Inverse relationship between testicular proliferation and apoptosis in mammalian seasonal breeders

Seasonal cycles of testicular activity occur in many mammals and can include transitions between total arrest and recrudescence of spermatogenesis. We hypothesize that involution and reactivation of testis result from two antagonistic processes, proliferation and programmed cell death (apoptosis), which are activated at different times. To test this hypothesis, quantitative measurements of both proliferation-specific marker and apoptotic produced nucleosomes have been compared with sperm and testosterone production in testes from adult roe deer during breeding and non-breeding seasons (May to September). Testes of brown hare were included from periods of testes regression (June to August) and recrudescence (November to December). The highest testicular weights in roe deer were found in the rutting period from late July to early August (27.25 +/- 8.56 g), corresponding with the highest number of testicular sperm/g parenchyma. The peak of sperm production coincided with a peak in testosterone concentration (1.19 +/- 0.53 microg/g testis). The maximum level of proliferation-specific marker was also found during the breeding season (98.6 +/- 58.2 U/g testis in comparison to 20.1 +/- 22.0 U/g in the prerutting period). In contrast, the most significant apoptosis was observed in the nonbreeding season than the breeding period (71.11 +/- 5.79 U/mg testis and 18.88 +/- 6.79 U/mg, respectively). Testicular proliferation was low in the brown hare (0.061 +/- 0.062 U/g) during involution of the testes. It was newly activated in November and December (0.85 +/- 0.33 U/g), preceding the increase in testicular volume. Testosterone production increased in conjunction with testicular proliferation. At this time, testicular apoptosis was significantly lower (14.16 +/- 2.12 U/mg testis) than during the period of pronounced testicular regression (30.16 +/- 19.95 U/g). These results suggest that regulation of seasonal testicular activity is characterized by an inverse relationship of proliferation and apoptosis.