Effects of vitamin E on arachidonic acid cascade in platelets and aorta of acute cadmium-poisoned rats

Abstract

The purpose of this study was to investigate the effects of vitamin E on several factors related to cardiovascular disease in acute cadmium-poisoned rats. Sprague-Dawley male rats weighing 100 ± 10 g were randomly divided into one control group and three groups for cadmium injection. For four weeks the latter three groups were fed a vitamin E-free diet (0E-Cd group), 40 mg vitamin E per kg diet (40E-Cd group), and 400 mg vitamin E per kg diet (400E-Cd group), respectively, and the control group was fed a 40 mg vitamin E per kg diet. Then the three groups selected for cadmium poisoning were injected intraperitoneally with 2.0 mg of CdCl 2/kg BW for 4 days. The effects of the vitamin E were then investigated by observing both the phospholipase A 2 (PLA 2) activity and arachidonic acid cascade metabolism in the platelet and aorta. When compared with the control group, the results can be summarized as follows: the platelet activity of PLA 2 in the 0E-Cd, 40E-Cd, and 400E-Cd groups increased 172%, 73%, and 40%, respectively, whereas the cyclooxygenase(COX) activity increased 153%, 96% and 57%, respectively. The total concentration of serum thiobarbituric acid reactive substances (TBARS) in the 0E-Cd group was 2.2 fold higher, however, this was reduced by the vitamin E supplementation. The platelet formation of thromboxane A 2(TXA 2) and prostaglandin D 2(PGD 2) increased 100%, 60%, and 10% in the 0E-Cd, 40E-Cd, and 400E-Cd groups, respectively. The production of aortic prostacyclin (PGI 2) in the 0E-Cd, 40E-Cd and 400E-Cd groups, was lower by 34%, 35%, and 11%, respectively. The PGD 2/TXA 2 and PGI 2/TXA 2 ratios in the cadmium-poisoned groups were also lower. These results indicate that Cd-poison rats accelerates arachidonic acid metabolism. The inhibition of arachidonic acid metabolism due to vitamin E supplementation, however, decreases platelet aggreability. In conclusion, it would appear the vitamin E supplementation in acute cadmium-poisoned rats inhibits the arachidonic acid cascade by regulating the activity of PLA 2.