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| To identify the effects of 1,25(OH)2D3 deficient and calcium and phosphorus supplement on male reproductive system, mice with targeted deletion of 25-hydroxyvitamin D 1α-hydroxylase [1α(OH)ase-/-] were used in this paper. The 1α(OH)ase-/- mice and their wild-type littermates were fed either a normal diet or a rescue diet (high calcium, phosphate, and lactose) starting from weaning until 3 mo of age, then sperm spermatogenesis and motility were explored. Results showed that 1α(OH)ase-/- male mice displayed hypocalcemia and hypophosphatemia, lower concentration of intracellular calcium accompanied with reduced protein levels of calcium transport channels in testis, less sperm count, weaken sperm motility and abnormal sperm morphology at ultrastructure. Furthermore, the deficient spermatogenesis in 1α(OH)ase-/- male mice were deeply found to be concerned with decreased spermatogenic cells proliferation and increased spermatogenic cells apoptosis which might be caused by unusual serum gonadal hormone (estrogen and testosterone) and gonadotropic hormone (follicle-stimulating hormone and luteotrophic hormone) , unbalanced expression of apoptotic and pro-apoptotic proteins. When serum calcium and phosphorus were normalized by the rescue diet, the concentration of intracellular calcium in spermatogenic cells returned to normal level and the defective reproductive phenotype including impaired spermatogenesis and sperm motility in the 1α(OH)ase-/- male mice were reversed. These results indicate that the infertility seen in 1,25(OH)2D-deficient male mice is not a direct effect of active vitamin D deficiency on the reproductive system but is an indirect effect mediated by decreased extracellular /and or intracellular calcium concentration. |
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| Keywords:1,25(OH)2D3; spermatogenesis; sperm motility |
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