The importance of prostaglandins (PCs) in thyroid physiology has long been a controversial subject. In [l-3] 6-ketoprostaglandin Fr, was isolated and found to be an end-metabolite of the unstable compound, prostacyclin [4,.5]. Prostacyclin producing activity has been reported in many tissues and cells [6-81, and biological significance of prostacyclin in maintaining homeostasis has become apparent. Thromboxane Ba, an end-metabolite of thromboxane Aa, has been isolated [9] and this thromboxane A* seems to play some role to maintain homeostasis. However, prostacyclin and thromboxane Aa producing activities in the thyroid have not been reported and their biological significance needs to be studied. To evaluate the role of endogenous PGs in the regulation of thyroid function, we have estimated prostaglandin Ea (PGE,), prostaglandin Fzor (PGFa,), 6-ketoprostaglandin Fr, and thromboxane Bz (TXBa) and correlations of these PGs and thyroid functions were studied using cultured porcine thyroid cells. Here, we show that in the absence of TSH, the cells are unable to take up iodide or organify it but product; PGE2, PGFzo, and TXBz and that in the presence of TSH, the cells are able to take up iodide and organify it but preferentially produce 6-ketoprostaglandin Fr,, an end-metabolite of prostacyclin.