Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Testicular interstitial cells were utilized to study the effects of prostaglandins (PG) on in vitro testosterone production and to examine the role of cyclic adenosine-3',5'-monophosphate (cAMP) in this process. Testosterone production was assessed after 3 hour incubations while cAMP accumulation was examined after a 0.5 hour incubation period. Testosterone and cAMP were measured by radioimmunoassay. None of the PGs tested (PGA, PGA2, PGB1, PGE1, PGE2, PGF1alpha PGF2alpha) altered basal testosterone production when present in incubates at concentrations of 1.3 X 10(-8) M to 1.3 X 10(-4). However, at concentrations of 1.3 X 10(-4) M all of these PGs were capable of decreasing Luteinizing Hormone (LH; 100ng)-induced testosterone production. The inhibition of LH-induced testosterone production by the B, E and F series PGs was less pronounced than that for the A series. PGA1 and PGA2 exhibited 80% and 95% inhibition, respectively, at 1.3 X 10(4) M. The inhibitory action of 4 X 10(5) M PGA1 or PGA2 was evident within 30 minutes. Preincubation of interstitial cells with indomethacin (10(-5) or 10(-6) M) for 30 minutes did not alter subsequent basal or LH (100ng)-induced testosterone production. Accumulation of cAMP was stimulated by LH (10 microgram) or by PGs (1.3 X 10(-4) M PGA1, PGA2, PGB1, PGE1 or PGF2alpha). The PG-induced cAMP accumulation thus occurred at concentrations where LH-stimulated testosterone production was inhibited. Furthermore, PGA1 and PGA2 (1.3 X 10(-4) M) inhibited testosterone production induced by either 3-isobutyl-1-methyl xanthine (MIX; 10(-4) M or 10(-3) M) or dibutyryl cAMP (dbcAMP; 10(-4) M or 10(-3) M). These results indicate that PGs can block testosterone production by a direct effect on testicular interstitial cells and suggest that PGs exert their inhibitory action distal to stimulation of cAMP formation. PGs do not appear to play a role in the mechanism of LH action.
Steroids 1978 Oct
PMID:Prostaglandin inhibition of testosterone production induced by luteinizing hormone, dibutyryl cyclic AMP or 3-isobutyl-1-methyl xanthine in dispersed rat testicular interstitial cells. 8 81

Production of testosterone (T) by decapsulated mouse tests in vitro was significantly inhibited by adding prostaglandin (PG) A1, PGA2 or PGE1 to the incubation medium. Prostaglandin A1 at a concentration of 10(-6)M inhibited T production in this system both in the presence of moderate amounts of hCG (12.5 or 25.0 mIU/ml), and in the absence of gonadotropins. However, in the presence of very high levels of hCG (125.0 mIU/ml), all PGs tested appeared to have had a slight potentiating effect on T production when added in concentrations ranging from 10(-7) to 10(-5)M, and the inhibition of T accumulation in the medium was consistently observed only when the concentration of PGs was increased to 10(-3)M. These results suggest that a direct effect of PGs on testicular steroidogenesis may account for, or contributes to, the decrease in peripheral T levels observed after administration of PGs in vivo.
Steroids 1976 Jul
PMID:Prostaglandins inhibit testosterone secretion by mouse testes in vitro. 96 Jan 48

The generation of T-cell colonies from human peripheral blood lymphocytes is a sensitive in vitro measure of cell-mediated immunity, considered to be under different and/or additional regulatory controls than short-term liquid cultures. The influences of steroids (aldosterone, estradiol, diethylstilbestrol, hydrocortisone, prednisolone, progesterone, testosterone), prostaglandins (PGA1, PGA2, PGB1, PGB2, PGE1, PGE2, PGF1 alpha), bradykinin, cyclic adenosine monophosphate (AMP), cyclic guanosine monophosphate (GMP), epinephrine, glucagon, histamine, insulin, luteinizing hormone, luteotropic hormone, serotonin, and thyroxin on the generation of both T-cell colonies in semisolid phase and induction of transformation in liquid culture was assessed in parallel assays. Steroids uniformly suppressed both types of culture systems, although colony formation appeared more sensitive by several hours of magnitude. In contrast, significant differences in the response of lymphocytes in colony formation assay, compared to liquid transformation, was noted for the other agents. Prostaglandins significantly inhibited colony formation even in the presence of as little as 10(-12) M PGE2; however, liquid culture responses were suppressed only by higher concentrations (10(-5) M) and enhanced transformation was found at lower concentrations (10(-9) M). Bradykinin, glucagon, and luteinizing hormone did not significantly influence either colony formation or liquid transformation. In contrast, cyclic AMP inhibited and cyclic GMP stimulated colony formation and liquid transformation. Histamine, insulin, epinephrine, and serotonin all had significant positive or negative influences on colony formation in concentrations that produced no detectable effects using conventional liquid transformation assays. Finally, correlation analysis of drug effects for each system extends the thesis that these assays quantitate different parameters of T-cell function. T-lymphocyte colony formation is a promising diagnostic tool for rapid screening of immune modulating agents.
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PMID:Pharmacologic and biochemical modulation of human T-lymphocyte colony formation: hormonal influences. 697 65