Scand J Gastroenterol
March 1993
The mechanism for the damage to the alanine-preferring amino acid transport system (A system) of guinea pig intestinal brush border membrane vesicles induced by active oxygen species was studied in vitro. The transport activity of L-proline, which is a model amino acid for the A system, and the tryptophan fluorescence intensity of intestinal brush border membrane vesicles were decreased, and lipid peroxidation of these membrane vesicles was induced by ultraviolet irradiation, which generated active oxygen species. Thiourea (hydroxyl radical scavenger) protected L-proline transport activity and tryptophan fluorescence intensity of intestinal brush border membrane vesicles and also inhibited lipid peroxidation in these membrane vesicles in the presence of active oxygen radicals.
View Article and Find Full Text PDFA partial cDNA clone encoding cholesterol 7 alpha-hydroxylase (pHA 7 alpha-3) was isolated from a hamster liver cDNA library using rat P-450 ch7 cDNA (p 7 alpha-11) as a probe. In comparison with the complete base sequence of p 7 alpha-11, pHA 7 alpha-3 lacked about 500 base pairs at the 5' end. Circadian rhythms of mRNA for hamster liver 3-hydroxy-3-methylglutaryl coenzyme A reductase and cholesterol 7 alpha-hydroxylase were investigated with cDNA clones encoding 3-hydroxy-3-methylglutaryl coenzyme A reductase (pRed-227) and pHA 7 alpha-3.
View Article and Find Full Text PDFThe effect of dietary hydrogenated corn oil (trans-octadecenoate-rich oil) on plasma cholesterol and triglyceride concentrations was compared with dietary palmitic acid in hamsters given a cholesterol-rich diet. The addition of dietary palmitic acid and hydrogenated corn oil accelerated the increase in plasma VLDL- and LDL-cholesterol levels and plasma triglyceride level induced by dietary cholesterol loading. Dietary cholesterol, palmitic acid and hydrogenated corn oil showed no effect on plasma HDL-cholesterol concentration.
View Article and Find Full Text PDFThe proliferation of vascular smooth muscle cells (VSMC) was stimulated by co-incubation with macrophages. Further stimulation was observed when co-incubated macrophages were supplied with LDL or cholesterol. However, the stimulation of VSMC proliferation did not result from co-incubation with macrophages supplemented with acetylated LDL or delipidated LDL.
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