LAUSR

This study aimed to observe the influence of selenium (Se) deficiency on sperm quality and selenoprotein expression in rats. Four-week male Wista rats were randomly divided into three groups: Se-A, Se-L, and Se-D (respectively for Se- adequate, low, and deficient group). After 9 weeks, the rats were sacrificed by anesthesia, with the cauda epididymidis quickly fetched for sperm count, motility, and deformity. Meanwhile the blood, liver, brain, heart, and testis were collected for Se and biochemical analysis. It was found that the rats in Se-D had poor growth, while the Se concentrations in blood, liver, and heart for Se-D decreased significantly, compared with Se-A and Se-L (p < 0.01). But no significant difference was observed in testis and brain and also no statistical significance for sperm count. The sperm motility for Se-A (63.07%) was significantly higher than Se-L (53.91%) and Se-D (54.15%). Deformities were observed in both Se-L and Se-D. Both glutathione peroxidases (GPxs) and selenoprotein-P (SEPP1) levels in plasma and tissues of Se-D were significantly lower than those of Se-A and Se-L (p < 0.01). The SEPP1 levels in heart and brain of Se-L were lower than Se-A (p < 0.01). There was no statistical difference for GPx1 between Se-A and Se-L. The GPx4 level in testis of Se-L was lower than Se-A (p < 0.05). However, the SEPP1 in plasma, liver, testis, and the GPx3 level in plasma of Se-L were higher than those of Se-A (p < 0.05 or p < 0.01). Our results show that dietary Se deficiency could reduce GPx4 and SEPP1 expression in testis, which further influence sperm motility and may cause sperm deformity. Selenoprotein expression in some tissues of Se-L was higher than that of Se-A, but sperm quality and GPx4 expression in testis were not improved for Se-L. Low active pseudoselenoproteins might be synthesized in low-Se condition. The underlying mechanism needs to be further investigated.