg kg,1, intestinal and renal function were reduced as seen from the significantly reduced protein and glycogen digestibility and increased plasma creatinine levels. For dietary methylmercury (MeHg), highest accumulation was found in blood and muscle. Intestinal cell proliferation and liver MT significantly increased at 5 mg MeHg kg,1 after 2 months of exposure. At the end of the experiment, blood haematology was significantly affected in fish fed 5 mg MeHg kg,1 and these fish exceeded the current food safety limit for mercury. Tissue MT induction and intestinal cell proliferation appeared to be useful and quantifiable early indicators of toxic mercury exposures. Based on the absence of induction of these early biological markers such as MT and cell proliferation, nonobserved effect levels (NOELs) could be set to 0.5 mg Hg kg,1 for dietary methylmercury and 1 mg Hg kg,1 for inorganic mercury. Lowest observed effect levels (LOELs) levels could be set to 5 mg kg,1 for methylmercury and 10 mg Hg kg,1 for inorganic mercury. [source]