Release of arachidonic acid and the effects of corticosteroids on steroidogenesis in rat testis Leydig cells
| Autor: | L. Chaudry, D R E Abayasekara, Brian A. Cooke, M.S.K. Choi, L. H. Phipp, G. Dirami |
|---|---|
| Rok vydání: | 1991 |
| Předmět: |
Male
endocrine system medicine.medical_specialty medicine.drug_class Endocrinology Diabetes and Metabolism Clinical Biochemistry Radioimmunoassay Prostaglandin Biochemistry Dexamethasone Phospholipases A chemistry.chemical_compound Endocrinology Phospholipase A2 Adrenal Cortex Hormones Internal medicine Cyclic AMP medicine Animals Testosterone Molecular Biology Chromatography High Pressure Liquid Arachidonic Acid Leydig cell biology Leydig Cells Cell Biology Luteinizing Hormone Rats Phospholipases A2 medicine.anatomical_structure chemistry Quinacrine biology.protein Molecular Medicine Steroids Arachidonic acid Gonadotropin Luteinizing hormone medicine.drug |
| Zdroj: | The Journal of Steroid Biochemistry and Molecular Biology. 40:465-471 |
| ISSN: | 0960-0760 |
| DOI: | 10.1016/0960-0760(91)90216-r |
| Popis: | The release of arachidonic acid by luteinizing hormone (LH) and the effects of inhibiting phospholipase A2 (PLA2) in vivo and in vitro on LH stimulated steroidogenesis in rat testis Leydig cells has been investigated. It was found that arachidonic acid is rapidly incorporated into phospholipids and is released within 1 min after addition of LH. The effects of treating adult rats with dexamethasone and human chorionic gonadotropin (hCG) in vivo on steroidogenesis and prostaglandin synthesis in Leydig cells isolated 6 h later were determined. It was found that hCG caused a marked increase in prostaglandin F2 alpha formation which was inhibited by treatment with dexamethasone. LH-stimulated testosterone production was inhibited in the hCG treated rats and dexamethasone caused a further decrease. Treatment with dexamethasone alone also caused a decrease in the response to LH. HCG, but not dexamethasone, had similar inhibitory effects on LH-stimulated cyclic AMP production. Similarly, the PLA2 inhibitors quinacrine, dexamethasone and corticosterone, added to the Leydig cells in vitro, inhibited LH-stimulated testosterone production but not cyclic AMP production. 11-Dehydrocorticosterone also inhibited LH-stimulated testosterone production, but higher concentrations were required to give 50% inhibition compared to corticosterone (50 and 25 microM, respectively). Ring A-reduced metabolites of corticosterone and progesterone were also found to inhibit LH-stimulated steroidogenesis. The results obtained in this and previous studies are consistent with the activation of PLA2, (either directly by LH and/or via cyclic AMP), which results in the release of arachidonic acid and the formation of leukotrienes, which stimulate steroidogenesis in the Leydig cell. This study also indicates that corticosteroids and their metabolites may exert inhibitory effects at other sites in the steroidogenic pathways, in addition to PLA2. |
| Databáze: | OpenAIRE |
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