Incorporation of vitamin E (a-tocopherol) was measured in total membranes of pulmonary artery endothelial cells (PAEC) following treatment with eight synthetic
Effect of polyunsaturated fatty acids and phospholipids on “3H”-vitamin E incorporation into pulmonary artery endothelial cell membranes
✍ Scribed by K. Madhavi Sekharam; Jawaharlal M. Patel; Edward R. Block
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 957 KB
- Volume
- 145
- Category
- Article
- ISSN
- 0021-9541
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✦ Synopsis
Abstract
Vitamin E, a dietary antioxidant, is presumed to be incorporated into the lipid bilayer of biological membranes to an extent proportional to the amount of polyunsaturated fatty acids or phospholipids in the membrane. In the present study we evaluated the distribution of incorporated polyunsaturated fatty acids (PUFA) and phosphatidylethanolamine (PE) in various membranes of pulmonary artery endothelial cells. We also studied whether incorporation of PUFA or PE is responsible for increased incorporation of ^3^ H)‐vitamin E into the membranes of these cells. Following a 24‐hr incubation with linoleic acid (18:2), 18:2 was increased by 6.9‐, 9.2‐, and 13.2‐fold in plasma, mitochondrial, and microsomal membranes, respectively. Incorporation of 18:2 caused significant increases in the unsaturation indexes of mitochondrial and microsomal polyunsaturated fatty acyl chains (P <.01 versus control in both membranes). Incubation with arachidonic acid (20:4) for 24 hr resulted in 1.5‐, 2.3‐, and 2.4‐fold increases in 20:4 in plasma, mitochondrial, and microsomal membranes, respectively. The unsaturation indexes of polyunsaturated fatty acyl chains of mitochondrial and microsomal membranes also increased (P.01 versus control in both membranes). Although incubations with 18:2 or 20:4 resulted in several‐fold increases in membrane 18:2 or 20:4 fatty acids, incorporation of “^3^ H”‐vitamin E into these membranes was similar to that in controls. Following a 24‐hr incubation with PE, membrane PE content was significantly increased, and “^3^H”‐vitamin E incorporation was also increased to a comparable degree, i.e., plasma membrane > mitochondria > microsomes. Endogenous vitamin E content of the cells was not altered because of increased incorporation of PE and “^3^H”‐vitamin E. When “^3^H”‐vitamin E was incorporated into lipid vesicles prepared from the total lipid extracts of endothelial cells and varying amounts of exogenous PE, vitamin E content was directly related to PE content. These results demonstrate that PUFA and PE distribute in all pulmonary artery endothelial cell membranes. However, only increases in PE were associated with increased incorporation of “^3^H”‐vitamin E in membranes of these cells.
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