Low levels of methylmercury induce DNA damage in rats: protective effects of selenium

Grotto, Denise; Barcelos, Gustavo Rafael Mazzaron; Valentini, Juliana; Antunes, Lusânia Maria Greggi; Angeli, José Pedro Friedmann; Garcia, Solange Cristina; Barbosa, Fernando de Holanda

doi:10.1007/s00204-008-0387-6

Cited by 5 publications

(5 citation statements)

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“…Regarding methylmercuric chloride a recent study provide evidence for a genotoxic potential after oral exposure in rats. After 100 days of exposure to 100 µg methylmercuric chloride per day (by gavage), rat white blood cells showed statistically significantly more DNA damage (as measured by the Comet assay) than white blood cells in control animals; co-administration of selenium reduced DNA damage, probably by re-establishment of glutathione peroxidase activity (Grotto et al, 2009a). The same group demonstrated that in direct comparison with rats receiving commercial food or a diet rich in uncontaminated fish, a 12-week diet with methylmercury contaminated fish resulted in an increase of DNA damage in peripheral blood of the respective rats.…”

Section: Genotoxicitymentioning

confidence: 97%

Scientific Opinion on the risk for public health related to the presence of mercury and methylmercury in food

2012

EFS2

463

160

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EFSA was asked by the European Commission to consider new developments regarding inorganic mercury and methylmercury toxicity and evaluate whether the Joint FAO/WHO Expert Committee on Food Additives (JECFA) provisional tolerable weekly intakes for methylmercury of 1.6 µg/kg body weight (b.w.) and of 4 µg/kg b.w. for inorganic mercury were still appropriate. In line with JECFA, the CONTAM Panel established a tolerable weekly intake (TWI) for inorganic mercury of 4 µg/kg b.w., expressed as mercury. For methylmercury, new developments in epidemiological studies from the Seychelles Child Developmental Study Nutrition Cohort have indicated that n-3 long-chain polyunsaturated fatty acids in fish may counteract negative effects from methylmercury exposure. Together with the information that beneficial nutrients in fish may have confounded previous adverse outcomes in child cohort studies from the Faroe Islands, the Panel established a TWI for methylmercury of 1.3 µg/kg b.w., expressed as mercury. The mean dietary exposure across age groups does not exceed the TWI for methylmercury, with the exception of toddlers and other children in some surveys. The 95 th percentile dietary exposure is close to or above the TWI for all age groups. High fish consumers, which might include pregnant women, may exceed the TWI by up to approximately six-fold. Unborn children constitute the most vulnerable group. Biomonitoring data from blood and hair indicate that methylmercury exposure is generally below the TWI in Europe, but higher levels are also observed. Exposure to methylmercury above the TWI is of concern. If measures to reduce methylmercury exposure are considered, the potential beneficial effects of fish consumption should also be taken into account. Dietary inorganic mercury exposure in Europe does not exceed the TWI, but inhalation exposure of elemental mercury from dental amalgam is likely to increase the internal inorganic mercury exposure; thus the TWI might be exceeded. This opinion focuses only on the risks related to dietary inorganic mercury and methylmercury exposure and does not assess the nutritional benefits linked to certain foods (e.g. fish and other seafood).A call for annual collection of chemical contaminant occurrence data in food and feed, including mercury, was issued by EFSA in December 2010. In response, EFSA received 59 820 results on mercury in food from 20 European countries, mainly covering the period from 2004 to 2011. A total number of 59 650 results were described with sufficient detail to be used in the statistical analysis of the respective food groups; 98.2 % of the samples were for total mercury, 1.8 % for methylmercury and three samples for inorganic mercury.All the 20 food groups available at the first level of FoodEx were covered in the current data collection. The food groups 'Fish and other seafood' and 'Meat and meat products' dominated the food product coverage with 36.8 % and 17.6 % respectively. These were followed by 'Grain and grain-based products' at 7.8 % and 'Vegetables an...

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Section: Genotoxicitymentioning

confidence: 97%

Scientific Opinion on the risk for public health related to the presence of mercury and methylmercury in food

2012

EFS2

463

160

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“…Kashanian et al [38] reported that selenium diminished DNA damage induced by incubation of calf thymus DNA with diazinon. Grotto et al [39] reported that in rats chronically exposed to low levels of methylmercury, selenium co-administration showed a significant reduction in methylmercury-induced genotoxicity, reestablished glutathione peroxidase activity and reduced and Histochemical Alterations in Prostate of Albino Rats DNA damage. Selenium reduced the cadmium induced histopathological changes in testes of rat, oxidative stress, endocrine disorder and apoptosis [40,41].…”

Section: Figurementioning

confidence: 99%

Effect of Selenium on Carbimazole-Induced Histopathological and Histochemical Alterations in Prostate of Albino Rats

Sakr¹,

Mahran²,

Nofal³

2012

AJMMS

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Carbimazole is an antithyroid drug used in treatment of hyperthyroidism. The present study is undertaken to evaluate the effect of carbimazole in prostate of albino rats and the ameliorative role of selenium. Treating rats with carbimazole(1.35mg/Kg b.w) daily for 8 weeks caused distinct histological alterations in prostate gland compared with control group. The epithelial cells of prostatic acini exhibited degeneration. Hyperplasia were projected into the lumens of the prostatic acini or to the outside stroma. Most of the intertubular blood vessels were congested. Histomorphological results showed that the heights of the epithelial cells were significantly reduced and the thickness of smooth muscle layer increased. Prostate gland of animals treated with carbimazole showed gradual decrease in the polysaccharide, protein and nucleic acids contents. These results were time-dependent. Treating animals with carbimazole and selenium showed an improvement in the histological structure as well as histochemical components of the prostate gland. It is suggested that the ameliorative effect of selenium against the histological and histochemical changes induced by carbimazole may be due to its antioxidant properties.

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“…Oxidative stress has also been observed in blood after subchronic exposure of rats to 0.086-0.140 mg/kg b.w. per day (Grotto et al, 2009a;Grotto et al, 2009b;Grotto et al, 2011), accompanied by increased systolic blood pressure. Biochemical alterations indicative of first liver and kidney effects were produced by exposure of rats to low doses of MeHg via whale meat (LOAEL 0.0067 mg/kg b.w.…”

Section: Miscellaneous Endpointsmentioning

confidence: 99%

Collate the literature on toxicity data on mercury in experimental animals and humans (Part I – Data on organic mercury)

Hassauer

Kaiser

Schneider

et al. 2012

EFSA Supporting Publications

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It was the scope of this project to collate, compile and summarise the scientific literature on the toxicity of methyl mercury, inorganic mercury and total mercury in humans and experimental animals published since 2002 and not evaluated in former JECFA risk assessments. Epidemiological data on MeHg toxicity confirmed former findings on an association between prenatal exposure and developmental neurotoxicity. Recent findings also support an influence of methyl mercury on the cardiovascular and immune system. Existing epidemiological data reveal several shortcomings limiting their suitability for risk assessment. Developmental neurotoxicity seems to be the most critical effect of MeHg in animals. A LOAEL of 0.01 mg/kg b.w. per day has been reported in young mice for locomotor activity exposed in utero. Rats seem to be less sensitive towards this endpoint: a NOAEL of 0.04 mg/kg b.w. per day has been reported in this species for locomotor activity. Systemic effects other than neurotoxicity have been mostly observed at higher doses than those producing neurotoxicity. No qualified epidemiological data appropriate for the evaluation of the toxicity of inorganic mercury after oral intake have been identified due to several limitations of the studies, e.g. small study group, insufficient control for confounders, inadequate exposure assessment. Toxicological studies in experimental animals widely confirmed former findings with respect to the target organs (neuro-, liver-, kidney-, immune-and reproductive toxicity, oxidative stress). The animal studies indicate that there might be relevant toxicological effects (developmental toxicity, liver toxicity) of inorganic mercury at dose levels similar or below the BMDL 10 value used for the derivation of the existing PTWI. However, due to some limitations of the studies no final conclusions can be drawn from these studies and the findings need further confirmation.

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Low levels of methylmercury induce DNA damage in rats: protective effects of selenium

Cited by 5 publications

References 0 publications

Scientific Opinion on the risk for public health related to the presence of mercury and methylmercury in food

Scientific Opinion on the risk for public health related to the presence of mercury and methylmercury in food

Effect of Selenium on Carbimazole-Induced Histopathological and Histochemical Alterations in Prostate of Albino Rats

Collate the literature on toxicity data on mercury in experimental animals and humans (Part I – Data on organic mercury)

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