The effect of ascorbic acid depletion on the amidation of alphamelanocyte stimulating hormone (alpha MSH) was studied in vivo in guinea pig pituitary. After four weeks, the concentration of ascorbic acid was 1.20 +/- 0.11 mumol/g tissue (mean +/- SD) in the pituitary and 0.34 +/- 0.07 mumol/g tissue in the cerebral cortex from the depleted animals versus 7.58 +/- 0.08 and 1.51 +/- 0.32 mumol/g tissue, respectively, in the control animals. In the pituitaries from the animals depleted of ascorbate (N = 4), the relative amount of alpha MSH was reduced to approximately half the values obtained in the control group (from 66.5 +/- 4.6% of total ACTH-related peptides to 31.1 +/- 12.2% (P less than 0.0025]. A concomitant increase (from 5.9 +/- 3.1% to 19.4 +/- 4.3% (P less than 0.004] in ACTH (1-14) (the glycine-extended precursor of alpha MSH) immunoreactivity and a smaller increase in ACTH (1-39) immunoreactivity was observed in the depleted guinea pigs. Gel chromatography and reversed-phase high-performance luquid chromatography showed that the alpha MSH and ACTH (1-14) immunoreactivity was of low molecular weight and partly mono- or diacetylated. Depletion of ascorbic acid had no influence on the degree of acetylation of alpha MSH and ACTH (1-14). It is concluded that depletion of ascorbic acid reduces the in vivo amidation of ACTH (1-14) in the guinea pig pituitary.
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Fenger et al. (1988) studied this question.