Mercury (Hg) is an environmental toxicant being present in the environment as elemental Hg (Hg), inorganic and organic Hg compounds. The nervous system is supposed to be the key target for Hg toxicity. Research indicates that selenium (Se) may be used as a protective agent against Hg neurotoxicity. Therefore, the aim of this review is to examine new implications of the molecular biology of Hg neurotoxicity, and specifically to focus on the influence of Se compounds and interfering thiols on Hg neurotoxicity at the molecular level. Mercury and Se form stable coordination compounds, and Hg species are characterized by higher affinity to selenol groups as compared to thiol groups. Therefore, Se-containing molecules are targets for Hg binding that may at least partially mediate the biological outcome of Hg-Se interaction. Molecular interaction between these elements also involves mutual interaction between Hg and various selenoproteins. Experimental data demonstrate that Se treatment modifies brain Hg retention, modulates neurotoxicity and oxidative stress in the nervous tissue of animals. Human data also indicate that molecular interaction between Hg and Se may have a significant influence on neurodevelopment, brain functioning, and neurodegeneration. It is hypothesized that the effectiveness of Se protection against Hg neurotoxicity may be determined by the dose of elements as well as their particular chemical forms. Further studies are required to estimate the intimate mechanisms of Hg and Se interaction in vivo. (C) 2016 Elsevier B.V. All rights reserved.