Role and underlying mechanism of SPATA12 in oxidative damage

Spermatogenesis-associated gene 12 (SPATA12) functions as an inhibitor in spermatogenesis and tumorigenesis. Our previous study demonstrated that SPATA12 may be induced in tumor cells by ultraviolet (UV) C-mediated DNA damage, suggesting its importance in maintaining genomic integrity. In order to understand whether and how SPATA12 responds to oxidative damage, the present study established a cellular model of oxidative stress by detecting the effect of H(2)O(2) on cell viability and intracellular superoxide dismutase activity, and the levels of glutathione and malondialdehyde (MDA). Quantitative polymerase chain reaction results demonstrated that H(2)O(2) upregulated the expression of SPATA12, and a dual luciferase reporter gene assay indicated that transcription factor activator protein-1 (AP-1) was involved in the response of SPATA12 to oxidative stress. Through the exogenous expression of SPATA12, it was identified that SPATA12 decreased the level of reactive oxygen species and MDA, and also may reduce the degree of cellular oxidative damage and apoptosis induced by H(2)O(2). In addition, resveratrol was demonstrated to increase the expression of SPATA12 by activating AP-1, and it may be used as a nontoxic activator of the SPATA12 gene. In conclusion, these results suggest that SPATA12 is upregulated by oxidative stress via AP-1, and that the exogenous expression of SPATA12 protects against H(2)O(2)-induced oxidative damage and apoptosis.