| First Author | Kongmanas K | Year | 2021 |
| Journal | Antioxidants (Basel) | Volume | 10 |
| Issue | 6 | PubMed ID | 34199863 |
| Mgi Jnum | J:307603 | Mgi Id | MGI:6721206 |
| Doi | 10.3390/antiox10060912 | Citation | Kongmanas K, et al. (2021) Accumulation of Seminolipid in Sertoli Cells Is Associated with Increased Levels of Reactive Oxygen Species and Male Subfertility: Studies in Aging Arsa Null Male Mice. Antioxidants (Basel) 10(6) |
| abstractText | Seminolipid (also known as sulfogalactosylglycerolipid-SGG), present selectively in male germ cells, plays important roles in spermatogenesis and sperm-egg interaction. The proper degradation of SGG in apoptotic germ cells is also as important. Sertoli cells first phagocytose apoptotic germ cells, then Sertoli lysosomal arylsulfatase A (ARSA) desulfates SGG, the first step of SGG degradation. We have reported that aging male Arsa(-/-) mice become subfertile with SGG accumulation in Sertoli cell lysosomes, typical of a lysosomal storage disorder (LSD). Since reactive oxygen species (ROS) levels are increased in other glycolipid-accumulated LSDs, we quantified ROS in Arsa(-/-) Sertoli cells. Our analyses indicated increases in superoxide and H2O2 in Arsa(-/-) Sertoli cells with elevated apoptosis rates, relative to WT counterparts. Excess H2O2 from Arsa(-/-) Sertoli cells could travel into testicular germ cells (TGCs) to induce ROS production. Our results indeed indicated higher superoxide levels in Arsa(-/-) TGCs, compared with WT TGCs. Increased ROS levels in Arsa(-/-) Sertoli cells and TGCs likely caused the decrease in spermatogenesis and increased the abnormal sperm population in aging Arsa(-/-) mice, including the 50% decrease in sperm SGG with egg binding ability. In summary, our study indicated that increased ROS production was the mechanism through which subfertility manifested following SGG accumulation in Sertoli cells. |
