Tubulin polymerization-promoting protein2 (TPPP2) is one of the three paralogs of mammalian TPPP proteins. Its possible role in spermatogenesis is described in this narrative review. TPPP2 is expressed specifically in the male reproductive system, mainly in testes and sperm, and also in the epididymis. In testes, TPPP2 is exclusively expressed in elongating spermatids; in the epididymis, it is located in the middle piece of the sperm tail. TPPP2 is involved in spermiogenesis, in steps which are determinative for the formation and morphology of spermatids. The inhibition of TPPP2 decreases sperm motility (the curvilinear velocity of sperms), probably due to influencing mitochondrial energy production since TPPP2 knockout mice possess an impaired mitochondrial structure. There are data on the role of TPPP2 in various mammalian species: human, mouse, swine, and various ruminants; there is a significant homology among TPPP2s from different species. Experiments with Tppp2-/--mice show that the absence of TPPP2 results in decreased sperm count and serious dysfunction of sperm, including decreased motility; however, the in vitro capacitation and acrosome reaction are not influenced. The symptoms show that Tppp2-/--mice may be considered as a model for oligoasthenozoospermia.

In vitro techniques for investigating the toxic effects of environmental contaminants (EC) on fish spermatozoa motility kinetics and fertilizing ability are valuable tools to understand toxicity mechanisms and sites of action. In vitro techniques may also be well-suited to studies of endocrine disruption in male fertility in vivo. This review shows ECs to decrease or suppress spermatozoa motility kinetics and fertilizing ability in a dose-dependent manner, with toxic concentrations being much higher than those reported in the aquatic environment. Sites of action depend on EC concentration and duration of exposure. Both instant (immediate) and incubated exposure of spermatozoa to ECs results in damage to the plasma membrane and the axoneme, while disruption of energy metabolism appears only during incubated exposure. Spermatozoa lose fertilizing ability following exposure to ECs in vitro, not only due to inhibition or suppression of the initiation of motility, but also through damage to DNA. This review highlights the significant lack of information about disruption of spermatozoa function associated with exposure to water from polluted areas as well as combined effects of ECs. Specifics of alterations in intracellular signaling cascades involved in the initiation of spermatozoa motility following exposure to sublethal concentrations of ECs remain unknown. Further studies are also needed to elucidate in vitro EC effects during spermatozoa maturation, when spermatozoa acquire the potential for motility.