The influence of the thyroid gland on polyploid cell formation in the external orbital gland of the rat
Authors: Carriere Rita 
Published: February 2005

The influence of the thyroid gland on the progressive accumulation of polyploid acinar nuclei in the rat external orbital gland was investigated. The numbers of polyploid nuclei were determined from nuclear size distribution curves, having first ascertained the correspondence between increased nuclear size and the polyploid state by microspectrophotometric determinations of the DNA in Feulgen‐stained nuclei.

In the first experiment, the animals were kept 147 days, and controls showed increases in external orbital gland weight and polyploid cell formation with age. The presence of the thyroid was essential to these morphological changes, for they were prevented by thyroidectomy at 70 gm body weight. Treatment with thyroxine, begun 103 days after thyroidectomy, restored body and orbital gland weight gains and the formation of new polyploid cells. Treatment of thyroidectomized rats with growth hormone induced body growth, but failed to alter orbital gland weight and polyploidy. The action of thyroid hormone on orbital gland cells was therefore not mediated through its effect on the release of anterior pituitary growth hormone and this contrasts with previously reported results of polyploidy studies in the livers of these same animals.

A second experiment was designed to study the interrelationship of the observed thyroid effect with the stimulatory action of testis hormone reported in the literature. The animals weighed 49 gm at the beginning of the experiment, their orbital glands weighed 54 mg and contained 41.0% polyploid nuclei. Eighty days after castration at 49 gm body weight, orbital glands weighed 153 mg and contained 88.9% polyploid nuclei of which 24.9% were above tetraploid size, whereas the glands of sham‐operated controls weighed 214 mg and contained 91.5% polyploid nuclei of which 53.6% were above tetraploid size. Thus, the presence of the testis is not required for polyploid cell formation and orbital gland growth, although it can exert some stimulatory action in the course of normal development. On the other hand, thyroidectomy alone or thyroidectomy together with castration, prevented increases in gland weight or numbers of polyploid nuclei, again demonstrating the essential role of the thyroid. Treatment of thyroidectomized‐castrates with thyroxine for 42 days, beginning 38 days after operation, led to the resumption of orbital gland weight gains (107 mg) and polyploid cell formation (91.4%), but treatment with testosterone did not. Thus, the thyroid control is independent of any concomitant testicular influence on these cells, whereas the stimulatory effect of testicular hormone requires a permissive action of thyroid hormone.

In discussing these results, comparisons were made with the hormone control of liver growth and polyploidy, and it was concluded that the formation of new polyploid cells is stimulated by those specific hormones which can promote cell division in liver parenchyma and external orbital gland acini. It was further noted that in both these tissues, there is an increase of basic nuclear size with age, regardless of ploidy, and that this nuclear growth also can be influenced by thyroid hormone.