Can Vitamin D supplementation be used as adjunctive treatment for oligozoospermia or asthenozoospermia accompanied with Vitamin D deficiency?

25(OH) D3. Finally, the renal 1α-hydroxylase converts 25(OH) D3 to 1,25(OH) 2D3, which is the most biologically active metabolite of VD (Figure 1).3 The actions of 1, 25(OH) 2D3 are mediated by binding to its high-affinity receptor, the VDR. Furthermore, the cellular response to VD is not only dependent on VDR, but also on presence and activity of VD metabolizing enzymes. Previous studies suggested than 1,25(OH) 2D3 plays important roles in reproductive functions. VD deficiency in male rats reduced sperm counts, and female rats inseminated with semen from VD deficient male rats have lower fertility rates.4,5 Moreover, retardation of spermatogenesis due to disturbances in sertoli and leydig cell function in VD-deficient rats is reversible and can be corrected by supplementing VD.6 VD acts through VDR, and the expression of VDR has been shown in the mature human spermatozoa.7,8 Significant Dear Editor, We read the paper by Hammoud et al.1 in the issue of Asian Journal of Andrology with great interests. This paper revealed that sperm concentration, sperm progressive motility, sperm morphology, and total progressively motile sperm count were lower in men with 25(OH) D ≥ 50 ng ml−1 when compared with men with 20 ng ml−1 ≤ 25(OH) D < 50 ng ml−1. Total sperm count and total progressive motile sperm count were lower in men with 25(OH) D < 20 ng ml−1 when compared to men with 20 ng ml−1 ≤ 25(OH) D < 50 ng ml−1. Therefore, they draw the conclusion that serum Vitamin D (VD) levels at high and low levels can be negatively associated with semen parameters. Recent studies indicate that a great variety of actions mediated by VD/vitamin D receptor (VDR), including regulating transcription of several genes involved in mitotic activity in spermatogonial nuclei, affecting sperm metabolism, controlling estrogen synthesis in gonads, increasing intracellular Ca2+ levels and activating different signaling pathways (extracellular signal-regulated kinases 1/2 [ERK1/2], AKT and glycogen synthase kinase-3 [GSK3]) in human sperm, can influence spermatogenesis and sperm maturation. Hence, we propose that VD supplement may be a novel therapeutic opportunity in the treatment of oligozoospermia and asthenozoospermia for those accompanied with VD deficiency. Development of spermatozoa depends on a complex series of events that occur in the reproductive organs. Spermiogenesis is an orderly, strict process of cell division and differentiation. Following spermiogenesis, the spermatozoa are transported to epididymis where they are stored before ejaculation and become motile. It is only during transit through the epididymis that spermatozoa undergo maturation and acquire progressive motility and the ability to fertilize ova. Epididymis is also a place where spermatozoa are stored before ejaculation.2 Many factors have been implicated in sperm production and maturation, including VD, which attracts more and more attention. Vitamin D is synthesized mainly in the skin, where ultraviolet ray B radiation converts 7-dehydrocholesterol to Vitamin D3. Then, Vitamin D3 is metabolized by the hepatic 25-hydroxylases to become Can Vitamin D supplementation be used as adjunctive treatment for oligozoospermia or asthenozoospermia accompanied with Vitamin D deficiency?