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R Ostwald

Publications and source records attributed to R Ostwald.

At least 37 records · Page 2Linked to original sources
PubMed1972

Characterization of guinea pig plasma lipoproteins: the appearance of new lipoproteins in response to dietary cholesterol.

Dietary cholesterol induces a hemolytic anemia in guinea pigs, accompanied by changes in the lipid composition of red cells and of plasma lipoproteins. This report presents a characterization of the lipoprotein species present in each main density class in both control and cholesterol-fed guinea pigs. Traces of a typical high density lipoprotein (HDL) were detected in control plasma. HDL from cholesterol-fed, anemic guinea pigs differed from control HDL in electron microscopic appearance and lipid and peptide composition. Long stacks of discs were observed in the electron microscope in addition to smaller, spherical particles characteristic of control HDL. Low density lipoproteins (LDL) from cholesterol-fed, anemic guinea pigs had two main populations, which were separated by gel chromatography. One population appeared in the electron microscope as large transparent discs and contained mainly unesterified cholesterol and phospholipids in a 2:1 molar ratio. The other population resembled control LDL in size and composition except for its high unesterified cholesterol content. Dietary cholesterol also altered the composition and decreased the electrophoretic mobility of very low density lipoproteins. Gel electrophoretic and immunochemical evidence indicates that a peptide (mol wt 35,000) appears in lipoproteins from cholesterol-fed, anemic guinea pigs that is undetectable in those of controls. Similarities between the cholesterol-induced lipoprotein abnormalities in guinea pigs and those reported in patients with obstructive jaundice, biliary cirrhosis, type III hyperlipoproteinemia, or familial lecithin:cholesterol acyltransferase deficiency are discussed.

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PubMed1972

Effects of plasma lipoproteins from control and cholesterol-fed guinea pigs on red cell morphology and cholesterol content: an in vitro study.

When guinea pigs are fed cholesterol, the cholesterol content of their red cells increases progressively, a large number of cells become spurred, and a hemolytic anemia develops. Unesterified cholesterol is readily transferred from plasma, HDL, or LDL of cholesterol-fed, anemic guinea pigs to normal red cells in vitro. This transfer is reversible and is proportional to the concentration of unesterified cholesterol in the incubation medium. Red cells loaded in vitro with cholesterol develop spurs identical with those on red cells in the circulation of cholesterol-fed, anemic guinea pigs. Neither the cholesterol content nor the morphology of normal red cells is altered by incubation in control plasma or in concentrated control lipoproteins. Plasma infranates (d > 1.21 g/ml) of either group do not cause spurring of control red cells. We conclude: (a) that accumulation of cholesterol by guinea pig red cells in vitro requires an increased concentration of unesterified cholesterol in lipoprotein rather than an increased concentration of normal lipoproteins, and (b) that an increased cholesterol content in guinea pig red cell membranes is necessary for their abnormal morphology. The flux of cholesterol between cholesterol-loaded cells and plasma from cholesterol-fed guinea pigs is three times greater than that between control red cells and control plasma, and the fractional exchange rates are altered.

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PubMed1966

Effect of sex and gonadal hormones on rat plasma lipids during the development of an essential fatty acid deficiency.

1. Male, female and castrated rats treated with oestradiol (30mug./week) or testosterone (2mg./week) were given an essential fatty acid-deficient diet containing 10% of hydrogenated coconut oil for 9 weeks. The concentrations and fatty acid composition of plasma phospholipids, cholesteryl esters and triglycerides were determined. 2. Between the second and third weeks of the deficiency, concentrations of plasma cholesteryl esters, phospholipids and triglycerides decreased, then remained relatively constant. There were no significant differences between males and females, but oestradiol caused a significant rise in plasma phospholipids and triglycerides as compared with testosterone-treated animals. 3. During the first 2 weeks of the deficiency, linoleic acid in the plasma lipids of all groups decreased to low concentrations and changed very little thereafter. 4. Female rats maintained higher percentages and concentrations of arachidonic acid and stearic acid in plasma phospholipids and arachidonic acid in cholesteryl esters than did males. Males had higher proportions of eicosatrienoic acid and oleic acid. There was no sex difference in the fatty acid composition of plasma triglycerides. 5. Oestradiol-treated rats had concentrations of cholesteryl and phospholipid arachidonate comparable with those of female rats and higher than the testosterone-treated group. Eicosatrienoic acid in the oestradiol-treated rats was high and resembled that of the male rats, apparently because of the higher concentration of plasma phospho lipids in this group. 6. Supplementation of the essential fatty acid-deficient rats with linoleate restored plasma cholesteryl and phospholipid linoleate and arachidonate nearly to normal concentrations in a single day. The increase in arachidonic acid in these fractions was accompanied by a similar quantitative decrease in eicosatrienoic acid. 7. These sex differences appear to be related to the smaller size of the female rat and to a more direct influence of oestradiol on the formation or maintenance of phospholipids rich in arachidonic acid.

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