Abstract:

With the increase of male life span, the level of androgen secreted by testicular Leydig cells reduce continuously, which leads to the late onset of hypogonadism (LOH). Concurrently, spermatogenesis in the seminiferous tubules is compromised, leading to the reduction in both the quantity and quality of sperm, thereby decreasing male fertility. Males who suffered from testicular natural aging, influence of external environmental factors, metabolic factors, microcirculatory disorders, or certain disease states, generated reactive oxygen species in testes. Meanwhile, the mechanisms of antioxidant stress, such as superoxide dismutase, the Keap1/Nrf2 antioxidant pathway, the ubiquitination pathway, USP15, and the seminal plasma antioxidant system, exhibit relative inadequacy. Consequently, the continuous accumulation of oxidative stress inflicts the direct or/and indirect damage on the functions of Leydig cells and seminiferous tubules, which represents one of the primary pathophysiological mechanisms underlying LOH. Accumulating evidences have indicated that antioxidant therapy holds promise in retarding the progression of LOH. In this review, we comprehensively examine the oxidative stress in the testes of aging men and the occurrence of LOH, and discusse the potential application prospects of novel antioxidants in middle-aged and elderly male populations.

Key words: Testis, Oxidative stress, Reproductive health, Hypogonadism, Hormone replacement therapy