Physical, histological, endocrinological and steroidogenical evaluation of male cats postnatally exposed to sexual steroids

M. GRISOLIA ROMERO; M. FAYA; C. MARCHETTI; M.J. BELLINI ; P.G. BLANCO; M. LOPEZ MERLO; C. GOBELLO

Berlin

Congreso; 22nd EVSSAR Congress; 2019

European Veterinary Society For Small Animal Reproduction

To test the hypothesis that postnatal sexual steroids induce an impairment of domestic male catreproductive function, this study describes the physical, endocrine, steroidogenical and histological effectsof a single, high dose of a postnatal sexual steroid in this species. Twenty male kittens wererandomly assigned within the first 24 h of birth to: Testosterone enanthate 12.5 mg sc (TE; n ¼ 8),medroxyprogesterone acetate 10 mg sc (MA; n ¼ 6), or Placebo sc (PL; n ¼ 6). The cats were followeduntil puberty when they were castrated. Kittens achieved puberty without age differences among groups(P > 0.05). Two MA cats presented abnormal testicular descent. Histological evaluation of the MA(P < 0.01), but not of TE testes revealed decreased diameter (P < 0.01) and epithelial height (P < 0.01) ofthe seminiferous tubules. Leydig cell nuclear area was also reduced in this group. Conversely, tubular/intertubular ratio was increased in TE animals (P < 0.01). Quantitative real-time PCR analysis of mRNAexpression of testicular tissue revealed no significant differences among groups for StAR, CYP17A1 andandrogen receptors. TE animals showed decreased CYP19A1 mRNA expression (P < 0.05). In the first 4postnatal weeks, fecal testosterone (T) values were high, basal and intermediate in TE, MA and PL(P < 0.05), respectively. These differences progressively diminished and the three groups presented basalT concentrations from the 7th week on (P > 0.05). It was concluded that the postnatal progestageninitially suppressed the gonadal axis and caused an impairment of spermatogenesis and testiculardescent at puberty. Androgen treatment caused downregulation of the final steroidogenic cascade.