A study of environmental influence upon salivary gland neoplasia in rats

Abstract

An animal model system was used in an attempt to explore suspect relationships between 3 groups of possible carcinogenic co‐factors (nutritional, endocrine, and thermal) and the seemingly high salivary gland cancer experience of Arcticdwelling Eskimos. Two hundred and thirty weanling Sprague‐Dawley rats were randomized into 7 groups to study effects of vitamin A deficiency, hypercortisonism, hyperthyroidism, hypercortisonism plus hyperthyroidism combined, and a windy, cold, humid environment upon submaxillary salivary glands challenged with implanted 20 percent 7,12‐dimethylbenzanthracene pellets. Animals were sacrificed at 14 weeks. Of the 7 regimens, only vitamin A deficiency increased malignant epithelial neoplasm yield. Increased yield in vitamin A deficient group (I) compared to the sum of nutritionally adequate control groups (II and III) was significant at the 0.001 level, and with all groups II‐VII individually (p = 0.0001) or combined (p = 0.00004). No significant yield difference was found among the other 6 groups (II‐VII).

The effect of different levels of dietary ß‐carotene on DMBA‐induced salivary gland tumors

“…The DMBA-induced SMSG tumor model is well established (18)(19)(20) and has a distinct advantage in that the DMBA-injected experimental gland and the vehicle-injected contralateral control gland are in the same animal. This reduces variability caused by factors such as differences among rats in food intakes and physiological states.…”

A comparative assay of the in‐vitro and in‐vivo behavior of three chemically induced neoplasms of rat submandibular glands

“…Etid poitit: 16 weeks was selected as the termination date because Shafer (1962), Glucksmann & Cherry (1966), Rowe et al (1970) have shown that a significant percentage of animals treated with DMBA bear carcinomas by 16 weeks.…”

Morphologic effects of hypervitaminosis a on rat submandibular gland

“…As in other epithelia, squamous metaplasia with keratin production by ductal cells was demonstrated (HAYES, MCCOMBS and FAHERTY, 1970;PARNELL and SHERMAN, 1962;TROWBRIDGE, 1969). Also in vitamin A deficiency, potentiation of chemically induced salivary gland neoplasia has been described (ROWE et al, 1970). What effect excess vitamin A might have on cells of salivary gland tissue has not been reported.…”