Wu G, Thompson J R
Department of Animal Science, University of Alberta, Edmonton, Canada.
Biochem Int. 1988 Feb;16(2):227-34.
Arachidonic acid (5 microM), prostaglandin E2 (0.28 microM) and F2 alpha (14 microM) inhibited (P less than 0.01) the rates of net leucine transamination, leucine oxidative decarboxylation and total CO2 production from leucine in extensor digitorum communis muscles from fed ten-day-old chicks. Indomethacin (50 microM) markedly inhibited (P less than 0.01) the rate of PGE2 production in the presence of 5 microM arachidonic acid and prevented the inhibition of leucine degradation by arachidonic acid in skeletal muscle. These results demonstrate that the actions of arachidonic acid on leucine degradation in chick skeletal muscle are mediated by metabolites generated via the cyclooxygenase pathway and that prostaglandins may play a role in the regulation of leucine degradation in skeletal muscle.
花生四烯酸（5微摩尔）、前列腺素E2（0.28微摩尔）和F2α（14微摩尔）抑制（P<0.01）了10日龄喂食雏鸡的趾长伸肌中亮氨酸净转氨速率、亮氨酸氧化脱羧速率以及亮氨酸产生的总二氧化碳生成速率。吲哚美辛（50微摩尔）在5微摩尔花生四烯酸存在的情况下显著抑制（P<0.01）前列腺素E2的产生速率，并阻止了花生四烯酸对骨骼肌中亮氨酸降解的抑制作用。这些结果表明，花生四烯酸对雏鸡骨骼肌中亮氨酸降解的作用是由通过环氧化酶途径产生的代谢产物介导的，并且前列腺素可能在骨骼肌中亮氨酸降解的调节中发挥作用。
