Human semen cryopreservation in the clinical management of male infertility is complicated by cryodamage to spermatozoa. We aimed to clarify the full pattern of cryodamage and evaluate the protective effects of ascorbate and catalase on cryopreserved spermatozoa. Semen samples were collected from 30 fertile males. Each sample was divided into 6 groups: fresh semen, cryopreserved semen without treatment, and samples cryopreserved with ascorbate (300 or 600 mM) or catalase (200 or 400 IU/mL). Spermatozoa were examined for their viability, motility, reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP), apoptosis (positive for annexin V and negative for propidium iodide [ie, Ann, and DNA damage (Olive tail moment [OTM]) in the presence or absence of ascorbate or catalase during cryopreservation. In comparison with the fresh spermatozoa, there was a significant decrease in the viability, motility, and MMP but increase in Ann + /PI 2 and OTM in the cryopreserved spermatozoa (P , .01 and P , .05, respectively). Concurrently, ROS levels in the postthaw spermatozoa also increased significantly, and this elevation was well correlated with the quality variations of postthaw spermatozoa (P , .01 for all). Ascorbate (300 mM) and catalase (200 and 400 IU/mL) reduced the ROS levels in postthaw spermatozoa significantly, compared with those in the control (P , .05). Furthermore, these antioxidants also prevented those characteristics from being adversely affected (P , .05). This study demonstrated that cryopreservation results in cryodamage to human spermatozoa, possibly through the mechanism of ROS. Appropriate ascorbate or catalase supplementation of cryoprotective medium restrains ROS levels and the resultant cryodamage.

Leucine-rich-repeat-containing G protein-coupled receptors (LGRs) have been widely found to be implicated with development and progression in multiple cancer types. However, the clinical significance and biological functions of LGR6 in ovarian cancer remains unclear. In this study, LGR6 expression was mainly examined by immunohistochemistry. Functional assays in vitro and animal experiments in vivo were carried out to explore the effect of LGR6 on cancer stem cell (CSC) characteristics and chemotherapeutic responses in ovarian cancer cells. Luciferase assays and GSEA were used to discern the underlying mechanisms contributing to the roles of LGR6 in ovarian cancer. Here, we reported that LGR6 was upregulated in ovarian cancer, which positively correlated with poor chemotherapeutic response and progression survival in ovarian cancer patients. Loss-of-function assays showed that downregulating LGR6 abrogated the CSC-like phenotype and chemoresistance in vitro. More importantly, silencing LGR6 improved the chemoresistance of ovarian cancer cells to cisplatin in vivo. Mechanistic investigation further revealed that silencing LGR6 inhibited stemness and chemoresistance by repressing Wnt/b-catenin signaling. Collectively, our results uncover a novel mechanism contributing to LGR6-induced chemotherapeutic resistance in ovarian cancer, providing the evidence for LGR6 as a potential therapeutic target in ovarian cancer.

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