Stress hormone and male reproductive function
| Autor: | Wei Ran Chai, Qiang Dong, Chantal M. Sottas, Matthew P. Hardy, Xing Feng, Hui-Bao Gao, Ren-Shan Ge, Qian Wang |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Male
endocrine system medicine.medical_specialty Histology medicine.drug_class Stimulation Apoptosis Biology Pathology and Forensic Medicine chemistry.chemical_compound Glucocorticoid receptor Receptors Glucocorticoid Corticosterone Stress Physiological Internal medicine Testis medicine Animals Testosterone Receptor Glucocorticoids Leydig cell Reproduction Leydig Cells Cell Biology Luteinizing Hormone Androgen medicine.anatomical_structure Endocrinology chemistry hormones hormone substitutes and hormone antagonists Glucocorticoid medicine.drug |
| Zdroj: | Cell and tissue research. 322(1) |
| ISSN: | 0302-766X |
| Popis: | The Leydig cell is the primary source of testosterone in males. Levels of testosterone in circulation are determined by the steroidogenic capacities of individual Leydig cells and the total numbers of Leydig cells per testis. Stress-induced increases in serum glucocorticoid concentrations inhibit testosterone-biosynthetic enzyme activity, leading to decreased rates of testosterone secretion. It is unclear, however, whether the excessive glucocorticoid stimulation also affects total Leydig cell numbers through induction of apoptosis and thereby contributes to the stress-induced suppression of androgen levels. Exposure of Leydig cells to high concentrations of corticosterone (CORT, the endogenously secreted glucocorticoid in rodents) increases their frequency of apoptosis. Studies of immobilization stress indicate that stress-induced increases in CORT are directly responsible for Leydig cell apoptosis. Access to glucocorticoid receptors in Leydig cells is modulated by oxidative inactivation of glucocorticoid by 11 beta-hydroxysteroid dehydrogenase (11 betaHSD). Under basal levels of glucocorticoid, sufficient levels of glucocorticoid metabolism occur and there is likely to be minimal binding of the glucocorticoid receptor. We have established that Leydig cells express type 1 11 betaHSD, an oxidoreductase, and type 2, a unidirectional oxidase. Generation of redox potential through synthesis of the enzyme cofactor NADPH, a byproduct of glucocorticoid metabolism by 11 betaHSD-1, may potentiate testosterone biosynthesis, as NADPH is the cofactor used by steroidogenic enzymes such as type 3 17beta-hydroxysteroid dehydrogenase. In this scenario, inhibition of steroidogenesis will only occur under stressful conditions when high input amounts of CORT exceed the capacity of oxidative inaction by 11 betaHSD. Changes in autonomic catecholaminergic activity may contribute to suppressed Leydig cell function during stress, and may explain the rapid onset of inhibition. However, recent analysis of glucocorticoid action in Leydig cells indicates the presence of a fast, non-genomic pathway that will merit further investigation. |
| Databáze: | OpenAIRE |
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