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Department of Oral Pathology, College of Dentistry, University of Illinois at Chicago, P.O. Box 6998, Chicago, IL 60680
While most organs of young zinc-deficient rats atrophy, oral surface epithelia either convert from ortho- to parakeratosis with increased rates of proliferation and synthesis (e.g., buccal epithelium) or show no changes (e.g., palate). To test the possibility that oral epithelia sequester zinc, weanling rats were fed a zinc-deficient diet for 27 d, and zinc concentrations were assayed in buccal and palatal epithelium. Testis, duodenum, thymus, kidney, and submandibular and sublingual glands were assayed for comparison. In controls, zinc levels in the two epithelia were higher than in all other tissues except testis. Experimental epithelia showed no sequestering of zinc in the zinc-deficient state. After 27 d, experimental oral epithelium levels were 50% of controls. A marked deficit occurred in testis also; the other organs showed moderate or no reductions. The results show that loss of a major fraction of zinc occurs in tissues with inherently high zinc levels. It is evident that this loss does not interfere with the increased metabolic and proliferative performance in buccal epithelium. The mechanism by which oral epithelia, although losing half their zinc, are spared from the atrophic effects of zinc deficiency remains to be elucidated.
KEY WORDS: zinc epithelium oral
1 This investigation was supported in part by U.S. Public Health Service Research Grants DE 06307 and DE 02342 from the National Institute of Dental Research.
Manuscript received 14 January 1985. Revision accepted 8 February 1985.
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