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Biology of Reproduction, Vol 42, 677-682, Copyright © 1990 by Society for the Study of Reproduction
ARTICLES |
AM Van Pelt and DG De Rooij
Department of Cell Biology, State University of Utrecht, Medical School, The Netherlands.
In seminiferous tubules of vitamin A-deficient rats, the remaining spermatogonia were A spermatogonia. These cells were topographically arranged as single and paired cells and clones of 4, 8, or more cells. The bromodeoxy-uridine-labeling index and the mitotic index of these cells were found to be 9% and 1%, respectively, indicating that these cells were slowly proliferating. Administration of vitamin A (retinol- acetate) resulted in a reinitiation of spermatogenesis in such a way that the epithelium became stage-synchronized. The rate of development of the spermatogenic cells between 7 and 21 days after vitamin A replacement was found to be similar to that in normal rats. At 24-30 h after administration of vitamin A, a 4- to 6-fold increase in the labeling index was found. In contrast, after 2 days, the labeling index was low, while the mitotic index was elevated (10%). A high labeling index was found again after 3 days. Assuming that during the first 7 days after vitamin A replacement the rate of development of the spermatogenic cells also was normal, it could be deduced that the spermatogonia labeled 24-30 h after vitamin A administration were A1 spermatogonia. These cells would then divide into A2 spermatogonia after about 2 days, which in turn would traverse their S phase after about 3 days. Hence, spermatogenesis in vitamin A-deficient rats would be arrested shortly before the S phase of the A1 spermatogonia. After administration of vitamin A, the spermatogonia synchronously start the series of six divisions leading to the formation of spermatocytes and, ultimately, they develop into mature spermatids.(ABSTRACT TRUNCATED AT 250 WORDS)
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