Modeling of the phase equilibria of polystyrene in methylcyclohexane with semi-empirical quantum mechanical methods I

A method for calculating interaction parameters traditionally used in phase-equilibrium computations in low-molecular systems has been extended for the prediction of solvent activities of aromatic polymer solutions (polystyrene+methylcyclohexane). Using ethylbenzene as a model compound for the repeating unit of the polymer, the intermolecular interaction energies between the solvent molecule and the polymer were simulated. The semiempirical quantum chemical method AM1, and a method for sampling relevant internal orientations for a pair of molecules developed previously were used. Interaction energies are determined for three molecular pairs, the solvent and the model molecule, two solvent molecules and two model molecules, and used to calculated UNIQUAC interaction parameters, a _ij and a _ji . Using these parameters, the solvent activities of the polystyrene 90,000 amu+methylcyclohexane system, and the total vapor pressures of the methylcyclohexane+ethylbenzene system were calculated. The latter system was compared to experimental data, giving qualitative agreement. Figure Solvent activities for the methylcylcohexane(1)+polystyrene(2) system at 316 K. Parameters a _ij (blue line) obtained with the AM1 method; parameters a _ij (pink line) from VLE data for the ethylbenzene+methylcyclohexane system. The abscissa is the polymer weight fraction defined as ₂(x ₁)=(1–x ₁)M ₂/[x ₁ M ₁+(1–x ₁)M ₂], where x ₁ is the solvent mole fraction and M _i are the molecular weights of the components.An erratum to this article can be found at     

The meter of metabolism

The circadian system orchestrates the temporal organization of many aspects of physiology, including metabolism, in synchrony with the 24 hr rotation of the Earth. Like the metabolic system, the circadian system is a complex feedback network that involves interactions between the central nervous system and peripheral tissues. Emerging evidence suggests that circadian regulation is intimately linked to metabolic homeostasis and that dysregulation of circadian rhythms can contribute to disease. Conversely, metabolic signals also feed back into the circadian system, modulating circadian gene expression and behavior. Here, we review the relationship between the circadian and metabolic systems and the implications for cardiovascular disease, obesity, and diabetes.     

The metabolism of S-methyl-l-cysteine

1. Methylsulphinylacetic acid, 2-hydroxy-3-methylsulphinylpropionic acid and methylmercapturic acid sulphoxide (N-acetyl-S-methyl-l-cysteine S-oxide) were isolated as their dicyclohexylammonium salts from the urine of rats after they had been dosed with S-methyl-l-cysteine. 2. A fourth sulphoxide was isolated but not identified. 3. The excretion of sulphate in the urine of rats dosed with S-methyl-l-cysteine was measured. 4. The metabolism of S-methyl-l-cysteine by the hamster and guinea pig was examined chromatographically. 5. The preparation of the following compounds is reported: (−)-dicyclohexylammonium methyl-mercapturate sulphoxide; the dicyclohexylammonium salts of the optically inactive forms of 2-hydroxy-3-methylthiopropionic acid, 2-hydroxy-3-methyl-sulphinylpropionic acid and methylsulphinylacetic acid.     

The metabolism of diethylstilbestrol

This literature review presents available data on the metabolism of diethylstilbestrol (DES) to shed light on the fate and the mechanism of toxicity of this compound. Biotransformation effects reviewed include conjugation reactions of DES such as glucuronide formation in vivo and in vitro, enterohepatic circulation of DES and its glucuronide, and formation of steroid sulfatases and sulfates; oxidative metabolism of DES (aromatic hydroxylation followed by methylation); and species differences in DES metabolism. Excretion curves for 12 animal species show vast differences; whereas urinary excretion predominates in humans, chimps, rhesus monkeys, and guinea pigs; rats, hamsters, and mice show predominately fecal elimination. The difference among species seems due to capability of biliary excretion. A molecular weight threshold seems to exist, and this may account for the varying remnants of DES housed in different species' organs. Placental transfer is another major problem. Fetuses of many species seem capable of glucurondizing DES. The formation of reactive metabolites (i.e., affinity for estradiol 17-beta receptor attachment and affinity for other proteins bound by estrogen) through oxidative biotransformation suggests that DES metabolites affect hepatic systems and may activate or transform cells to malignancy. Theories of the organotropism of DES carcinogenicity are presented, as well as a discussion of the fate of DES in the environment.     

The metabolism of tetralin

1. [1-(14)C]Tetralin was synthesized and fed to rabbits. 2. Of the radioactivity, 87-90% was excreted in the urine within two days and 0.5-3.7% on the third day. The faeces contained 0.6-1.8%. No radioactivity was found in the breath and negligible amounts were retained in the tissues. About 90-99% of an administered dose was accounted for. 3. The main metabolite in the urine was the glucuronide of alpha-tetralol (52.4%). Other conjugated metabolites were beta-tetralol (25.3%), 4-hydroxy-alpha-tetralone (6.1%), cis-tetralin-1,2-diol (0.4%) and trans-tetralin-1,2-diol (0.6%). 4. beta-Tetralone, alpha-naphthol, 1,2-dihydronaphthalene and naphthalene, previously reported as metabolites, are artifacts, and tetralin, alpha-tetralone, beta-naphthol, 5-hydroxytetralin, and 6-hydroxytetralin are not metabolites. 5. The major metabolite of tetralin, alpha-tetralol and alpha-tetralone is the glucuronide of alpha-tetralol, which was isolated as methyl (1,2,3,4-tetrahydro-1-naphthyl tri-O-acetyl-beta-d-glucosid)uronate; the major metabolite of beta-tetralol and beta-tetralone is the glucuronide of beta-tetralol, which was characterized as methyl (1,2,3,4-tetrahydro-2-naphthyl tri-O-acetyl-beta-d-glucosid)uronate. 5-Hydroxytetralin is conjugated with glucuronic acid, and was characterized as methyl (5,6,7,8-tetrahydro-1-naphthyl tri-O-acetyl-beta-d-glucosid)uronate. 6-Hydroxytetralin is conjugated with glucuronic acid, and was characterized as methyl (5,6,7,8-tetrahydro-2-naphthyl tri-O-acetyl-beta-d-glucosid)uronate. 6. A metabolic sequence accounting for the observed biological transformation products is proposed.