The N-benzhydrylamido-1,1-diphenylphosphine−borane ligand [Ph 2 P(BH 3 )NH(CHPh 2 )] (1-H) has been prepared via the reaction of an equimolar ratio of the phosphine amine [Ph 2 PNH(CHPh 2 )] and the borane adduct [BH 3 •SMe 2 ] at an ambient temperature. The reaction of 1-H with ((trimethylsilyl)methyl)lithium (neosilyllithium), [LiCH 2 SiMe 3 ], afforded a three-membered lithium amidophosphine−borane complex with the composition ([η 2 -Ph 2 CHNP(BH 3 )Ph 2 )Li(THF) 2 ] (2). Analogous reactions with sodium and potassium bis(trimethylsilyl)amides at ambient temperature yielded the respective alkali-metal amidophosphine−borane complexes [{(Ph 2 CHNP(BH 3 )Ph 2 )Na(THF) 2 } 2 ] (3) and [{(Ph 2 CHNP(BH 3 )Ph 2 )K(THF) 2 } 2 ] (4), with the loss of hexamethyldisilazane, [(Me 3 Si) 2 NH]. The corresponding heavier alkaline-earth-metal complexes [M-(THF) 2 {Ph 2 P(BH 3 )N(CHPh 2 )} 2 ] (M = Ca ( 5), Sr (6), Ba ( 7)) can be obtained via the reaction of [M{N(SiMe 3 ) 2 } 2 (THF) n ] (M = Ca, Sr, Ba) and 1-H. The metal complexes 5−7 can also be prepared via a salt metathesis route, where the alkali-metal salts 3 and 4 were reacted with the respective metal diiodides in THF at ambient temperature. The molecular structures of 1-H and 2−7 have been established by X-ray diffraction analyses, and from the solid-state structures of 3−7, it was confirmed that, in all of the compounds, the metal ions are chelated through the nitrogen atom and the hydrogen atoms of the borane group of ligand 1-H.

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Cadmium(II) is an omnipresent environmental toxicant emitted from various industrial sources and by anthropogenic sources such as smoking. Cadmium(II) enters our body through various sources including contaminated food and drinks and from active or passive smoking. It spares no organs in our body and the calamities it invites include primarily nephrotoxicity, osteotoxicity, teratogenicity, endocrine disruption, hepatotoxicity and carcinogenicity above all. It brings about a bolt from the blue in the cellular biochemistry by generating reactive oxygen species (ROS), disrupting the factors involved in the repair of DNA lesions and many other toxic nuisances otherwise by modulating the cell signalling machinery and acting as a potent carcinogen above all. In this review, we have tried to decipher some of the mechanisms played by cadmium(II) in exhibiting its toxic effects on various system of our body.

The Cβ–Cβ bond fission of a tantallacyclopentadiene moiety bridged over low-valent Ta­(V)–Ta­(III) dinuclear tantalum complex 2, having an infinite structure, was facilitated by the coordination of 1,10-phenanthroline (PHEN) to give a doubly η2-alkyne-bridged ditantalum complex (phen)­Cl2Ta­(μ,η2-C2Et2)2TaCl2(phen) (8), while the corresponding high oxidation Ta­(V)–Ta­(V) complex, Cl2Ta­(μ,η4-C4Et4)­(μ-Cl)­TaCl3 (1), afforded Cl3Ta­(μ,η4-C4Et4)­(μ-Cl)­TaCl2(phen) (7) with an intact metallacyclopentadiene structure. Characterization of 2 was confirmed by isolating a DME adduct 9 derived from a mixture of complex 2 and DME. In contrast, no Cβ–Cβ bond cleavage was observed for azine-coordinated ditantalum complexes 5 and 6 as well as their reduced species: PHEN was found to be essentially required for the transformation of the tantallacyclopentadiene.