Effects of Prostaglandin E1Ethanol and TSH on the Adenylate Cyclase Activity of Beef Thyroid Plasma Membranes and Cyclic AMP Content of Dog Thyroid Slices1

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Abstract
Prostaglandin E1 (PGE1) stimulated adenylate cyclase activity in beef thyroid homogenates and isolated plasma membranes in a dose dependent manner. Effects were significant with, 1.4 × 10−7M PGE, and maximal with 1.4 × 10−5M PGE1. Larger doses (1.4 × 10−3M PGE1)had no effect on homogenates but caused a further stimulation of membrane adenylate cyclase. However, this was due to the ethanol used to dissolve the PGE1. The ethanol induced stimulation was linear over the concentration range 0.25% (v/v) t o 5%. Five percent ethanol stimulated adenylate cyclase activity in rat liver and kidney plasma membranes but not in homogenates of these tissues or of beef thyroid. Ethanol (1%) did not affect cyclic 3′,5′-adenosine monophosphate (cyclic AMP) levels in dog thyroid slices. It is suggested that ethanol can activate adenylate cyclase as a result of membrane perturbation. Neither aspirin (100 μg/ml), or indomethacin (10 μg/ml), blocked the effect of TSH on cyclic AMP levels or l−14C-glucose oxidation in dog thyroid slices. Maximal effects of thyrotropin (TSH) on adenylate cyclase activity in beef thyroid plasma membranes or cyclic AMP levels in dog thyroid slices were much larger than those of PGE1. Combinations of maximal doses of TSH and PGE1 or submaximal doses of one stimulator with maximum doses of the other did not produce any inhibition when cyclic AMP concentrations in dog thyroid slices or adenylate cyclase in plasma membranes were measured. Combinations of low doses of these stimulators, or a low dose of TSH with a maximal dose of PGE1, were additive. These data do not support the concept that the effects of TSH on the thyroidal adenylate cyclase-cyclic AMP system are mediated by PGE1. (Endo-crinology94: 370, 1974)

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