Some effects of selenium status on inorganic mercury metabolism in the rat

Burk, Raymond F.; Jordan, Hilliard E.; Kiker, Kenneth W.

doi:10.1016/0041-008x(77)90118-1

Cited by 52 publications

(11 citation statements)

References 14 publications

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“…A similar Se‐induced shift of inorganic Hg from low‐molecular‐weight to high‐molecular‐weight proteins was also demonstrated in rabbit blood, kidneys, and liver [104]. Several other studies, however, suggested that the Se status of the animals had no effect on the distribution of inorganic Hg [105] and MeHg [21,106].…”

Section: Possible Pathways Leading To Biological Hg‐se Antagonismmentioning

confidence: 62%

Mercury‐selenium compounds and their toxicological significance: Toward a molecular understanding of the mercury‐selenium antagonism

Khan

Wang

2009

Enviro Toxic and Chemistry

401

294

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The interaction between mercury (Hg) and selenium (Se) is one of the best known examples of biological antagonism, yet the underlying mechanism remains unclear. This review focuses on the possible pathways leading to the Hg-Se antagonism, with an emphasis on the potential Hg-Se compounds that are responsible for the antagonism at the molecular level (i.e., bis[methylmercuric]selenide, methylmercury selenocysteinate, selenoprotein P-bound HgSe clusters, and the biominerals HgSe(x)S(1-x)). The presence of these compounds in biological systems has been suggested by direct or indirect evidence, and their chemical properties support their potentially key roles in alleviating the toxicity of Hg and Se (at high Hg and Se exposures, respectively) and deficiency of Se (at low Se exposures). Direct analytical evidences are needed, however, to confirm their in vivo presence and metabolic pathways, as well as to identify the roles of other potential Hg-Se compounds. Further studies are also warranted for the determination of thermodynamic properties of these compounds under physiological conditions toward a better understanding of the Hg-Se antagonism in biota, particularly under real world exposure scenarios.

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Section: Possible Pathways Leading To Biological Hg‐se Antagonismmentioning

confidence: 62%

Mercury‐selenium compounds and their toxicological significance: Toward a molecular understanding of the mercury‐selenium antagonism

Khan

Wang

2009

Enviro Toxic and Chemistry

401

294

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“…According to some authors, in the case of mercuric chloride the mechanism of the detoxifying action of selenium involves a decrease in the renal level of mercury, and therefore a diminution of the nephrotoxic effect (22,24,29,36), the effect of selenite depending on its concentration as well as on the time and kind of exposure (37)(38)(39)(40)(41)(42).…”

Section: Introductionmentioning

confidence: 99%

Interaction of Alkylmercuric Compounds with Sodium Selenite. I. Metabolism of Ethylmercuric Chloride Administered Alone and in Combination with Sodium Selenite in Rats

Brzeznicka¹,

Chmielnicka²

1981

Environmental Health Perspectives

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The effect of sodium selenite administered intragastrically in repeated doses to rats receiving ethylmercuric chloride po in various repeated doses (0.25 or 2.5 mg Hg/kg) on the excretion, whole-body retention, and organ distribution of mercury was studied.Selenium was found to affect the distribution of ethylmercury among tissues and subcellular fractions of the kidneys and liver as well as its binding to proteins of soluble fractions in these organs.Similarities and differences between the effect of interaction of sodium selenite with ethylmercuric chloride and methylmercury as well as inorganic mercury are also discussed. IntroductionEmployment of alkylmercury compounds, especially methylmercurials, in agriculture has resulted in several epidemic intoxications of humans (1)(2)(3)(4). Ethylmercuric compounds are believed to be generally less toxic due to more rapid clearance (5,6). However, these compounds have been used for a long time not only in agriculture (1, 7) but also as antiseptics, among others for preservation of blood plasma (8).Numerous poisonings by ethylmercurials have been noted, however, in humans (9-13) and in animals (14,15 and concern mainly single-dose experiments (5,10,(16)(17)(18)(19)(20)(21). On the other hand, for estimation of chronic toxicity of alkylmercury compounds, of primary importance is the extent of their accumulation in the body, determined by the magnitude and duration of exposure, uptake rate, biotransformation efficiency and excretion rate.Moreover, in the last decade considerable information has been gained on the detoxifying role of sodium selenite in experimental poisoning of animals with mercuric chloride (22-28) and methylmercury (28-35).According to some authors, in the case of mercuric chloride the mechanism of the detoxifying action of selenium involves a decrease in the renal level of mercury, and therefore a diminution of the nephrotoxic effect (22,24,29,36), the effect of selenite depending on its concentration as well as on the time and kind of exposure (37)(38)(39)(40)(41)(42).Results of studies on the mechanism of protective action of selenium in poisoning by methylmercury 131 compounds are equivocal and sometimes contradictory (27,43 At 24 hr after administration of the last dose of ethylmercuric chloride, rats were sacrificed under ether narcosis by heart puncture and then appropriate organs and tissues were removed.Mercury was estimated directly by a radiochemical method from measurement of gamma-radiation in a USB-2 scintillation counter with a NaI/Tl crystal. The time of measurement was 100 sec.Liver and kidneys were fractionated at a temperature of 0-4°C. The organs were homogenized in 7 volumes of 0.25M sucrose + 0.01% NaOH (pH 7.0) in a glass homogenizer (44). The homogenates were ifitered through a gauze and centrifuged twice at 600g for 15 min to sediment the nuclear fraction (N). The postnuclear supernatant was centrifuged twice at 7000g for 15 min to sediment the mitochondrial fraction (M). The postmitochondrial supernatant was centrifuged once a...

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“…There are several studies, in which the retention and distribution of mercuric chloride given together with selenium have been reported (Parizek et al 1967(Parizek et al & 1969Chen et al 1974;Moffitt et al 1974;v. Eybl et al 1975;Burk et al 1976;Magos & Webb 1976;Wada et al 1976). In only a few studies were the rats fed for more than a week with the test compounds (Johnson & Pond 1974;Potter & Matrone 1974;Burk et at.…”

Section: Group B (Meohg) and E (Meohgf Se)mentioning

confidence: 99%

Studies on the Interaction and Distribution of Selenite, Mercuric, Methoxyethyl Mercuric and Methyl Mercuric Chloride in Rats. I. Analysis of Brain, Liver, Kidney and Faeces

Mengel

Karlog²

1980

Acta Pharmacologica et Toxicologica

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The interaction of selenium with methyl mercury, methoxyethyl mercury and mercuric chloride was studied in a 37 days' experiment with rats. Liver, kidney, brain and faeces were analysed for mercury and selenium at the end of the experimental period. Selenium supplementation increased the retention of mercury in liver, when mercuric chloride was given, in liver and brain when methyl mercury was given, and in all tissues examined when methoxyethyl mercury was given. The Hg/Se molar ratios in the tissues have been calculated and are found to vary considerably.

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Some effects of selenium status on inorganic mercury metabolism in the rat

Cited by 52 publications

References 14 publications

Mercury‐selenium compounds and their toxicological significance: Toward a molecular understanding of the mercury‐selenium antagonism

Mercury‐selenium compounds and their toxicological significance: Toward a molecular understanding of the mercury‐selenium antagonism

Interaction of Alkylmercuric Compounds with Sodium Selenite. I. Metabolism of Ethylmercuric Chloride Administered Alone and in Combination with Sodium Selenite in Rats

Studies on the Interaction and Distribution of Selenite, Mercuric, Methoxyethyl Mercuric and Methyl Mercuric Chloride in Rats. I. Analysis of Brain, Liver, Kidney and Faeces

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