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)

Melatonin-binding sites in membrane preparation immature rat testes were demonstrated by utilizing 2-[125I]-iodomelatonin as a radioligand. Binding at these sites was found to be reversible, saturable, specific and of, high affinity. Scatchard analysis of the specific binding revealed an equilibrium binding constant (kd) of 215 +/- 23 pmol/L and a total number of binding sites (Bmax) of 0.94 +/- 0.1 fmol/mg protein. The Hill coefficient of 1.0 suggests a single class of 2-[125I]-iodomelatonin-binding site in the rat testes. The Kd value determined from kinetic analysis was 179 pmol/L, which is in close agreement with the value determined from equilibrium studies. In competition studies, the order of pharmacological affinity for 2-[125I]-iodomelatonin binding sites in the rat membrane testes was: melatonin > 6-hydroxymelatonin > N-acetylserotonin > 5-hydroxyindole-3-acetic acid > 5-hydroxytryptamine > 5-hydroxy-L-tryptophan > tryptamine > > 5-methoxytryptamine, 5-methoxyl-DL-tryptophan, D-L-tryptophan. The 2-[125I]-iodomelatonin binding was markedly reduced by guanine nucleotides; treatment with nonhydrolyzable GTP analog guanosine 5'-O-(3-thiotriphosphate) caused a 10-fold decrease in receptor affinity. In this paper, we report evidence indicating the presence of binding sites in immature rat tests, suggesting a possible direct role of melatonin on testicular steroidogenesis.
Steroids 1997 Feb
PMID:Melatonin and testicular function: characterization of binding sites for 2-[125I]-iodomelatonin in immature rat testes. 905 81

BACKGROUND: Development of steroid cataract is a likely outcome following prolonged exposure to glucocorticoids. It has been suggested that formation of steroid-protein adducts is a key event in this lens opacification. In order to explore this possibility, we have monitored the reaction of bovine lens proteins with glucocorticoids and examined the effects of adduct formation on their structures. METHODS: Bovine lens proteins were incubated with high (10(-4) M) and low (10(-8) M) concentrations of dexamethasone or prednisolone for up to 56 days at 37 degrees Celsius. Changes in molecular size and solubility of the crystallins and their polypeptide subunits were examined using gel permeation chromatography and SDS gel electrophoresis. Conformational changes were assessed with the aid of tryptophan fluorescence spectroscopy and oxidation was monitored by measuring protein sulphydryl content. RESULTS: Covalent incorporation of glucocorticoids was observed for all crystallins with relative reactivities for alpha-: beta-: gamma-crystallin of 20: 5: 1. The maximum incorporated was one steroid molecule per 40 to 50 subunits of alpha-crystallin. The proportions and sizes of the soluble crystallins and their subunits were unchanged. Protein sulphydryl contents decreased by eight to 10 per cent more than controls but no intermolecular disulphide bonds were detected. There were no alterations in tryptophan microenvironments. CONCLUSIONS: Steroids form adducts with lens proteins, in particular alpha-crystallin, but it appears unlikely that this reaction is responsible for steroid cataract formation.
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PMID:Steroid adduct formation with lens crystallins. 1248 87

Estrogen results in the suppression of experimental allergic encephalomyelitis (EAE), a frequently used experimental animal model of multiple sclerosis (MS). The mechanism by which estrogen acts in diseases with an autoimmune background is less clear. Here, we used splenic dendritic cells (DC) from the Lewis rats EAE model as target cells, and explored the pathway of estrogen in immune modulation. Estrogen did not affect the expression of MHC class II, CD80 and CD86 by DC, but inhibited the ability of DC to stimulate T cell proliferation and production of both Th1 and Th2 cytokines. This was accompanied by increased T cell apoptosis. Estrogen up-regulated DC to express indoleamine 2,3-dioxygenase (IDO) which can limit T cell responses. The effects of estrogen-exposed DC on T cell proliferation and apoptosis were partly abolished by addition of an IDO inhibitor (1-methyl-dl-tryptophan, 1-MT), indicating that estrogen-exposed DC induced IDO-dependent T cell suppression. Our data support the hypothesis that the estrogen-induced suppression of EAE, as well as the reduction in number of MS relapses observed during pregnancy, may be related to the estrogen-DC-IDO axis. This observation could open up a novel therapeutic target for influencing the course of MS and other diseases with an autoimmune diseases background.
Steroids 2004 Sep
PMID:Antigen-specific T cell functions are suppressed over the estrogen-dendritic cell-indoleamine 2,3-dioxygenase axis. 1546 10