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Glutathione peroxidase (GSH-Px) contains 4 selenium atoms/molecule; its activity is increased by selenium dietary intake. The enzyme destroys H2O2 and organic hydroperoxides, contributing to the integrity of biological membranes. GSH-Px activity increased (+100%) in washed platelets of rats administered selenium (0.3 ppm given as sodium selenite) for 60 days from 10.44 +/- 1.10 U/g protein (control rats fed a standard diet) to 20.50 +/- 1.21 U/g protein (mean +/- SE; P less than 0.001). GSH-Px in washed erythrocytes was also stimulated (+70%) after 80 days of selenium dietary intake from 11.60 +/0 0.82 U/g Hb to 19.74 +/- 0.94 U/g Hb (P less than 0.001). Malondialdehyde (MDA), the typical breakdown product of peroxidized lipid and a suitable indicator of platelet prostaglandin production, increased from 0.343 +/- 0.035 nM/3 X 10(8) platelets (control) to 0.478 +/- 0.052 nM/3 X 10(8) platelets after 30 days of selenium treatment (P less than 0.05) and to 0.527 +/- 0.051 nM/3 X 10(8) platelets after 80 days (P less than 0.01). MDA was measured by the thiobarbituric acid method after stimulation with 25 X 10(-4) M arachidonic acid. It is concluded that platelets are very rich in GSH-Px, i.e., activity is greatly increased by oral administration of selenium and that the synthesis of prostaglandins is stimulated too.

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Factors contributing to the antioxidant power of plasma may play a role in the control of arachidonic acid (AA) metabolism. The purpose of this study was to evaluate the possible effects of vitamin E deficiency on platelet and vascular prostaglandin synthesis. CD-COBS male rats were fed for 7 mo a diet containing either 1 or 75 mg/kg vitamin E. At the end of this period, serum levels of vitamin E were 0.4 +/- 0.1 and 10 +/- 0.6 micrograms/ml in the two groups, respectively. Malondialdehyde (MDA) generation by AA was significantly higher in platelet-rich plasma from vitamin E-deficient rats. Thromboxane B2 (TxB2) in serum from vitamin E-deficient rats increased about 16 times compared with controls, whereas 6-keto-PGF1 alpha levels increased only 3 times. The ratio between TxB2 and 6-keto-PGF1 alpha, increased therefore manyfold in vitamin E-deficient animals. MDA formation and [14C]AA metabolism in washed platelets were similar in the two groups of animals. No significant difference was found in the PGI2 (prostacyclin) antiaggregating activity released from the aortic rings resuspended in buffer. In contrast, the capacity of plasma to stimulate PGI2 activity from "exhausted" aortic rings (prostacyclin-stimulating factor) was significantly reduced in vitamin E-deficient animals. In conclusion, vitamin E deficiency induces an unbalanced plasma regulation of AA metabolism. This results in an excessive production of platelet TxA2 compared with vascular PGI2 generation. On the other hand, vitamin E deficiency does not seem to affect directly the enzymatic pathways of AA metabolism.

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