Biology of Reproduction, Vol 21, 891-904, Copyright © 1979 by Society for the Study of Reproduction

Spermatogenic Response to Vitamin A in Vitamin A Deficient Rats

¹ Department of Obstetrics and Gynecology, Columbia University College of Physicians and Surgeons, New York, New York 10032
² Department of Obstetrics and Gynecology, Columbia University College of Physicians and Surgeons, New York, New York 10032Department of Obstetrics and Gynecology and Department of Medicine Columbia University College of Physicians and Surgeons, New York, New York 10032

Male Holtzman rats were given a vitamin A deficient (VAD) diet from 21 days of age and retinoic acid after the onset of vitamin A deficiency. At 130 days of age, seminiferous tubules contain Sertoli cells, spermatogonia and preleptotene spermatocytes; serum LH and testosterone values are low normal, while FSH levels are high. Oral feeding of a single dose of 1 mg vitamin A (followed by a regular commercial rat pellet diet) causes reinitiation of spermatogenesis, although testosterone remains low and FSH does not return to normal for 60 days. After vitamin A treatment (PVA), kinetic characteristics based upon histologic criteria of the reinitiated spermatogenesis in VAD rats were normal. Pachytene spermatocytes can be seen by Day 14 PVA and spermatids by Day 24 PVA; elongation of spermatids was completed by Day 31 PVA and spermatozoa were formed by Day 41. Quantitatively, sperm production remained below normal at 150 days PVA, although epididymal sperm counts had continued to increase PVA to 50% of that in mature controls. The qualitative normalcy of spermatogenesis in PVA-VAD rats was demonstrated by fertility with normal litter size. Thus, VAD causes reversible germ cell depletion. Reinitated spermatogenesis in the VAD rat provides a kinetically normal, in vivo system in which functionally normal spermatozoa are produced and in which it may be possible to study the biochemical and morphological events of specific stages of spermatogenesis.

Note:
ACKNOWLEDGMENTS The authors wish to express their gratitude to Dr. I. Dyrenfurth for the testosterone assay, Dr. J. E. Smith for advice in the preparation of vitamin A deficient rats and Dr. A. F. Parlow and the NIH Rat Pituitary Hormone Distribution Program for supplying FSH and LH assay kits.

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