A mechanism of action of the gonadotropins.

in recent years tends more or less to support the view that the biosynthetic pathways involved in the synthesis of the steroid hormones by the endocrine organs are qualitatively similar. One outstand ing exception to this is the ability of the adrenal cortex to hydroxylate the steroid molecule at C-il, which phe nomenon is not shared by any other normal mammalian tissue. In a very broad sense one can assume also that the contoffling mechanisms at the pituitary level are aLso similar and that the major difference among these tissues is their specific responsivity to their respective anterior pituitary hormones. Several mechanisms have been suggested over the past few years in attempts to explain the action of these pro tein hormones on their respective target organs. Hechter and Lester (7) proposed that adrenocortico tropin (ACTH)3 acts on the adrenal cortex by enhancing the permeability of the cell to glucose. This, in addition to furnishing the energy requirements of the cell, would give rise to increased TPNH (reduced triphosphopyridine nucleotide) as glucose 6-phosphate is made available to the various TPNH-generating systems. The TPNH would then be available to satisfy the co-factor require nients of the hydroxylating enzyme systems involved in steroid hormone biosynthesis. Konitz amid Peron (10) have suggested that ACTH may do 2 things : 1) make more TPNH available for crucial hydroxylat.ions involved in steroid biosynthesis; and 2) release hormone precursor material intracellulanly from some previously unavailable form. This is based on ob servations that freezing quartered rat adrenal glands and subsequently incubating them prevented the stimulatory 1 This investigation has been supported by USPHS Grant AM-02672. 6-phosphate; G-6-P DHase, glucose 6-phosphate dehydrogenase. action of ACTH omi corticoid output by the quartered glands. If they incubated the prefrozen glands with TPN and glucose 6-phosphate, they observed more corti coid production than with ACTH stimulation of unfrozen glands. ACTH addition to TPN and glucose 6-phosphate produced no further increase in corticoid output. They suggested that the results of the freezing mimicked the ACTH effect. Haynes and Berthet (5), from observations obtained in bovine adrenal cortex slices, advanced the suggestion that ACTH acted by activating adrenal phosphorylase and that the glucose 6-phosphate resulting from this activation was metabolized via the hexose monophosphate shunt. The TPNH thus generated increased the rate of steroido genesis. This was modified by further observations (4) which showed that 3' , 5'-AMP (adenosine-3' , 5'-mono phosphate) was …