Detoxification of methylmercury by formation of mercury selenide in muscle of toothed-whale

Sakamoto, Masatoshi; Itai, Takaaki; Nakamira, M.; Sawada, Masumi

doi:10.1016/j.toxlet.2015.08.317

Cited by 2 publications

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“…Selenium supplementation and selenoprotein activity is likely responsible for in vivo demethylation of MeHg þ and conversion to inorganic Hg 2þ in tissues, including the brain [101,103,138,153,155]. In comparing chronic exposure in mice (30 days), rats (18 weeks) and post-natal rat pups (10 days), both mercury exposure groups (mercury vs mercury plus selenium) showed increases in brain mercury, but the selenium supplementation groups did not display the clinical and pathological evidence of mercury toxicity [100,102,156].…”

Section: Effects On Mercury Kinetics After Selenium Supplementationmentioning

confidence: 99%

“…The supplemental selenium may produce this protective effect by binding with the available mercury, producing an inert colloidal mercury:selenium complex [101,119,120,127,135,137,155,[157][158][159]. Support for this theory comes from autopsy studies in occupationally exposed mercury mine workers in Indrija Slovenia (compared with non-exposed population), who had elevated brain mercury content found 5 to 16 years after retirement [157].…”

Section: Effects On Mercury Kinetics After Selenium Supplementationmentioning

confidence: 99%

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Rethinking treatment of mercury poisoning: the roles of selenium, acetylcysteine, and thiol chelators in the treatment of mercury poisoning: a narrative review

Spiller

Hays

Casavant

2021

Toxicology Communications

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We reevaluate the treatment of mercury poisoning, incorporating recent advances in understanding of mercury toxicity and the mercury:selenium interaction. This review focuses on: 1) the role, limitations and benefits of chelation (Unithiol, succimer and N-Acetylcysteine); 2) the role of selenium supplementation; and 3) how the different forms of mercury are impacted by use of chelation and selenium. Unithiol and succimer produce increases in urinary excretion of mercury and to a lesser degree blood and total body mercury. The primary role of N-acetylcysteine is increasing renal mercury excretion, similar to the thiol-chelators. Additional unique features of acetylcysteine include increased efflux of methylmercury from the brain, and reduced oxidative stress via increased glutathione production. The role of selenium includes: 1) restoration of selenoprotein activity, 2) protection against mitochondrial injury and DNA damage, 3) demethylation of methylmercury, 4) sequestering of mercury via Hg:Se complexes, and 5) redistribution of Hg inside organisms. Selenium may increase blood Hg, via a "sink" effect, causing a redistribution of mercury away from the brain. A combined approach for mercury poisoning treatment was developed focusing on restoration of selenoprotein function, reduction of oxidative stress and increased mercury elimination.

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Section: Effects On Mercury Kinetics After Selenium Supplementationmentioning

confidence: 99%

Section: Effects On Mercury Kinetics After Selenium Supplementationmentioning

confidence: 99%

Rethinking treatment of mercury poisoning: the roles of selenium, acetylcysteine, and thiol chelators in the treatment of mercury poisoning: a narrative review

Spiller

Hays

Casavant

2021

Toxicology Communications

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Rethinking mercury: the role of selenium in the pathophysiology of mercury toxicity

Spiller

2017

Clinical Toxicology

159

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The interaction with selenium is a central feature in mercury toxicity. This interaction is complex depending on a number of features such as the form of mercury, the form of selenium, the organ and dose. The previously suggested "protective effect" of selenium against mercury toxicity may in fact be backwards. The effect of mercury is to produce a selenium deficiency state and a direct inhibition of selenium's role in controlling the intracellular redox environment in organisms. Selenium supplementation, with limitations, may have a beneficial role in restoring adequate selenium status from the deficiency state and mitigating the toxicity of mercury.

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Detoxification of methylmercury by formation of mercury selenide in muscle of toothed-whale

Cited by 2 publications

References 0 publications

Rethinking treatment of mercury poisoning: the roles of selenium, acetylcysteine, and thiol chelators in the treatment of mercury poisoning: a narrative review

Rethinking treatment of mercury poisoning: the roles of selenium, acetylcysteine, and thiol chelators in the treatment of mercury poisoning: a narrative review

Rethinking mercury: the role of selenium in the pathophysiology of mercury toxicity

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