Pediatric mercury poisoning, brain MRI, and white matter hyperintensities

Costa, A.; Branca, V.; Pigatto, P. D.; Guzzi, Gianpaolo

doi:10.1007/s00431-011-1420-y

Cited by 5 publications

(1 citation statement)

References 3 publications

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“…Several alternate markers of mercury toxicity have been suggested to monitor ongoing injury and perhaps response to therapy: 1) neurologic injuryserum neuron-specific enolase (NSE), S100B, and glutamate receptor levels, and 2) evidence of oxidative stressserum malondiadehyde and urinary malondiadehyde and 8-hydroxy-2-deoxyguanosine [131,133,[175][176][177]. However, further validation of these markers are needed and may not be widely available.…”

Section: Alternate Markers Of Mercury Toxicitymentioning

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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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: Alternate Markers Of Mercury Toxicitymentioning

confidence: 99%