Effects of vitamin E and aspirin on the incidence of encephalomalacia, fatty acid status and serum thromboxane levels in chicks.
This study was initiated to examine the role of prostanoids (thromboxane) in the development of nutritional encephalomalacia (NE). Chicks were fed diets deficient in or supplemented with vitamin E in the presence or absence of a known prostaglandin inhibitor, acetylsalicylic acid (ASA). When the incidence of NE was approximately 50% in the vitamin E--deficient group without ASA supplement, the chicks were killed, and serum thromboxane B2 (TxB2) and serum and brain fatty acid (FA) composition were determined. The incidence of NE was not altered by ASA treatment. Plasma arachidonate levels were increased by ASA treatment on the vitamin E--deficient diet. Furthermore, the serum TxB2 levels in vitamin E--deficient versus vitamin E--adequate chicks, unlike changes noted for rats, were decreased. Aspirin treatment drastically reduced TxB2 levels in all groups but did not alter the incidence of NE. Therefore, it is unlikely that the development of NE is a result of thromboxane-mediated thrombosis.
D000818:Animals; D001241:Aspirin / Q000494:pharmacology*; D002645:Chickens / Q000097:blood*; D004678:Encephalomalacia / Q000097:blood / Q000453:epidemiology* / Q000209:etiology; D005227:Fatty Acids / Q000097:blood*; D013931:Thromboxanes / Q000097:blood*; D014810:Vitamin E / Q000008:administration & dosage*; D014811:Vitamin E Deficiency / Q000097:blood
D005227:Fatty Acids; D013931:Thromboxanes; D014810:Vitamin E; D001241:Aspirin