AJP - Heart and Circulatory Physiology, Vol 245, Issue 5 867-H870, Copyright © 1983 by American Physiological Society
Unbalanced plasma control of TxA2 and PGI2 synthesis in vitamin E-deficient rats
A. Falanga, M. G. Doni, F. Delaini, G. De Bellis Vitti, L. Imberti, M. B. Donati and G. de Gaetano
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.
