No abstract

The unrestricted Hartree-Fock and unrestricted Kohn-Sham calculations generally result in spincontaminated solutions. Moreover, the energies from these calculations cannot be directly compared with the results of corresponding restricted calculations since the latter yield higher energies due to restrictions imposed on the form of the wave function. We present here a simple method of correcting the mixed spin energies resulting from unrestricted Hartree-Fock or density-functional theory calculations and removing the foreign spin components. The method allows for elimination of higher-multiplet components from the given mixed spin state solution by performing unrestricted calculations at the same fixed geometry for the higher multiplets and the state under consideration. The performance of the method is illustrated with several examples of density-functional calculations of radical species. The current method is also variational in nature and can be further extended in a self-consistent field fashion.

The kinetics of transport of L-lactate, pyruvate, ketone bodies, and other monocarboxylates into isolated hepatocytes from starved rats were measured at 25 degrees C using the intracellular pH-sensitive dye, 2',7'-bis(carboxyethyl)- 5(6)-carboxyfluorescein, to detect the associated proton influx. Transport kinetics were similar, but not identical, to those determined using the same technique for the monocarboxylate transporter (MCT) of Ehrlich Lettré tumor cells (MCT1) (Carpenter, L., and Halestrap, A. P. (1994) Biochem. J. 304, 751-760). Km values for L-lactate (4.7 mM), D-lactate (27 mM), D,L-2-hydroxybutyrate (3.3 mM), L-3-hydroxybutyrate (12.7 mM), and acetoacetate (6.1 mM) were very similar in both cell types, whereas in hepatocytes the Km values were higher than MCT1 for pyruvate (1.3 mM, cf. 0.72 mM), D-3-hydroxybutyrate (24.7 mM, cf. 10.1 mM), D-2-chloropropionate (1.3 mM, cf. 0.8 mM), 4-hydroxybutyrate (18.1 mM, cf. 7.7 mM), and acetate (5.4 mM, cf. 3.7 mM). In contrast, the hepatocyte carrier had lower Km values than MCT1 for glycolate, chloroacetate, dichloroacetate, and 2-hydroxy-2-methylpropionate. Differences in stereoselectivity were also detected; both carriers showed a lower Km for L-lactate than D-lactate, while hepatocyte MCT exhibited a lower Km for D- than L-2-chloropropionate and for L- than D-3-hydroxybutyrate; this is not the case for MCT1. A range of inhibitors of MCT1, including alpha-cyanocinnamate derivatives, phloretin, and niflumic acid, inhibited hepatocyte MCT with K0.5 values significantly higher than for tumor cell MCT1, while stilbene disulfonate derivatives and p-chloromercuribenzene sulfonate had similar K0.5 values in both cell types. The branched chain ketoacids alpha-ketoisocaproate and alpha-ketoisovalerate were also potent inhibitors of hepatocyte MCT with K0.5 values of 270 and 340 microM, respectively. The activation energy of L-lactate transport into hepatocytes was 58 kJ mol-1, and measured rates of transport at 37 degrees C were considerably greater than those required for maximal rates of gluconeogenesis. The properties of the hepatocyte monocarboxylate transporter are consistent with the presence of a distinct isoform of MCT in liver cells as suggested by the cloning and sequencing of MCT2 from hamster liver (Garcia, C. K., Brown, M. S., Pathak, R. K., and Goldstein, J. L. (1995) J. Biol. Chem. 270, 1843-1849).

No abstract

A bond and group equivalent scheme that allows the calculation of heats of formation for carboxylic acids and esters from ab initio 6-31G* energies has been developed. For a group of 16 compounds, the rms error for the calculated heats of formation was 0.64 kcalimol. Heats of formation have been predicted for an additional seven compounds for which the experimental values are either unknown or suspect. 0 1992 by