Ang-(1-7) plays an important role in regulating spermatogenesis in Trachemys scripta elegans under salinity stress

Elevation in water salinity can threaten the fertility of freshwater animals, including spermatogenesis. The role of the renin-angiotensin system (RAS) in regulating spermatogenesis has attracted considerable attention. Our previous study found that red-eared sliders (Trachemys scripta elegans), could survive in 10 PSU water for over one year. To understand the chronic impact of salinity on testicular spermatogenesis and underlying mechanisms, male T. s. elegans was subjected to treatment with 5 PSU (S5) and 10 PSU (S10) groups for a year, and spermatogenesis and regulation of the RAS signal pathway were elaborated. Results showed that the S10 group induced inflammation in the testes of T. s. elegans, as evidenced by a decrease in the number of testicular germ cells from 1586 to 943. Compared with the control group, the levels of proinflammatory genes, including TNF-α, IL-12A, and IL-6 were elevated by 3.1, 0.3, and 1.4 times in the S10, respectively. Testicular antiapoptotic processes of T. s. elegans might involve Ang-(1-7) in the RAS, as its level was significantly increased to 419.2 ng mL−1 in the S10. As expected, specific inhibitor (A-779) for Ang-(1-7) acceptor effectively prevented the salinity-induced upregulation of anti-inflammatory and antiapoptotic genes (TGF-β1, Bcl-6) in the testis of the S10, whereas it promoted the upregulation of proinflammatory and proapoptotic genes (TNF-α, IL-12A, IL-6, Bax, and Caspase-3). Our data indicated that Ang-(1-7) attenuated the effect of salinity on inflammation and apoptosis of the testis in T. s. elegans. A new perspective to prevent salinity-induced testis dysfunction is provided.