Haye B, Gerard C, Jacquemin C
FEBS Lett. 1982 Nov 8;148(2):281-8. doi: 10.1016/0014-5793(82)80825-9.
The arachidonate inhibition of the adenylate-cyclase system of cultured pig thyroid cells was not mediated by cyclooxygenase, lipoxygenase or peroxidase metabolites. Indeed ETYA, an inhibitor of cyclooxygenase and lipoxygenase, and methimazole, an inhibitor of peroxidase and iodination were without effect on the arachidonate inhibition. Moreover the effect of arachidonate was amplified by a combination with ETYA. In 32P incorporation experiments we observed a modification of the labelling of individual phospholipids of cultured pig thyroid cells resulting in a decrease into phosphatidylinositol (PI) and an increase into phosphatidate (PA) of arachidonate and ETYA-treated cells. These results may be explained by an inhibition of CDP-diacylglycerol: inositol transferase and conversely a stimulation of PI specific phospholipase C yielding a decrease in PI and an increase in PA, which inhibits in turn adenylate cyclase activity possibly by Ca2+ translocation.
花生四烯酸对培养的猪甲状腺细胞腺苷酸环化酶系统的抑制作用并非由环氧化酶、脂氧化酶或过氧化物酶代谢产物介导。事实上，环氧化酶和脂氧化酶的抑制剂ETYA以及过氧化物酶和碘化作用的抑制剂甲巯咪唑对花生四烯酸的抑制作用均无影响。此外，花生四烯酸与ETYA联合使用时其作用会增强。在³²P掺入实验中，我们观察到培养的猪甲状腺细胞中个别磷脂的标记发生了改变，花生四烯酸和ETYA处理的细胞中磷脂酰肌醇（PI）减少而磷脂酸（PA）增加。这些结果可能是由于CDP - 二酰甘油：肌醇转移酶受到抑制，相反，PI特异性磷脂酶C受到刺激，导致PI减少而PA增加，PA可能通过Ca²⁺转运反过来抑制腺苷酸环化酶活性。
