One of the reasons for the toxic effects of mercury has been attributed to its influence on the biochemical roles of selenium. For this reason, it is important to understand details pertaining to the nature of Hg−Se interactions and this has been achieved by comparison of a series of mercury chalcogenolate complexes that are supported by tris(2-mercapto-1-t-butyl-imidazolyl)hydroborato ligation, namely [Tm^But]HgEPh (E = S, Se, Te). In particular, X-ray diffraction studies on [Tm^But]HgEPh demonstrate that although the Hg−S bonds involving the [Tm^But] ligand are longer than the corresponding Cd−S bonds of [Tm^But]CdEPh, the Hg−EPh bonds are actually shorter than the corresponding Cd−EPh bonds, an observation which indicates that the apparent covalent radii of the metals in these compounds are dependent on the nature of the bonds. Furthermore, the difference in Hg−EPh and Cd−EPh bond lengths is a function of the chalcogen and increases in the sequence S (0.010 Å) < Se (0.035 Å) < Te (0.057 Å). This trend indicates that the chalcogenophilicity of mercury increases in the sequence S < Se < Te. Thus, while mercury is often described as being thiophilic, it is evident that it actually has a greater selenophilicity, a notion that is supported by the observation of facile selenolate transfer from zinc to mercury upon treatment of [Tm^But]HgSCH₂C(O)N(H)Ph with [Tm^But]ZnSePh. The significant selenophilicity of mercury is in accord with the aforementioned proposal that one reason for the toxicity of mercury is associated with it reducing the bioavailability of selenium.