Apoptosis is a complex process, which is adjusted on many levels by a wide range of pro- and anti-apoptotic proteins. It has been established that the long-term damage to the balance between the two groups causes apoptotic changes in cells. Cell apoptosis is also an active process which occurs in the course of aging. The key factors, not only the age-related ones, but also those linked to the overall process of apoptosis affecting the steroidogenic Leydig cells (LCs) and germinative epithelium in the testes are mitochondrial damages caused by free radicals (ROS - Reactive oxygen species). The direct result of the aging of the testis is reduction in the levels of testosterone and the results of this are disruption of the physiological processes and dramatically deteriorated the quality of life. A number of studies reported involvement of the proteins p53 and Cyclin D1 in the regulation of some of the mechanisms of apoptosis. P53 promotes the expression of many apoptotic genes (transcription factor) and has an important role in the apoptosis in normal spermatogenesis and in the response to DNA damage. The role of Cyclin D1 is examined in two directions - cell proliferation and provoking apoptotic changes in major damage to the DNA of the cells. At this stage, the role of p53 and Cyclin D1 in the control of apoptosis in human LCs in the aging testis is not well investigated, which determines the aim of the present study. In this study we used material from human testes from patients between 56, 68 and 80 years of age, embedded in paraffin and prepared for immunohistochemistry. Our results demonstrated an increased intensity of the immunoexpression of p53 and Cyclin D1 in the course of aging. These findings marked the role of these proteins in the regulation of testicular apoptosis.
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