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Query: UMLS:C0036474 (scurvy)
 685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of ascorbic acid deficiency on adrenal hydroxylation of cholesterol and deoxycorticosterone in guinea pigs was studied by using mitochondria and isolated cytochrome P-450 fractions. The effects obtained were compared with the effects of long-term treatment with ACTH. Advanced scurvy as well as treatment with ACTH resulted in an increase in the weight of the adrenals, the total amount of cytochrome P-450, the cholesterol side-chain cleavage activity, the cortisol level in plasma, and the excretion of unconjugated cortisol in urine. Total 11beta- and 18-hydroxylation of deoxycorticosterone were not stimulated or were stimulated only to a small extent. It is suggested that the major effects observed in advanced scurvy are due to ACTH, the level of which was significantly increased, most probably as a consequence of the stress. In animals kept on a scorbutogenic diet for 2-4 weeks or, with a small dose of ascorbate added, for several weeks, changes were observed that could not be fully explained as effects of ACTH on normal adrenals. Although the plasma levels of ACTH and cortisol were increased only to a small extent and excretion of unconjugated cortisol in urine was unaffected, there was a significant increase in the total capacity of adrenal mitochondria to hydroxylate exogenous cholesterol. It is concluded that the level of ascorbate in the adrenals might be of some importance for the capacity to convert cholesterol into pregnenolone. The normal feed-back regulation is, however, intact in moderate ascorbate deficiency and the plasma level of cortisol is kept within normal limits.
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PMID:Effects of ascorbic acid deficiency on adrenal mitochondrial hydroxylations in guinea pigs. 21 Nov 71

Effects of deficiency in ascorbic acid on in vivo production of corticosterone and testosterone were examined using a mutant strain of rats unable to synthesize ascorbic acid. The adrenal weight of scorbutic rats was larger, and corticosterone levels in plasma and adrenal tissues were higher than those of ascorbic acid-supplied (ascorbutic) rats. Acute and chronic stimulation with ACTH increased corticosterone levels in both ascorbutic and scorbutic rats. In contrast, weights of seminal vesicles and ventral prostates in unstimulated scorbutic rats were smaller, and testosterone levels in plasma and testicular tissues were lower than those in ascorbutic rats. Acute stimulation with hCG increased testosterone levels only slightly in plasma and not in testicular tissues of scorbutic rats, when testosterone levels in ascorbutic rats reached a maximum. Chronic stimulation with hCG increased testosterone levels remarkably in both ascorbutic and scorbutic rats. These findings seem to indicate that ascorbic acid is not essential for the synthesis of steroid hormones. The scurvy seems to increase plasma ACTH levels secondary to the stress, resulting in the stimulation of the adrenals. In contrast, a prolonged deficiency in ascorbic acid appears to decrease plasma gonadotropin levels, and may reduce the sensitivity of testes to gonadotropins.
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PMID:Production of corticosterone and testosterone in scorbutic mutant rats: difference of in vivo production between adrenal gland and testis. 185 91

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