The transport of l-ascorbic acid by quartered rat adrenal glands was measured using l-ascorbic acid-l-14C. The transport is dependent upon an aerobic atmosphere and the presence of Na+, K+ and Ca++ in the medium. After 150 min of incubation the ratio of intracellular to extracellular radioactivity is 7.5 ± 0.2 (se) for adrenal glands from male rats and 4.3 ± 0.5 for adrenal glands from females. ACTH, added in vitro, inhibits the transport of ascorbic acid by about 30%. The inhibition by ACTH is correlated with increased steroidogenesis. 17β-Estradiol and progesterone also inhibit the transport of ascorbic acid and, in their presence, corticosteroid production is increased. Substances extracted by methylene dichloride from the medium of adrenal glands incubated with ACTH in vitro inhibit the transport of l-ascorbic acid to a greater extent than several corticosteroids tested. Of the steroids examined, aldosterone is the most potent inhibitor at concentrations between 10−6 and 10−4m. Corticosterone at 10−4m or less has little effect. ACTH also inhibits ascorbic acid transport in isolated zona fasciculatareticularis of adrenal tissue, ruling out aldosterone as a unique inhibitor. The transport of ascorbic acid appears to be independent of protein synthesis because puromycin inhibits leucine incorporation into adrenal gland proteins without affecting the uptake of ascorbic acid. In the presence of 0.1 HIM puromycin, however, ACTH no longer inhibits the uptake of l-ascorbic acid-l-14C, suggesting that protein synthesis is required for the inhibition of ascorbic acid transport by ACTH. (Endocrinology82: 436, 1968)
No takes yet. Share an insight, caveat, or question.
Nicola et al. (1968) studied this question.
Synapse has enriched 5 related papers. Consider them for comparative context: