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

FAYA, M.; D´FRANCISCO, F.; GRISOLIA, M.; MERLO, M.LÓPEZ; GOBELLO, C.; GRISOLIA, M.; MERLO, M.LÓPEZ; GOBELLO, C.; MARCHETTI, C.; BELLINI, M.J.; MARCHETTI, C.; BELLINI, M.J.; FAYA, M.; D´FRANCISCO, F.

THERIOGENOLOGY

ELSEVIER SCIENCE INC

Lugar: Amsterdam; Año: 2019 vol. 138 p. 47 - 51

0093-691X

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.