[Testicular functions in mice bearing an autosomal translocation (T 145H)].
In the mouse, the autosomal reciprocal translocation T (7; 19) 145 H caused complete male sterility. The spermatogenesis was arrested at prophase or early metaphase I stages during the first meiotic division. The exocrine and endocrine testicular functions of azoospermic males (T 145 H/+) were compared with those of normal male littermates (+/+) at 63 days of age. Testis and epididymis weights in T 145 H/+ were significantly lower than those in +/+. By histological examination, the interstitial cells appeared preponderant but this was probably illusory due to the decrease in seminiferous tubular size and diminished testicular size. Moreover, androgen activity in T 145 H/+ seemed normal judging by weights of androgen target tissues (prostate, seminal vesicles), and plasma testosterone level.
D000818:Animals; D003433:Crosses, Genetic; D004822:Epididymis / Q000503:physiopathology; D005260:Female; D008297:Male; D008540:Meiosis; D008677:Metaphase; D051379:Mice; D008817:Mice, Mutant Strains; D009845:Oligospermia / Q000235:genetics; D013737:Testis / Q000473:pathology / Q000503:physiopathology*; D014178:Translocation, Genetic
Fonctions testiculaires chez des souris porteuses d'une translocation autosomique (T 145H).