A series of mono- and disubstituted complexes, FeI(2)(CO)(x)L(4-x), x = 2 or 3, is conveniently accessed from simple mixing of N-heterocyclic carbenes, phosphines, and aromatic amines with FeI(2)(CO)(4), first reported by Hieber in 1928. The highly light sensitive complexes yield to crystallization and X-ray diffraction studies for six complexes showing them to be rudimentary structural models of the monoiron hydrogenase, [Fe]-H(2)ase or Hmd, active site in native (Fe(II)(CO)(2)) or CO-inhibited (Fe(II)(CO)(3)) states. Diatomic ligand (nu(CO)) vibrational and Mossbauer spectroscopies are related to those reported for the Hmd active site. The importance of a serial approach for relating such parameters in model compounds to low spin Fe(II) in the diverse ligation of enzyme active sites is stressed.

Pentacoordinate iron dicarbonyls, (NS)Fe(CO)(2)P (NS=2-amidothiophenylate, P=PCy(3) (4), PPh(3), (5), and P(OEt)(3) (6)) were prepared as potential biomimetics of the active site of the mono-iron hydrogenase, [Fe]-H(2)ase. Full characterization including X-ray diffraction, density functional theory (DFT) computations, and Mössbauer studies for complexes 5 and 6 find that, despite similar infrared v(CO) pattern and absorption frequencies as the active site of the [Fe]-H(2)ase, the geometrical distortions towards trigonal bipyramidal, the negative isomer shift parameters, and the differences in CO-uptake reactivity are due to the "non-innocence" of the NS ligand. Ligand-based protonation with a strong acid, HBF(4).Et(2)O, interrupted the extensive pi-delocalization over Fe and NS ligand of complex 4 and switched on CO uptake (1 bar) to form a CO adduct, mer-[(H-NS)Fe(CO)(3)(PCy(3))](+) or 4(CO)-H(+). The extrinsic CO is reversibly removed on deprotonation with Et(3)N to regenerate complex 4. In a (13)CO atmosphere, concomitant CO uptake by 4-H(+) and exchange with intrinsic CO groups provide a facile route to (13)C-labeled 4(CO)-H(+) and, upon deprotonation, (13)C-labeled complex 4. DFT calculations show substantial Fe character in the LUMO of 4-H(+) typical of the d(6) Fe(II) in a regular square-pyramidal geometry. Thus, the Lewis acidity of 4-H(+) makes it amenable for CO binding, whereas the dianionic NS ligand renders the iron center of 4 insufficiently electrophilic and largely of Fe(I) character.

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Cardiac enlargement that develops during pregnancy is an important yet under‐studied adaptation to physiologic stress. In light of recent evidence of resident stem cell pools in the heart, we tested the hypothesis that pregnancy‐induced cardiac enlargement may involve both myocyte hypertrophy and new myocyte formation. 6 nonpregenant age matched controls (C) and 6 mice in late pregnancy (LP, 17–19 days) were studied. Hearts were formalin fixed and 5μ sections were examined. Laminin staining was used to identify cell perimeter and determine myocyte cross‐sectional area (MCSA). Wet weights of LP hearts were 23% greater than C (240±9 vs 195±13mg). Increases in MCSA were not proportional to increases in heart mass. MCSA of LP (262±3μ2, n=225) was 11% greater than of C (236± 3μ2, n=225). Analysis of sections from different regions of the heart showed different degrees of MCSA hypertrophy. Apex, mid and basal sections were analyzed from all hearts. No difference in MCSA among sections was found in C. MCSA of all sections were greater in LP than C, but MCSA of the mid‐heart in LP (275 ±4μ2, n=75) were greater than MCSA of apex (252± 5μ2, n=75) and base (259 ±4μ2, n=75). Myocyte hypertrophy during pregnancy is not sufficient to account for the whole‐heart enlargement suggesting that new myocytes are generated during pregnancy. Hypertrophy is not evenly distributed during pregnancy suggesting an unequal distribution of wall stress.