Germ cell degeneration in normal and microwave-irradiated rats: Potential sperm production rates at different developmental steps in spermatogenesis

Authors

  • Dr. L. Johnson,

    Corresponding author
    1. Departments of Cell Biology and Physiology, The University of Texas Health Science Center at Dallas, Dallas, TX 75235
    • Departments of Cell Biology and Physiology, The University of Texas Health Science Center at Dallas, Dallas, TX 75235
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  • R. M. Lebovitz,

    1. Departments of Cell Biology and Physiology, The University of Texas Health Science Center at Dallas, Dallas, TX 75235
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  • W. K. Samson

    1. Departments of Cell Biology and Physiology, The University of Texas Health Science Center at Dallas, Dallas, TX 75235
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Abstract

Germ cell degeneration in 14 normal and 14 microwave-irradiated, adult (400–500 gm), Sprague-Dawley rats was compared by evaluating potential sperm production rates at different developmental steps in spermatogenesis. Following 9 days of irradiation at 1.3 GHz (6 hours/day at 6.3 mW/gm using 1-μsec pulsewidth at 600 pulses/second) or sham treatment, rats were killed at 6.5, 13.0, 26.0, or 52.0 days following treatment. Testes were perfused with 2% glutaraldehyde, embedded in Epon, and sectioned at 0.5 μm for morphometric analyses. Plasma LH and FSH concentrations were determined by radioimmunoassay from blood collected on the day of death. Considering nuclear size, percentage of nuclei in the parenchyma, and life span of different cells, potential daily sperm production was determined for type B spermatogonia, preleptotene or pachytene primary spermatocytes, or spermatids with round nuclei. No differences (P > .05) in parameters tested were found among time periods following irradiation. With the possible exception of sperm production per testis (P < .05) based on pachytene spermatocytes, microwave irradiation had no effect on the parameters evaluated. No degeneration was detected in spermatogenesis when potential sperm production rates were determined either from type B spermatogonia to spermatids or from type B spermatogonia to a posttesticular approximation of sperm production rate. Thus, it appears that regulation of sperm production rates must take place during spermatogonial mitoses, since once the number of type B spermatogonia is determined, there is essentially no subsequent alteration in sperm production potential in normal or irradiated adult rats.

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