Adrenal Gland in Vitamin E Deficiency: III. INHIBITION OF ADRENOCORTICOTROPIC HORMONE-INDUCED STEROIDOGENESIS IN ISOLATED ADRENAL CELLS BY ASCORBIC ACID

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Isolated adrenal cells from vitamin E-deficient and control rats were prepared by a trypsin digestion method. Corticosterone formation and lipid peroxidation in vitro were measured in these cells in response to adrenocorticotropin (ACTH) and dibutyryl cyclic adenosine 3′, 5′-monophosphate ((bt)2 cAMP) in the presence and absence of ascorbate. The addition of ascorbate to adrenal cells of vitamin E-deficient rats stimulated lipid peroxidation in the presence and absence of ACTH or (bt)2 cAMP. Ascorbate inhibited ACTH-induced steroidogenesis in adrenal cells of vitamin E-deficient rats, but not in the control group. Ascorbate did not affect (bt)2 cAMP-induced steroidogenesis in either group. Intraperitoneal injection of tocopherol to the deficient rat, 16 hours prior to sacrifice, abolished the inhibitory effect of ascorbate on ACTH-induced steroidogenesis and prevented the stimulation of lipid peroxidation by ascorbate. Butylated hydroxytoluene treatment did not have any effect on lipid peroxidation or steroidogenesis in vitamin E-deficient rat adrenal cells. Addition of manganese, cobalt, EDTA, and α-tocopherol to adrenal cells from vitamin E-deficient rats in vitro reduced the inhibition of ACTH-induced steroidogenesis by ascorbate, but only the doses of EDTA and α-tocopherol (5.8 µg per ml or higher) caused diminution of lipid peroxidation. Based on these studies, we suggest that tocopherol deficiency in the presence of ascorbic acid may affect steroidogenesis through interaction of ACTH with the cell membrane prior to the formation of the second messenger.