Paper
VITAMIN A AND MUCOUS METAPLASIA *
Published Mar 1, 1963 · D. J. Lawrence, H. Bern
Annals of the New York Academy of Sciences
23
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Abstract
The term “metaplasia” has been defined in various ways (Weiss, 1949; Grobstein, 1959). We use the term to refer to a change in a tissue from one adult or differentiated pattern to another fully differentiated pattern. In our usage, no particular mechanism of transformation is implied, and the term is employed only in its descriptive sense. The processes of mucus production and keratinization represent distinct alternate pathways of differentiation and adult function of epithelia in higher vertebrates. We are concerned here with the metaplastic transformation of one of these patterns into the other. In the two processes of mucification and keratinization, the end products are mucin or keratin, respectively. Both end products are variable in structure and chemical composition and actually represent two classes of macromolecular materials, rather than specific chemical entities. Although both classes of materials include protein as a major constitutent and both have an important content of sulfur, they are otherwise chemically distinct. In mature keratin (Matoltsy, 1958; Ryder, 1958; Rogers, 1959; Mercer, 1961), sulfur is present largely in the form of disulfide (S-S) bonds serving as multiple cross-links between fibrillar polypeptide chains; these S-S bonds seem to explain many of the characteristic resistant qualities of keratin. Earlier studies in our laboratory (Bern, 1954; Bern et aE., 19553; Harkness and Bern, 1957) and elsewhere (for example Ryder, 1958) established that many if not all varieties of keratin-forming tissues exhibit a characteristic zone of uptake of V5-labeled cyst(e)ine within a delimited, partially keratinized region of the tissue. This uptake and fixation of cysteine to form later a permanent component of keratin have been interpreted as representing a specific stage in keratin synthesis wherein cysleine is incorporated into an amorphous “cement” protein in which the fibrils become embedded. Since the first reports in 1922 by Mori and by Evans and Bishop, vitamin A deficiency has been known to promote a keratinizing change of many epithelia in mammals and birds (see Wolbach and Bessey, 1942; Moore, 1957). In the animal deficient in vitamin A, keratinization is somehow favored. Normally keratinizing areas produce a thicker layer of keratin; many, if not eventually all, mucous membranes undergo keratinizing metaplasia. This change to a keratin-producing state appears to result from altered differentiation of the progeny of undifferentiated basal cells of the original epithelium (rather than from an ingrowth of normally keratinizing cells from elsewhere). Recent studies of the effects of vitamin A deficiency in the rat have been reviewed by Parnell and Sherman (1962). In an attempt to obtain the reverse effect, the inhibition of normal keratini-
Vitamin A deficiency promotes keratinization in mucous membranes, leading to a thicker layer of keratin, affecting the function of the epithelia in mammals and birds.
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