title: Acute immobilization stress disrupts testicular steroidogenesis in adult male rats by inhibiting the activities of 17 alpha-hydroxylase and 17,20-lyase without affecting the binding of LH/hCG receptors.
abstract: We have investigated the effect of acute immobilization (3 hours) stress on testicular steroidogenesis in the adult rat. Immobilization did not alter plasma luteizing hormone (LH) levels, but plasma testosterone (T) levels were reduced by 82%. Plasma levels of corticosterone in stressed rats were elevated more than ninefold over control levels. After 3 hours of stress, testicular levels of progesterone were elevated 33%, and levels of 17 alpha-hydroxyprogesterone and T were reduced 47% and 37%, respectively, compared to controls. Immobilization for 3 hours had no effect on the association or dissociation rate constants of LH/human chorionic gonadotropin (hCG) receptors of testicular interstitial cells and did not alter specific hCG binding. The effect of 3 hours of immobilization on testicular 17 alpha-hydroxylase and 17,20-lyase was assessed by incubating testicular microsomes from stressed and control animals in the presence of 21[14C]progesterone and [3H]17 alpha-hydroxyprogesterone. Immobilization of rats reduced the Vmax values of 17 alpha-hydroxylase and 17,20-lyase by 47% and 48%, respectively, but had no effect on the Km values. These results support the hypothesis that stress for 3 hours disrupts rat testicular steroidogenesis via a mechanism that is independent of changes in circulating levels of LH and the binding characteristics of LH/hCG receptors. The effects of immobilization on the content of testicular steroids and on the activities of 17 alpha-hydroxylase and 17,20-lyase suggest that stress inhibits the activities of both 17 alpha-hydroxylase and 17,20-lyase.
authors.affiliation: Department of Physiology, Morehouse School of Medicine, Atlanta, Georgia 30310-1495.
authors.forename: T E
authors.initials: TE
authors.lastname: Orr
authors.forename: M F
authors.initials: MF
authors.lastname: Taylor
authors.forename: A K
authors.initials: AK
authors.lastname: Bhattacharyya
authors.forename: D C
authors.initials: DC
authors.lastname: Collins
authors.forename: D R
authors.initials: DR
authors.lastname: Mann
mesh_terms: D000446:Aldehyde-Lyases / Q000037:antagonists & inhibitors*; D000735:Androstenedione / Q000032:analysis / Q000378:metabolism; D000818:Animals; D006063:Chorionic Gonadotropin / Q000378:metabolism; D003345:Corticosterone / Q000097:blood; D065607:Cytochrome P-450 Enzyme Inhibitors; D007103:Immobilization / Q000502:physiology*; D007986:Luteinizing Hormone / Q000097:blood*; D008297:Male; D011374:Progesterone / Q000032:analysis / Q000378:metabolism; D011863:Radioimmunoassay; D051381:Rats; D017207:Rats, Sprague-Dawley; D011974:Receptors, LH / Q000032:analysis / Q000378:metabolism*; D013254:Steroid 17-alpha-Hydroxylase / Q000037:antagonists & inhibitors*; D013312:Stress, Physiological / Q000503:physiopathology*; D013737:Testis / Q000737:chemistry / Q000378:metabolism* / Q000503:physiopathology; D013739:Testosterone / Q000097:blood*; D013997:Time Factors
chemical_list: D006063:Chorionic Gonadotropin; D065607:Cytochrome P-450 Enzyme Inhibitors; D011974:Receptors, LH; D013739:Testosterone; D000735:Androstenedione; D011374:Progesterone; D007986:Luteinizing Hormone; D013254:Steroid 17-alpha-Hydroxylase; D000446:Aldehyde-Lyases; D003345:Corticosterone