There is a stereoselective difference in the interaction of the hexobarbital enantiomers with rat liver microsomes. The metabolism of the hexobarbital isomers was elevated in microsomes isolated from rats pretreated with phenobarbital and the (+)-isomer metabolized to a greater degree in control and phenobarbital-induced preparations. (+)-Hexobarbital was observed to be more effective than the (–)-isomer in the stimulation of endogenous NADPH oxidation and inhibition of ethylmorphine N-demethylation. In binding spectral experiments, the (+)-isomer exhibited larger Amax (maximum absorbance) values and slightly lower apparent Ks (spectral dissociation) constants than the (–)-form in control and phenobarbital-induced microsomal preparations.
Rats were placed on a basal diet supplemented with 0, 0.03, or 3 ppm selenium and 0 or 20 ppm vitamin E for 41-43 wk. Selenium deficiency decreased hepatic glutathione peroxidase activity and lowered both aortic prostacyclin (PGI2) and platelet thromboxane (TXA2) production compared to selenium- and vitamin E-supplemented animals. Vitamin E deficiency increased hepatic lipid peroxidation and decreased aortic PGI2 synthesis. Rats exposed daily for 31-32 wk to fresh smoke from a UK 2R1 reference cigarette had carboxyhemoglobin levels of 0.75 +/- 0.12 and 4.73 +/- 0.12% in sham- and smoke-exposed groups, respectively. Animals chronically exposed to cigarette smoke displayed a nearly twofold increase in pulmonary arylhydrocarbon hydroxylase activity. Smoke exposure produced a 26-33% decrease in aortic PGI2 synthesis compared to shams in the Se3E20, Se0.03E20, and Se3E0 groups. Smoking also increased platelet thromboxane 91% and 98% in the Se3E20 and Se3E0 groups compared to shams. It is concluded that cigarette-smoke exposure and selenium or vitamin E deficiency alter aortic PGI2 and platelet TXA2 production.
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