Hormonal regulation of ascorbic acid in the adrenal of the rat

Abstract

Fifteen days after hypophysectomy of rats the concentrations of ascorbic acid (AA) in adrenals, liver, blood and urine are lower than in normal rats or in rats 1 day after hypophysectomy. Despite the low levels the percentage AA depletion after administration of ACTH and the subsequent repletion to the pre-ACTH level are normal. Lack of corticosteroids is not the cause of the low AA levels, as shown by experiments in 15 days adrenalectomized rats and in rats treated with low doses of dexamethasone.Fifteen days treatment with high doses of dexamethasone lowered the AA concentrations in adrenals, liver and blood. Treatment with long-acting ACTH maintained adrenal weight but not adrenal and blood AA. A high dose of ACTH lowered these levels. The administration of AA markedly increased the AA levels in blood, but did not normalize its concentration in the adrenals, not even when the size of the adrenals was maintained by treatment with long-acting ACTH. Growth hormone, in particular when administered together with long-acting ACTH, markedly raised the AA concentration in the adrenals but hardly affected the AA blood level. Rats with high blood levels of prolactin induced by pituitary grafts in the kidney also had clearly higher AA levels in adrenals, but not in blood. These results indicate that, although acute AA release from the adrenal is caused by ACTH, AA uptake to a certain concentration is not controlled by the pituitary gland, and above this concentration is promoted by growth hormone and prolactin. In the liver AA release may also be caused by ACTH but the AA production is promoted by other as yet unidentified pituitary factors.In rats 15 days after hypophysectomy the adrenals are markedly atrophied and contain little ascorbic acid (AA) both absolutely (mg/adrenal) and rela¬ tively (mg/100 g adrenal). This was described by Stähelin et al. (1965) and confirmed by Overbeek (1981a,b). It was to be expected that the atrophied adrenals would contain only small amounts of AA but the fact that the concentration is well below normal was unexpected and requires an explana¬ tion.Several explanations are conceivable such as: a decreased supply of AA to the adrenals as a con¬ sequence of an increased urinary excretion of AA; or a decreased production of AA; or a decreased ability of the adrenal to store A A.Such possibilities have been explored in the present study.It was also studied if the lowered corticosterone production in the adrenals influences AA levels in adrenals, blood and liver and if one of the lacking pituitary hormones could be held responsible for the abnormal AA levels in the long-term hypophysectomized rats. Materials and MethodsThe experiments were carried out with male Wistar rats purchased from TNO, Zeist, The Netherlands (body weight about 300 g). Hypophysectomy was performed by the parapharyngeal route. Ascorbic acid (AA) was deter¬ mined in adrenals with the dichlorophenol-indophenol method (USP XX) and in blood, liver and urine with the dinitrophenylhydrazine (DNPH) method described by György &...

Vitamin E Depletion Enhances Liver Oxidative Damage in Rats with Water-Immersion Restraint Stress

“…Therefore, it is assumed that the damaged liver of VE-D-fed rats with WIRS releases ascorbic acid accumulated in the liver into the bloodstream more easily than the damaged liver of N-fed rats with WIRS. In addition, it has been shown in rats with a single administration of ACTH that ascorbic acid is released from the adrenal gland into the bloodstream (22). It has also been shown that human adrenal glands secrete ascorbic acid in response to ACTH (23).…”

Water‐immersion restraint stress disrupts nonenzymatic antioxidant defense systems through rapid and continuous ascorbic acid depletion in the adrenal gland of rats

“…Serum ascorbic acid concentration in rats exposed to WIRS for a 6‐h period began to increase 0.5 h after the onset of the stress and continued to increase thereafter, reaching 2.5‐fold higher than that concentration in unstressed rats at 6 h. In addition, the content of adrenal ascorbic acid was well correlated with the concentration of serum ascorbic acid in a negative fashion in all stressed rats. It is known that a single treatment of rats with ACTH causes a rapid ascorbic acid depletion in the adrenal gland . It is also known that ACTH inhibits the uptake of ascorbic acid by isolated rat adrenal glands or isolated rats adrenocortical cells .…”

“…Therefore, we have suggested that ascorbic acid in the liver of rats with WIRS is, at least in part, released from the tissue into the bloodstream . It has also been suggested that a single ACTH administration and acute release of ACTH from the pituitary after acute stress might cause an acute release of ascorbic acid from liver tissues into bloodstream in rats . Therefore, it cannot be ruled out that the release of ascorbic acid from the liver tissue of rats with WIRS contributes to the increase in serum ascorbic acid concentration found in the stressed rats.…”

“…To confirm the disruption of nonenzymatic antioxidant defense systems through ascorbic acid depletion in the adrenal gland of rats with WIRS, we examined the effect of preadministered l ‐ascorbic acid on the changes in LPO, ascorbic acid, GSH and α‐tocopherol levels in the serum and adrenal gland of rats with 6 h of WIRS. As described earlier, it is known that ACTH and sympathomimetic amines such as adrenaline and noradrenaline cause ascorbic acid depletion in the adrenal gland of rats . Therefore, we checked whether preadministered l ‐ascorbic acid affects the stress response via the HPA axis and the sympathetic–adrenal system in rats with 6 h of WIRS.…”

“…It has also been reported that a single exposure of rats to 6 h of WIRS causes increases in serum adrenocorticotropic hormone (ACTH) and corticosterone levels through activation of the HPA axis and serum glucose level through activation of the sympathetic–adrenal system . It is known that a single treatment with ACTH causes a rapid reduction of ascorbic acid level in the adrenal gland of rats . It is also known that ACTH inhibits the uptake of ascorbic acid by isolated rat adrenal glands or isolated rats adrenocortical cells .…”