Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036474 (scurvy)
 685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concentration of ascorbic acid (vitamin C) in the adrenal cortex is higher than in any other organ. The role of vitamin C in the adrenal cortex is unknown, but data obtained with bovine adrenocortical cells in vitro favour its role as an antioxidant that especially protects aldosterone synthesis from damaging lipid peroxides. Alternatively, vitamin C could act as part of an auxiliary electron transport system for the last step of aldosterone synthesis. The effects of vitamin C depletion on adrenocortical function cannot be studied in the human for ethical reasons, so we subjected different groups of guinea pigs to vitamin C depletion, sodium depletion and combined vitamin C and sodium depletion. Other groups of animals on normal or vitamin C-deficient diets received high-dose adrenocorticotrophin (ACTH) injections for 3 days before sacrifice. Fifteen days of a vitamin C-free diet led to very low vitamin C levels in adrenals, liver and plasma without clear signs of scurvy. At this time, plasma aldosterone and aldosterone secretion by isolated adrenal cells were stimulated significantly by sodium deficiency. Simultaneous vitamin C depletion completely abolished the rise in aldosterone in vivo and in vitro, significantly reduced the conversion of [3H]deoxycorticosterone to [3H]aldosterone and impaired renal sodium conservation. Plasma renin activity (PRA), plasma ACTH and serum potassium were not different in the sodium-depleted and sodium plus vitamin C-depleted groups. Sodium depletion did not affect cortisol. Vitamin C depletion led to a significant increase in plasma cortisol without an increase in ACTH, while in vitro secretion of cortisol was slightly decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ascorbate depletion prevents aldosterone stimulation by sodium deficiency in the guinea pig. 758 76

Ascorbate (Vit.C) and alpha-tocopherol (Vit.E) are highly concentrated in the adrenal. Both vitamins support steroid synthesis in vitro. Vitamin depletion experiments in guinea pigs were done to study the role in aldosterone synthesis of these antioxidants in vivo. We stimulated aldosterone secretion by sodium depletion in vitamin depleted animals and compared the effects with those in vitamin replete guinea pigs. We analysed plasma hormone levels and measured ex vivo steroid secretion by isolated adrenal cells and conversion of[3H]deoxycorticosterone to [3H]aldosterone. Fifteen days of a Vit.C-free diet led to very low Vit.C levels in adrenals, liver and plasma, without signs of scurvy. Plasma ACTH and plasma renin activity (PRA) were not influenced. Vit.C depletion abolished a rise of plasma aldosterone and of aldosterone secreted in vitro stimulated by sodium depletion. The in vitro conversion of [3H]deoxycorticosterone to [3H]aldosterone was reduced and sodium conservation was impaired by Vit.C depletion. Vit.E depletion did not abolish but significantly attenuated the rise in plasma aldosterone stimulated by sodium depletion. Aldosterone secretion by adrenal cells isolated from these animals was suppressed to control levels. Both antioxidants Vit.C and Vit.E seem to play a permissive role in aldosterone synthesis, possibly by protecting the cytochrome P450(11 beta) from lipidperoxides. Vit.C may also act as part of an auxiliary electron transport system for the last step of aldosterone synthesis.
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PMID:Ascorbate and alpha-tocopherol depletion inhibit aldosterone stimulation by sodium deficiency in the guinea pig. 896 17