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

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