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Whether the alterations in the synthesis of thromboxane A2 (TXA2) is the direct mechanism underlying the blood pressure-lowering effect of fish oil was investigated in this study. Six groups of 11 male spontaneously hypertensive rats were fed semipurified diets containing corn or fish oils and graded levels (50, 5000 or 15,000 ppm) of dietary vitamin E for 8 weeks. Plasma TXA2, assayed by RIA, was significantly greater in the corn oil group than in the fish oil group (P < 0.05). Compared to 50 ppm dietary vitamin E, 5000 and 15 000 ppm dietary vitamin E, respectively, significantly decreased plasma TXA2 (P < 0.05). Systolic, mean or diastolic blood pressure, evaluated by the tail cuff method, were significantly higher in the corn oil group than in the fish oil group (P < 0.05). However, vitamin E had no effect on blood pressure. No relationship between TXA2 and blood pressure was found. Experimental results indicated that the alterations in the synthesis of TXA2 were not the direct antihypertensive effect of fish oil.

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.