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In Vitro and In Vivo Interactions of Triton 1339 with Plasma Lipoproteins of Normolipidemic Rhesus Monkeys

In Vitro and In Vivo Interactions of Triton 1339 with Plasma Lipoproteins of Normolipidemic... Triton WR-1339 was incubated in vitro in various proportions with plasma from normolipidemic rhesus monkeys or with ultracentrifugally purified lipoproteins, and the products were examined by isopycnic density gradient ultracentrifugation, agarose column chromatography, electrophoretic and immunochemical techniques, and electron microscopy. Some experiments used apo A-I, apo A-II, or Triton labeled with either 125I or 131I. At concentrations of less than 10 mg/ml plasma, Triton interacted preferentially with HDL, changing lipoprotein size and density; Triton was progressively incorporated into the HDL particles, displacing apo E, apo A-I, and apo A-II. At concentrations above 10 mg/ml plasma, Triton displaced all apo A-I from the particle, and much lipid was dissolved into the Triton micelles. When Triton-treated HDL particles were used as a substrate for the enzyme LCAT, enzyme activity decreased in parallel to the displacement of apo A-I. There was no displacement of apo B from LDL nor any loss of lipids; but the particles became deformed and formed rouleaux. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis Wolters Kluwer Health

In Vitro and In Vivo Interactions of Triton 1339 with Plasma Lipoproteins of Normolipidemic Rhesus Monkeys

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Copyright
© 1984 by American Heart Association, Inc.
ISSN
0276-5047

Abstract

Triton WR-1339 was incubated in vitro in various proportions with plasma from normolipidemic rhesus monkeys or with ultracentrifugally purified lipoproteins, and the products were examined by isopycnic density gradient ultracentrifugation, agarose column chromatography, electrophoretic and immunochemical techniques, and electron microscopy. Some experiments used apo A-I, apo A-II, or Triton labeled with either 125I or 131I. At concentrations of less than 10 mg/ml plasma, Triton interacted preferentially with HDL, changing lipoprotein size and density; Triton was progressively incorporated into the HDL particles, displacing apo E, apo A-I, and apo A-II. At concentrations above 10 mg/ml plasma, Triton displaced all apo A-I from the particle, and much lipid was dissolved into the Triton micelles. When Triton-treated HDL particles were used as a substrate for the enzyme LCAT, enzyme activity decreased in parallel to the displacement of apo A-I. There was no displacement of apo B from LDL nor any loss of lipids; but the particles became deformed and formed rouleaux.

Journal

Arteriosclerosis – Wolters Kluwer Health

Published: Jul 1, 1984

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