| Selenium,an essential trace element for humans and animals,plays an important biological role in the growth,development,reproduction,immunity enhancement and disease resistance of livestock and poultry through selenoproteins.Notably,there is a U-shaped relationship between the intake of selenium and optimal health,selenium deficiency and excess will harm the health of livestock and poultry,resulting in the decline of their production performance.Meanwhile,selenium deficiency and excess also impair male reproductive function,but the mechanism is not very clear.Therefore,the present study was designed to explore the effects and mechanisms of two extreme selenium doses on sperm quality in mice by establishing dietary selenium deficiency and excess mice models,to explore the important role of selenium in male animal reproduction and provide some scientific basis for the rational use of selenium in breeding livestock and poultry production.In this study,30 C57BL/6J mice aged 21 days were randomly divided into three treatment groups,including a Se-deficient diet group(Se D,0.02 mg Se/kg),a control group(Se A,0.2 mg Se/kg)and an excess-Se diet group(Se E,2.0 mg Se/kg).After the five-month feeding period,all mice were killed by cervical dislocation.Blood,testis and epididymis samples were collected for follow-up analysis.The main results of the study are as follows:1)Compared with Se A,Se D reduced(P < 0.05)the body weight(10.4%)and sperm density(84.3%)but increased(P < 0.05)sperm deformity(32.8%);Se E decreased(P <0.05)the sperm density(78.5%)and sperm motility(35.9%)of the mice.Meanwhile,Se D and Se E caused the vacuolar degeneration of the spermatogenic cells and detachment of spermatogenic epithelium from the basal membrane,and increased(P < 0.05)serum FSH concentrations(10.4%–25.6%)in comparison to the control.Furthermore,compared with the Se A,Se D increased(P < 0.05)the concentration of 8-OHd G by 25.5%,and Se E increased(P < 0.05)the concentrations of 8-OHd G and MDA by 180.3% and 118.8% in the testis of mice,respectively.2)Compared with Se A,the transcriptomic results showed that 1,325 and 858 genes were altered(P < 0.05)in the mice testis by Se D and Se E,respectively.KEGG pathway analysis revealed that these differentially expressed genes were mainly enriched in the PI3K/AKT signaling pathway,which is regulated by oxidative stress.Moreover,western blotting analysis revealed that Se D and Se E dysregulated PI3K/AKT-mediated apoptosis and cell proliferation signaling,including upregulating(P < 0.05)Caspase 3,Cleaved-caspase 3,BCL-2 and(or)P53 and downregulating(P < 0.05)PI3K,p-AKT,p-m TOR,p-4E-BP1 and(or)4E-BP1,p-p70S6 K in the testis of mice compared with Se A.Additionally,compared with Se A,both Se D and Se E increased(P < 0.05)GPX3 and SELENOO;Se D decreased(P < 0.05)GPX1,TXRND3 and SELENOW,but Se E increased(P < 0.05)production of three selenoproteins in the testis.Conclusively,the results of this study show:Both dietary selenium deficiency and excess cause testicular injury and a decrease in sperm quality in mice,potentially with the induction of oxidative stress,dysregulation of PI3K/AKT-mediated apoptosis and cell proliferation,and dysregulation of the expression of several key testicular selenoproteins in the testis. |
