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

Abstract

Abstract 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.