Metaplasia produced in cultures of chick ectoderm by high vitamin A / by Honor B. Fell and E. Mellanby.

  • Fell, Honor B.
Date:
[1953?]
Catalogue details

Licence: In copyright

Credit: Metaplasia produced in cultures of chick ectoderm by high vitamin A / by Honor B. Fell and E. Mellanby. Source: Wellcome Collection.

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    obscure, but whatever it may be it appears to act on those cells which are basic to the growth of the tissue, in this case those of the stratum germinativum (cf. Wolbach & Howe, 1925, 1933). This direct action of the vitamin on master structural cells is also seen in bone. As shown by one of us (Mellanby 1938, 1944, 1947), when vitamin A becomes deficient in young growing animals, the position and degree of activity of the osteoblasts and osteoclasts are greatly altered, the mechanism of bone modelling breaks down and the bone becomes thickened, coarse and malformed. When the vitamin A is sufficiently above normal, there is also an alteration of bone cell activity in the opposite sense, and the bones become rarified and fracture easily. Another instance of vitamin A acting on structural cells can be seen in embryonic bone growing in tissue culture. There the high vitamin A stimulates the chondroblasts to destroy the matrix of the cartilage prior to their own disappearance (Fell & Mellanby, 1952). These, of course, are effects of vitamin A on mesodermal cells in contrast to its action on ectodermal cells described in the present work. The fact that vitamin A acts on basic structural cells in both ectodermal and mesodermal tissues may be of significance, and may lead to a better under¬ standing of this interesting biological effect of the vitamin. Whereas there are probably different threshold values of vitamin A for controlling the structure and function of different epithelia in an animal, it is also probable that there are differences of threshold, controlling the same epithelium in different species. This seems likely from the great differences of vitamin A concentration in the blood of different species. Normally rat plasma contains 50-80 i.u./lOO ml., a level which would correspond to hypovitaminosis in dogs or chickens in which normal values lie between 200 and 350 i.u./lOO ml., values corresponding with induced hypervitaminosis in rats. The great difficulty in producing hypervitaminosis A and the need to give massive doses of the vitamin to produce this condition, shows how important to the well¬ being of the animal is the mechanism of keeping the plasma concentration constant at the level normal to each species. Whereas the significance of this control is now obvious, except for the storage phenomenon in the liver, knowledge of the mechanism of control is meagre. In view of these great differences in the normal amount of vitamin A present in the blood of different animals, it may well be that the ectoderm of species other than that of chick embryos may vary in their susceptibility to excessive vitamin A. Preliminary experiments with the early embryonic mouse ectoderm in culture, have shown that it is far less reactive than that of the chick, and while there was evidence of an inhibitory effect on hair-formation and eventually on epidermal keratinization, for the first week at least, plentiful keratin was formed in the presence of a concentration of vitamin A which completely prevented cornification in the chick cultures. Further experiments will be made with mammalian tissues.