Rapid Glucocorticoid Mediation of Suppressed Testosterone Biosynthesis in Male Mice Subjected to Immobilization Stress

Wiley - Tập 25 Số 6 - Trang 973-981 - 2004
Qiang Dong1, Antonio Salva1, Chantal M. Sottas1, En-Mei Niu1, Michael Holmes1, Matthew P. Hardy1
1From the Center for Biomedical Research, Population Council, and the Rockefeller University, New York, New York.

Tóm tắt

ABSTRACT: Physical and psychosocial stress challenge homeostasis, increasing glucocorticoid secretion (in rodents, corticosterone [CORT]) while decreasing testosterone (T) levels. The dynamics of stress‐induced changes in T, CORT, and luteinizing hormone (LH) concentrations in mice have not been investigated previously. In particular, it remains to be established whether there is a rapid effect of CORT that is directly mediated by glucocorticoid receptors (GRs) in the testis. Therefore, serum and intratesticular T, serum CORT, and LH levels were measured during acute immobilization (IMO) stress, using the C57BL/6 strain of mice. The effects of testicular GR blockade were investigated by administration of the GR antagonist, RU486, via intratesticular (IT) or intraperitoneal (IP) injection. CORT levels increased in stressed males starting at 15 minutes, reaching a fivefold higher plateau by 1 hour compared with controls (P < .01). Conversely, starting from 30 minutes on, both serum and intratesticular T levels decreased in stressed males to 30% and 8% of control values, respectively, by 6 hours (P < .01). In contrast, LH was unchanged by IMO stress for up to 6 hours. Intratesticular treatment with RU486 partially prevented the IMO‐induced decline in T levels. CORT treatment reduced intracellular cyclic adenosine monophosphate (cAMP) content in Leydig cells by 15 minutes and T production by 30 minutes in vitro. We conclude that 1) the rapid changes in T suggest a suppression of T biosynthesis by glucocorticoid through a nongenomic mechanism, lowering the production of cytoplasmic cAMP; 2) changes in gonadotropic stimulation of Leydig cells are unlikely to explain the suppression of T levels during acute stress; and 3) the results are consistent with a direct inhibitory action of CORT on Leydig cells.

Từ khóa


Tài liệu tham khảo

10.1016/0031-9384(84)90304-4

10.1093/humrep/9.suppl_1.1

10.1210/endo.133.2.8344212

10.1139/y84-195

Brann DW, 1991, Role of corticosteroids in female reproduction, FASEB J, 5, 2691, 10.1096/fasebj.5.12.1655548

10.1146/annurev.med.48.1.129

10.1016/0039-128X(88)90052-9

10.1210/endo-109-4-1254

10.1001/jama.1992.03480090092034

Cochran RC, 1981, Serum levels of follicle stimulating hormone, luteinizing hormone, prolactin, testosterone, 5α‐dihydrotestosterone, 5α‐androstane‐3α, 17β‐diol, 5α‐androstane‐3β, 17β‐diol, and 17β‐estradiol from male beagles with spontaneous or induced benign prostatic hyperplasia, Invest Urol, 19, 142

10.1159/000122860

10.1002/j.1939-4640.1989.tb00089.x

10.1146/annurev.ph.50.030188.002411

10.1016/0960-0760(95)00091-D

10.1002/j.1939-4640.1997.tb01900.x

10.1210/en.137.5.1714

10.1210/endo.143.1.8604

Ge RS, 1997, Developmental changes in glucocorticoid receptor and 11beta‐hydroxysteroid dehydrogenase oxidative and reductive activities in rat Leydig cells, Endocrinology, 138, 5089, 10.1210/endo.138.12.5614

10.1159/000126973

10.1038/328624a0

10.1038/336695a0

10.1210/endo-124-5-2099

10.1095/biolreprod36.3.769

10.1210/endo-86-6-1298

Landers JP, 1991, The Male Germ Cell: Spermatogonium to Fertilization, 26

Landers JP, 1992, New concepts in steroid hormone action: transcription factors, proto‐oncogenes, and the cascade model for steroid regulation of gene expression, Crit Rev Eukaryot Gene Expr, 2, 19

10.1021/bi00426a017

10.1016/0960-0760(91)90217-S

10.1016/0092-8674(95)90199-X

10.1016/0024-3205(90)90398-B

10.1016/0960-0760(96)00044-1

10.1016/S0006-8993(00)02950-4

10.1016/0959-4388(95)80028-X

Moberg GP, 1987, Influence of the adrenal axis upon the gonads, Oxf Rev Reprod Biol, 9, 456

Monder C, 1994, 11β‐Hydroxysteroid dehydrogenase alleviates glucocorticoid‐mediated inhibition of steroidogenesis in rat Leydig cells, Endocrinology, 134, 1199, 10.1210/endo.134.3.8119160

10.1210/en.134.3.1193

10.1016/0018-506X(90)90013-N

10.1016/0018-506X(92)90005-G

10.1002/j.1939-4640.1994.tb00455.x

10.1210/endo-109-5-1331

10.1210/edrv.22.4.0436

Pacak K, 1998, Heterogeneous neurochemical responses to different stressors: a test of Selye's doctrine of nonspecificity, Am J Physiol, 275, R1247

10.1210/endo-106-5-1424

10.1210/endo-129-3-1429

10.3109/09513599809024971

10.1159/000064411

10.1095/biolreprod45.4.523

Rohlf S, 1995, Electrosurgical safety considerations for minimally invasive surgery, Minim Invasive Surg Nurs, 9, 26

10.1046/j.0953-816x.2001.01876.x

10.1016/0960-0760(95)00038-2

10.1016/0306-4530(95)00020-8

10.3181/00379727-204-43658

10.1530/ror.0.0050105

Kar LD, 1999, Forebrain pathways mediating stress‐induced hormone secretion, Front Neuroendocrinol, 20, 1, 10.1006/frne.1998.0172

Veldhuis JD, 1997, Infertility in the Male, 47

10.1146/annurev.physiol.59.1.365

10.1095/biolreprod27.5.1138

Xiao E, 1999, Stress and the menstrual cycle: short‐ and long‐term response to a five‐day endotoxin challenge during the luteal phase in the rhesus monkey, J Clin Endocrinol Metab, 84, 623

Thông tin
Thông tin xuất bản

Wiley

Tập 25 Số 6

973-981

Thông tin tác giả