Structural characterization of anti- and syn-allyltricarbonyliron bromide: rotational spectra, quadrupole coupling, and density functional calculations.

Rotational transitions for two distinct structural isomers of allyltricarbonyliron bromide have been clearly observed in the cold molecular beam of a pulsed-beam Fourier transform microwave spectrometer. Rotational transitions exhibiting quadrupole splitting patterns for each isomer were measured for the 79Br and 81Br isotopomers. Both isomers are accidental near-prolate symmetric tops. The measured rotational constants for the 79Br isotopomer are A(anti) = 920.6148(2) MHz, B(anti) = 582.8866(12) MHz, C(anti) = 581.3027(12) MHz, A(syn) = 919.5055(1) MHz, B(syn) = 584.1865(1) MHz, and C(syn) = 581.6392(1) MHz. Analysis of the isotopic substitution data and possible transition assignments indicates that these molecules have Cs symmetry. Both isomers are found to have a dipole component along the a axis. However, the anti isomer has a "c" type dipole component, whereas a "b" dipole component is found for the syn isomer. It was found necessary to carefully analyze both rotational constants and the quadrupole coupling data in order to determine the correct assignment of dipole moment components for each isomer. This change in dipole assignments implies that there is a switch of inertial axes upon isomerization resulting from a subtle shift of the allyl center of mass coordinates, upon reorientation of the allyl ligand. The X-ray and DFT calculated structures for the anti isomer are in excellent agreement with the present data. No previous structural data for the syn isomer were available, and the present analysis strongly supports the expected conformation.

Generation of furazolidone radical anion and its inhibition by glutathione.

Furazolidone is a nitrofuran drug which causes dilated cardiomyopathy in turkeys and serves as an important model of human dilated cardiomyopathy. Although extensively investigated, the chemical mechanism by which furazolidone produces injury remains unknown. In this work we used electron paramagnetic resonance (EPR) spectroscopy to show that furazolidone was reduced to its corresponding nitro anion radical by ascorbate and hypoxanthine. Glutathione prevented the generation of this anion radical. These results document directly, with EPR spectroscopy, the presence of furazolidone anion radical during biochemical reduction and suggest a protective role of glutathione in furazolidone-induced injury. These data enhance our understanding of furazolidone metabolism and may be useful in defining its role in furazolidone-induced dilated cardiomyopathy.