ABSTRACT
The aim of the present study was to examine whether vitamin E deficiency and dietary linoleate had additive or synergistic effects on serum thromboxane (TX) status and therefore on thrombogenesis. Eight groups of five male weaning Sprague-Dawley rats were fed semipurified diets containing 3.5 or 18.4% of energy from linoleate (en% linoleate) and 0, 100, 5000, 15,000 ppm vitamin E for 8 weeks. Rats fed no vitamin E had the lowest serum vitamin E while rats fed 15,000 ppm vitamin E had the highest serum vitamin E (p < 0.05). Serum 18:2, n-6 (linoleic acid; LA) and 20:4, n-6 (arachidonic acid; AA) were significantly greater in the 18.4 en% linoleate group than in the 3.5 en% linoleate group (p < 0.05). Serum TXA2, measured as its stable metabolite TXB2, was significantly greater in the vitamin E-deficient rats than in the vitamin E-adequate and vitamin E-supplemented rats (p < 0.05). Serum lipid peroxidation, measured as thiobarbituric acid reactive substances (TBARS), was significantly greater in the 0 and 100 ppm vitamin E groups than in the 5000 and 15,000 ppm vitamin E groups (p < 0.05). No interaction between dietary linoleate and vitamin E deficiency on serum TX status was found. However, it seemed that vitamin E deficiency had a more potent effect on TX synthesis than dietary linoleate. The result suggested that vitamin E deficiency may be prothrombogenic via its effect on TX synthesis.
