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American Journal of Clinical Nutrition, Vol. 87, No. 1, 191, January 2008
© 2008 American Society for Nutrition

LETTER TO THE EDITOR

Is there a need for vitamin C supplementation of the normal diet? Effects of in vivo ascorbate depletion on adrenal function

Volker Bähr and Andreas FH Pfeiffer

Department of Endocrinology, Diabetes, and Nutrition
Charité Campus Benjamin Franklin
Hindenburgdamm 30
12200 Berlin
Germany
E-mail: volker.baehr{at}charite.de

Wolfgang Oelkers

Endokrínologikum Berlin
Center for Endocrine and Metabolism Diseases
Jägerstrasse 61
10117 Berlin
Germany

Dear Sir:

In a recent article in the Journal, Padayatty et al (1) described a fast increase in the secretion of vitamin C from human adrenals in response to adrenocorticotrophic hormone, preceding the rise in cortisol secretion. The function of the vitamin C released from the adrenals is not clear. The authors considered oral and intravenous vitamin C supplementation in the context of a putative paracrine function of adrenal vitamin C.

Our group has shown that vitamin C deprivation of guinea pigs for 15 d reduced the vitamin C content of their adrenals to <1/20 of the normal concentration in this tissue (2). These animals showed an impaired plasma aldosterone response to sodium depletion. Cells isolated from the adrenals of these vitamin C–deprived animals secreted less aldosterone than did cells isolated from the adrenals of animals without vitamin C depletion. A reduced conversion of labeled deoxycorticosterone to aldosterone by these cells seemed to indicate an impaired activity of CYP11B2 (2). Guinea pigs also have shown reduced in vivo and in vitro aldosterone responses after depletion of {alpha}-tocopherol (3). These findings are compatible with the need for antioxidants to protect the function of the adrenal cortex against reactive oxygen species generated by lipid peroxydation in the adrenal cortex (4). We did not see an impaired cortisol response after vitamin C or {alpha}-tocopherol depletion, perhaps because of the higher expression of the cortisol-synthesizing enzyme CYP11B1 than of the aldosterone-producing enzyme CYP11B2. In addition to these antioxidants, superoxide dismutase and gluthatione peroxidase are highly concentrated in the adrenals, and they may add to the defense against reactive oxygen species. Our depletion experiments concerning the role of vitamin C in the function of the adrenal cortex do not support the necessity of vitamin C supplementation in addition to a normal diet.

ACKNOWLEDGMENTS

None of the authors had a personal or financial conflict of interest.

REFERENCES

  1. Padayatty SJ, Doppman JL, Chang R, et al. Human adrenal glands secrete vitamin C in response to adrenocorticotrophic hormone. Am J Clin Nutr 2007;86:145–9.[Abstract/Free Full Text]
  2. Redmann A, Möbius K, Hiller HH, Oelkers W, Bähr V. Ascorbate depletion prevents aldosterone stimulation by sodium deficiency in the guinea pig. Eur J Endocrinol 1995;133:499–506.[Abstract/Free Full Text]
  3. Möbius K, Redmann A, Hiller HH, Oelkers W, Bähr V. Permissive role of {alpha}-tocopherol in the stimulation of aldosterone by sodium depletion in the guinea pig. Eur J Endocrinol 1996;134:758–63.[Abstract/Free Full Text]
  4. Hornsby PJ, Crivello JF. The role of lipid peroxidation and biological antioxidants in the function of the adrenal cortex. Part 2. Mol Cell Endocrinol 1983;30:123–47.




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