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Sertoli cell death contributes to spermatogenesis impairment, which is associated with male infertility. Testicular ischemia‑reperfusion (I/R) injury induces the cell death of germ cells and Sertoli cells, whereas inhibition of cell death ameliorates acute testicular I/R damage. The aim of the present study was to investigate the mechanism of I/R stress-induced cell death in TM4 cells. Oxygen‑glucose deprivation and reoxygenation (OGD/R) was demonstrated to induce I/R injury and cell death in TM4 cells. Cell death was blocked by the reactive oxygen species (ROS) inhibitor N‑acetylcysteine, as well as lipid peroxidation inhibitors Liproxstatin‑1 and iron chelator deferoxamine; however, inhibitors of apoptosis, necrosis or autophagy had no effect. It was also demonstrated that iron and lipid ROS levels were elevated in I/R injury and that mitochondria decreased in size and increased in membrane density, which is indicative of ferroptosis. Furthermore, the generation of lipid ROS suggests iron accumulation and glutathione (GSH) depletion. The expression of ferroportin (Fpn) protein and mRNA was decreased in TM4 cells. Notably, overexpression of Fpn inhibited ferroptosis, lipid ROS generation and iron accumulation. In addition, GSH‑dependent peroxidase 4 (GPX4) was inactivated via GSH depletion following I/R injury, whereas GPX4 activation blocked I/R‑induced ferroptosis by reducing lipid ROS levels. The mitogen‑activated protein kinase (MAPK) pathway was also investigated in the present study; it was observed that I/R‑induced ferroptosis was blocked by inhibiting p38 MAPK activation. The results of the present study demonstrate that ferroptosis is a pervasive and dynamic type of cell death induced by OGD/R injury in Sertoli cells. This may provide a novel insight into the application of cytoprotection in testicular I/R damage‑induced cell loss.

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Abstract. The syntheses of DNA, RNA and protein in the livers of aging mice was studied by electron microscopic radioautography using radioactive precursors. Labeling with 3H-thymidine was observed in the nuclei of some hepatocytes at various prenatal and postnatal ages. The percentage of labeled cells decreased after birth, then slowly fell to the lowest value at 2 years. The silver grains with 3H-uridine labeling were observed in both the nuclei and cytoplasm of hepatocytes at various ages. There was a peak in uridine labeling at 14 days, and then it slowly decreased until old age. The number of silver grains with aH-leucine labeling in the cytoplasm of hepatocytes was small. It increased after birth, reached the maximum at 1 month, and continued to decrease with aging.

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Abstract. The ultrastructural difference between 3H-thymidine labeled and unlabeled germ cells in mouse testis was observed by electron microscopic radioautography. The RNA and protein syntheses in the seminiferous tubules of aging mice were also studied using 3H-uridine and leucine radioautography. At embryonic day 19, the Sertoli cells and myoid cells labeled with 8H-thymidine were often observed. The gonocytes labeled with aH-thymidine that were not rich in cell organelles appeared from the early postnatal stage. The silver grains were located mainly over the nuclei of labeled gonocytes, but a few were over the mitochondria. The labeling index of spermatogonia for 3H-thymidine rapidly increased from 2 weeks on, and stayed relatively constant until old age. The labeling indices of the other two kinds of cells, i.e., Sertoli and myoid cells, decreased to low levels with aging, while these cells continued RNA and protein syntheses through aging, as detected by the incorporation of 3H-leucine and uridine.

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