Marginal Zinc Deficiency in Mice Increased the Number of Abnormal Sperm and Altered the Expression Level of Spermatogenesis-Related Genes.

Marginal zinc deficiency is more common than severe zinc deficiency, and the effect of marginal zinc deficiency on male reproduction is unknown. This study investigated the effect of marginal zinc deficiency on spermatogenesis and its mechanism. Male ICR mice were fed normal zinc (30 mg/kg) and marginal zinc deficiency (10 mg/kg) diets for 35 days. Zinc-dependent proteins and enzymes were measured as biomarkers of zinc levels in the body. Metallothionein and Cu-Zn SOD levels in the control group were higher than those in the marginal zinc deficiency group. Hematoxylin and eosin staining showed that the marginal zinc deficiency diet caused histopathological changes in the testis and destruction of the sperm head under scanning electron microscopy. Sperm parameters and sex hormone levels were also affected by marginal zinc deficiency. In addition, marginal zinc deficiency led to alter expression level of several important spermatogenesis-related genes in the epididymis and testes. These results indicate that although zinc intake in marginal zinc deficiency is close to the recommended reference value, low zinc intake interferes with the expression of genes related to spermatogenesis and may lead to sperm abnormalities in mice.

Zinc-Enriched Yeast May Improve Spermatogenesis by Regulating Steroid Production and Antioxidant Levels in Mice.

Zinc (Zn) is an essential nutrient for the human body. This nutrient is involved in numerous physiological functions and plays an important role in spermatogenesis. Zn-enriched yeast (ZnY) is considered a Zn supplement with high bioavailability and is widely used as a functional food. However, the effect of ZnY on male reproductive function remains unclear. This study aimed to investigate the beneficial effects of ZnY on the treatment of male spermatogenesis disorders. The spermatogenic dysfunctional mice were established by using cyclophosphamide (CP). CP was administered in saline at a dose of 50 mg/kg bw/day for 5 days by intraperitoneal injection (i.p.). Then, ZnY was orally supplemented at the dose levels of 2, 4, and 8 mg Zn/kg bw/day for 30 days. CP significantly decreased the sperm density and viability, testicular marker enzymes, serum testosterone, follicular stimulating hormone (FSH), and luteinizing hormone (LH). ZnY supplementation significantly improved these sperm parameters and hormone levels. Additionally, ZnY decreased the CP-induced lipid peroxidation and increased the glutathione levels. Moreover, ZnY increased the gene expression of anti-apoptotic proteins and steroid synthetase in mouse testes. The low-dose ZnY supplementation has a better effect on improving spermatogenesis, while the other two groups are less beneficial roles possibly due to excessive Zn intake. The present results suggest that appropriate ZnY can act as an accessory factor to improve steroid production and antioxidant levels in spermatogenic dysfunction mice.