Alterations in the testicular parenchyma of Foxn1⁺/^- and Foxn1^-/^- adult mice

Nude mice carry an autosomal recessive mutation in the Foxn1 gene and therefore are homozygous recessive animals (Foxn1 ^-/^-). The fertility rate of homozygous male (Foxn1^-/^- ) is low, which seems to be related to the delay in the production of gametes at the beginning of sexual maturity. The present study evaluated the structural and organizational aspects of the testicles of homozygous and heterozygous offspring related to the Foxn1 gene in mice, describing its implications on spermatogenesis. Adult males Balb/c, Foxn1⁺/^- and Foxn1^-/^- mice were used. Testes and epididymis were harvested for histological, biochemical, and sperm transit analyses. Gonadal weight was significantly lower in Foxn1⁺/^- and Foxn1^-/^- animals, the same behavior was noticed for the activity of antioxidant enzymes. In addition, tubular parameters such as epithelial proportion, length, and area, as well as germ and Leydig cell’s populations were significantly reduced in the aforementioned groups, leading to lower sperm production. In conclusion, our results indicate the importance of the Foxn1 in Leydig cell’s function, reflecting in the preservation of spermatogenesis, thus in germ cell’s population and sperm cell production.

Key words
Spermatogenesis; germ cells; Leydig cells; androgen; oxidative stress