Fluoride Action Network

Excerpt:

A.P. Tarinsky (4) revealed a 2-3 fold increase of symptoms of oligospermia and azoospermi a in male W¢rkers suffering from industrial fluorosis compared with healthy men o f the same age. Tokar (5, 6) found an association between fluorosis and hypogonadism. These data made it necessary to study the changes of synthetic processes in the testes of mice in experimental fluorosis. A total scintillation method of probe computing on the counter revealed certain shifts of RNA and prote in metabolism in this organ, but the dAta were no t statistically significant. More informative, was the cytoche·m.ical investigation of certain cell types in the testes on the separate stages of spermatogenesis, particularly on tbe 7tb stage. The cells of spermatogenic epithelium with fairly stable DNA content – Sertoli cells, spermatogones of A type, spermatides and also interstitial cells of Leidig – were studied. Between the second and third week after the beginning of the experiment there was a decrease of rRNA in the basal part of the Sertoli cells, in Leidig cells and in spermatides.

In the spermatogones this index was not significantly changed (Fig. 6a). During the course of hyperfluoridation a decrease of the dry weight
appeared in Leidig cells and in spermatides (Fig. 6b). An adaptation of the cells to the toxic influence of fluoride is suggested since at the
termination of the experiment a tendency to normalization of the rRNA content developed and the dry weight of the spermatides and the interstitial cells reached almost the control level. It is known that Sertoli cells constitute a part of the hematotesticular barrier and are actively attacked by fluoride ions, which is perhaps the cause of the decrease of rRNA in these cells. On the other hand, these cells play a trophic role
for spermatides and probably supply them with rRNA. Consequently the decrease of the rRNA content and of the: dry weight in spermatides is caused by the disturbance of the metabolism in Sertoli cells and therefore presents a secondary event.

The noted cytochemical alterations in Leidig cells and in the basal parts of Sertoli cells reflect the di.sturbances in the protein synthesizing system of these cells in fluorosis and to a certain degree explain the hormonal imbalance in this disease, since Leidig cells synthesize testosterone and Sertoli cells produce protein-binding androgens. The high resistance of the spermatogones to the influence of fluoride in comparison
with Sertoli cells is difficult to explain since in most cases the unfavorable factors affect primarily the sperm cells.

Since the various stages of spermatogenesis are controlled by different hormones (e.g. testosterone controls the process of meiosis) (2) the present findings allow one to develop a more complete concept of the alteration of the germinative epithelium in fluorosis – not only through the disturbance of the functioning of the cell enzyme systems but also by the way of induction of hormonal i.mbala.nce in the body.