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At least 163 records · Page 9Linked to original sources
PubMed1996

The effects of steroidal and non-steroidal ovarian hormones on pituitary responsiveness to gonadotrophin surge-attenuating factor.

Primary pituitary cultures from adult female rats were used to investigate the effects of steroidal (oestradiol and progesterone) and non-steroidal (inhibin, follistatin) ovarian hormones on the suppressive actions of the ovarian factor gonadotrophin surge-attenuating factor (GnSAF) in the control of gonadotrophin secretion. The source of GnSAF was a chromatographic preparation from follicular fluid containing four distinct protein bands as resolved on SDS-PAGE. Oestradiol and progesterone added alone had no effect on gonadotrophin secretion but had a wide range of effects on the suppression of both LH and FSH secretion caused by the non-steroidal factors. Oestradiol, progesterone and oestradiol+progesterone enhanced the suppressive actions of GnSAF on GnRH-induced LH secretion (causing 19.3 +/- 5.2% (P < 0.05), 41.9 +/- 3.4% (P < 0.001) and 32.2 +/- 5.3% (P < 0.001) greater suppression than GnSAF alone). Progesterone and oestradiol+progesterone completely abolished the suppression of basal FSH secretion caused by inhibin (causing 157.1 +/- 22.2%, P < 0.001, and 160.9 +/- 11.3%, P < 0.001, stimulation compared with inhibin alone). Separately the steroids had no effect on the suppression of gonadotrophin secretion caused by follistatin. However, in combination, oestradiol+progesterone potentiated the suppressive actions of follistatin on GnRH-induced LH secretion causing 29.9 +/- 5.3% (P < 0.05) greater suppression than follistatin alone. In combination, high-dose follistatin and GnSAF caused 31.1 +/- 6.5% (P < 0.01) greater suppression than GnSAF alone. Thus in combination high-dose follistatin and GnSAF have additive effects on the suppression of GnRH-induced LH secretion. Recombinant human inhibin and GnSAF added in combination had little further effect compared with either alone suggesting that they may have a similar mechanism of action at the pituitary level. These results demonstrate that while FSH secretion in vitro is mainly controlled by inhibin and follistatin, LH secretion is affected by the presence of a whole range of factors. We have demonstrated that oestradiol and progesterone potentiate the suppressive actions of GnSAF in vitro. These data are compatible with the suggestion that in the late follicular phase it is falling levels of GnSAF that allow positive feedback of the steroids on the pituitary to elicit the LH surge, rather than increases in the stimulatory effects of the ovarian steroids overcoming GnSAF. The actions of GnSAF on the pituitary may be modulated by follistatin but it is unlikely that inhibin has any modulatory effects on the GnSAF-induced suppression of LH secretion.

Animals↗
PubMed2005

Excessive use of Steroid Hormone & beneficial effects of True St. 36 acupuncture on malignant brain tumors--part I; how to estimate non-invasively presence of excess dose of Steroid Hormone in patients, baseball players & other professional athletes from its toxic effects on heart & pancreas, as well as persistent or recurrent infection--part II.

Using accurate organ representation areas map of the face, originally mapped by the author using Bi-Digital O-Ring Test Resonance Phenomena between two identical substances, one can make quick non-invasive screening of diseases by visual inspection, particularly if it is chronic degenerative disease, as they often develop deep crease or creases or discoloration on the pathological organ representation area. However, even if there are no visible abnormalities in the organ representation areas, the author found that when the individual is using excessive Steroid Hormones for malignant brain tumors, other medical purposes, and competitive sports, not only did the left ventricle and pancreas become very abnormal when examined by the Bi-Digital O-Ring Test, and Steroid Hormone accumulate in these organs with abnormally increased 8-OH-dG & TXB2, and Folic Acid & Telomere markedly reduce, but also the organ representation areas of the pancreas and left ventricle on the face showed similar abnormalities. Thus, using the Bi-Digital O-Ring Test, one can quickly and non-invasively screen the Steroid Hormone induced abnormalities of the heart and pancreas, and their organ representation areas of various parts of the body, including the face, tongue, ears, hands and feet. For malignant tumors including brain tumors, acupuncture on True ST. 36 or ST. 37 was found to be highly beneficial by reducing cancer cell telomere to practically 0, while increasing normal cell telomere moderately. The author's study over the past 15 years indicates that photographs of the human body, including pictures that appear in newspapers and magazines, have almost identical information as the information taken directly from the body surfaces of patients or individual athletes. Some examples of the application of this principle for the noninvasive estimation of the presence of Steroid Hormones using a photograph of the individual receiving the Steroid Hormone for medical reasons, or for the purpose of gaining an advantage in competitive sports, are shown in this article. While excessive Steroid Hormone use damages the heart and pancreas and hides symptoms of infection, additional use of Vitamin C also inhibits antibiotics and antiviral agents and cannot control severe infection, as suspected in the cases of late Pope John Paul II and late Palestinian leader Yasser Arafat.

Acupuncture↗
PubMed1976

Determination of mycelial steroids with the aid of polyene antibiotics. II. Quantitative determination of the mycelial steroids of Mucor hiemalis.

UV absorption spectrum of polyene antibiotics was dramatically altered in the presence of steroids. The introduction of a steroid to an aqueous solution of polyene antibiotics resulted in a change in the ratio of absorbance of peak 3 (with shorter wavelength) to peak 1 (with longer wavelength), E3/E1. Interactions between 28 steroids and 4 polyene antibiotics were studied and the results revealed that the structures of steroids essential for the optimal interaction with polyene antibiotics were C-17 side chain, substitution C-3 hydroxyl group, intact steroid nucleus and aromatic A-ring. The ratio of E3/E1 was used for the determination of steroids in mycelium of Mucor hiemalis and the result was in good agreement with that obtained from gas chromatograph. The (-) strain had a greater change in the ratio of absorbance, E3/E1, than that of the (+) strain. The ratio of absorbance, E3/E1, decreased in the following order: the (-) strain, the (-) strain with the addition of the filtrate of (+) strains, the mated strains, the (+) with the addition of the filtrate of (-) strain and the (+) strain.

Amphotericin B↗
PubMed1992

Botulinum C2 toxin and steroid production in adrenal Y-1 cells: the role of microfilaments in the toxin-induced increase in steroid release.

Exposure of adrenal Y-1 cells to C2 toxin results in an increase in steroid release that is accompanied by a rounding of the cell. The actions of C2 toxin mimic those of adrenocorticotropin and cholera toxin except that there is no increase in intracellular cyclic AMP content. In the present study we provide evidence that C2 toxin increases steroid output from Y-1 cells through an alteration in the microfilament network of the cell. C2 toxin significantly increased steroid output after 3 hr of exposure. This effect was accompanied by a significant increase in the transport of [3H]cholesterol to the mitochondrial fraction, independent of cholesterol uptake by the cell. The toxin was unable to increase steroid output from cells prerounded in suspension culture. The protease inhibitors benzamidine and phenylmethylsulfonyl fluoride did not attenuate the ability of C2 toxin to alter the morphology of Y-1 cells. A 3-hr exposure to C2 toxin resulted in the ADP-ribosylation of 50 to 60% of the total actin pool. Fluorescein isothiocyanate-labeled phalloidin visualization of the cytoskeleton of toxin-treated cells confirmed that the toxin caused a decrease in the stress fiber network. C2 toxin treatment of a protein kinase A mutant Y-1 cell (Kin 8) resulted in morphological changes and an increase in steroid output that was not different from that observed for wild type Y-1 cells. The data suggest that C2 toxin increases steroid output from adrenal Y-1 cells by a cyclic AMP-independent mechanism that involves the microfilament network of the cell.

Actin Cytoskeleton↗
PubMed2006

Non-steroidal steroid receptor modulators.

The discovery and launch of non-steroidal ligands for estrogen receptors (ERs) and for androgen receptors (ARs) demonstrated the potential of these ligands as therapeutic agents. Based on these successes, substantial attention in the past ten years has been focused on identifying non-steroidal ligands for all of the classic steroid receptors. Non-steroidal ligands are currently in the discovery phase or in early clinical development for glucocorticoid, mineralocorticoid and progesterone receptors, and therefore must still provide evidence of their beneficial features over their steroidal counterparts. Although many new compounds for ERs and ARs are also undergoing discovery phase investigation or (early) development, none have been launched in the past ten years. The complexity of steering functional selectivity remains an ongoing challenge in the development on non-steroidal ligands.

Animals↗
PubMed1984

Studies on steroid receptors in human and rabbit skeletal muscle - clues to the understanding of the mechanism of action of anabolic steroids.

The mechanism of action of steroid hormones in target tissues include the binding of the steroid molecule to specific receptors in the cytoplasm. Steroid receptors may therefore be regarded as mediators of hormone action. The presence of such receptors in tissues reflects their hormone-sensitivity and the receptor levels are indicative of the relative potential for a direct hormonal action on the tissue in question. Using 3H-labeled synthetic ligands and a charcoal adsorption assay, the presence of specific androgen, glucocorticoid and estrogen (in rabbits only) receptors was demonstrated in human and rabbit skeletal muscle cytosol. These tissues can therefore be regarded as targets for these steroids. Scatchard analysis was then used to quantitate the receptors in muscle in different conditions. In back muscle of scoliotic patients, the concentrations of androgen and glucocorticoid receptors were similar on the convex and concave sides, except the concentration of glucocorticoid receptors (per g of wet weight), which was higher on the convex side. The tissue concentration (per g of wet weight) of glucocorticoid and estrogen receptors (but not of androgen receptor) was higher in rabbit soleus (slow-twitch) muscle than in the gastrocnemius/plantaris (fast-twitch) muscle complex. When the concentrations were related to the number of nuclei (i.e. expressed per mg of DNA), however, only the estrogen receptor concentration differed between the muscles (higher in soleus). Muscle atrophy in rabbit gastrocnemius muscle was induced by tenotomy or denervation and led to similar changes with an increase with time in androgen and glucocorticoid receptor levels (expressed per g of wet weight or per mg of protein) and a concomitant loss of muscle weight and protein. The total muscle content of receptors or the receptor concentration expressed per mg of DNA were also increased, but to a lesser extent. Synthetic anabolic-androgenic steroids can act directly on skeletal muscle in view of their capacity to bind to the androgen receptor as shown in the present study. Relative binding affinities of anabolic-androgenic steroids to the androgen receptor were similar in rabbit and rat skeletal muscle and in rat prostate. The protein/DNA ratio in the muscle samples was used as an estimation of the size of the "functional DNA-unit". The results indicate that slow-twitch fibers have smaller "DNA units", but also that muscle atrophy causes a decrease of the size of the "DNA unit".(ABSTRACT TRUNCATED AT 400 WORDS)

Androgens↗
PubMed1975

Effect of plasma, steroids, or steroid products on the adhesion of human opsonized thrombocytes to human leukocytes.

An in vitro system was designed in which human thrombocytes were opsonized with rabbit antihuman platelet antibody and incubated with human leukocytes in EDTA-plasma in order to measure opsonized platelet-leukocyte adhesion. Antiplatelet antibody opsonization enhanced platelet-leukocyte adhesion 2.6-fold over control nonopsonized platelets in 50 out of 56 experiments. A plasma factor was found necessary for the support of opsonized platelet-leukocyte adhesion. This factor was EDTA-stable, heat labile, and labile to freezing and thawing. Hydrocortisone at 10-2 M was extremely effective in preventing opsonized platelet-leukocyte adhesion in 11 out of 14 experiments (2 S.D. below test-control value). Plasmas from 23 different patients ingesting 20 to 120 mg. of prednisone per day, were also tested. Seventeen out of 23 (74 per cent) did not support opsonized platelet-leukocyte adhesion at in vivo steroid concentrations of 10-6 M. Dilutions of 6 of these plasma samples with pooled normal plasma from 8- to 16-fold were still incapable of supporting opsonized platelet-leukocyte adhesion, whereas higher dilutions were capable. "Nonsteroid" plasma from 9 out of 17 (53 per cent) hospitalized "sick" patients were also incapable of supporting opsonized platelet-leukocyte adhesion. "Steroid plasma" from 5 out of 6 patients with severe thrombocytopenic purpura refractory to steroid treatment, did support leukocyte adhesion of opsonized platelets. It is concluded that a plasma factor is required for opsonized platelet-leukocyte adhesion. A steroid metabolite or byproduct factor is capable of inhibiting the adhesion of antibody-coated human platelets to leukocytes at an in vivo "steroid" concentration of 10-7 M. This factor does not appear to be present in most patients refractory to steroid treatment for autoimmune thrombocytopenic purpura.

Adult↗
PubMed1996

Monoclonal antibody analysis of glomerular and renal interstitial immune cells in steroid-resistant and steroid-responsive minimal change disease in children.

Glomerular and interstitial leukocyte infiltrates were studied by indirect immunoperoxidaze technique using monoclonal antibodies against all leukocytes, pan-T lymphocytes, helper/inducer CD4 cells, suppressor/cytotoxic CD8 cells, pan-B lymphocytes, monocytes/macrophages and polymorphs in 23 renal biopsy samples obtained from children with minimal change disease (MCD). The cases were classified on the basis of light, electron microscopy and immunofluorescence. Nephrotic syndrome was steroid-sensitive in 15 patients (group I) and steroid-resistant in 8 subjects (group II). Both groups did not differ in the type or number of glomerular immune cells, quantified as immunopositive cells per glomerular cross section. Intraglomerular cellular infiltrates were mainly constituted of monocytes/macrophages; among T lymphocytes T helper/inducer cells predominated over T cytotoxic/suppressor cells. Enumeration of interstitial immune cells showed significantly higher number of all leukocytes and T lymphocytes, quantified as immunopositive cells/mm2, in steroid-resistant group. T helper/inducer cells predominated over T cytotoxic/suppressor cells in the renal interstitium in steroid-responsive and in steroid-resistant MCD. The leukocyte infiltrates did not correlate with a degree of proteinuria at the tine of biopsy and with the renal cortical interstitial volume in both studied groups. Our data suggest, that steroid resistance in minimal change nephropathy in children seems to be related to interstitial T lymphocytes.

Antibodies, Monoclonal↗
PubMed1998

Steroid hormone receptors and steroid action in rat glial cells of the central and peripheral nervous system.

The nervous system is a target for sex steroid hormones which have profound actions on the growth, maturation, differentiation and functioning of brain cells. We found that some steroids, termed "neurosteroids", are synthesized within the brain by glial cells. The term "neurosteroids" designates their site of synthesis--the nervous system, either de novo from cholesterol or from steroid hormone precursors. The biological effects of steroid hormones are mediated by specific high-affinity intracellular receptors, which, after hormone binding, function as activated transcription factors. The presence of such receptors was shown in primary cultures of oligodendrocytes and astrocytes, derived from forebrains (CNS), and in Schwann cells, derived from sciatic nerves (PNS), of newborn rats. In glial cells of the CNS, progesterone-, glucocorticoid-, estrogen and androgen-receptors (PR, GR, ER, AR) were demonstrated and of these receptors, only PR was estrogen-inducible. In glial cells of the PNS, the presence of PR and ER was shown, but the PR in Schwann cell cultures was not inducible by estrogen treatment. Different effects of steroids on glial cell growth and differentiation during primary culture were observed. In particular, a striking increase of myelin-specific proteins such as myelin basic protein (MBP) and cyclic nucleotide phosphodiesterase (CNPase) was observed when oligodendrocytes, the myelinating glial cells of the CNS, were cultured in the presence of progesterone, as determined by indirect immunofluorescence staining and immunoblotting. Insulin also increases MBP and CNP-ase in oligodendrocytes and the combined treatment (insulin + progesterone) promotes a strong synergistic stimulation (14-fold increase) of myelin protein expression. Estradiol also increases MBP- and CNPase expression in oligodendrocytes, although to a lesser extent than progesterone. In the search for optimal stimulation of myelin-protein expression, several progesterone analogues were tested and the results are discussed.

Animals↗
PubMed1983

Properties of porcine liver and testicular steroid sulphotransferases: reaction conditions and influence of naturally occurring steroids and steroid sulphates.

Sulphotransferase activity has been assayed in porcine liver and testis cytosol using either 3'-phosphoadenosine-5'-phospho [35S]sulphate (PAPS) or unlabelled PAPS as sulphate donors. In porcine liver the sulphotransferase for DHA was linear for up to 10 min, the optimum pH was 7.7 and optimum temperature, 37 degrees C. The apparent Km value was found to be 91 mumol/l and the activity was inhibited non-competitively by 5 alpha-androst-16-en-3 beta-yl sulphate, with all concentrations used (0.02-25 mumol/l) inhibiting the enzyme to the same extent. Time courses for sulphoconjugation of pregnenolone and 5 alpha-androst-16-en-3 beta-ol were linear for up to at least 10 min or up to only 5 min, respectively. The optimum pH values and temperatures were pH 8.0 and 37 degrees C in each case. The porcine testicular sulphotransferase activity for DHA as substrate was linear with time up to 10 min, the apparent Km for the reaction was 2 mumol/l and apparent Vmax 10 nmol/l/mg/min. 5 alpha-Androst-16-en-3 beta-yl sulphate (11.3-45.2 mumol/l) failed to inhibit the enzyme activity. The time-course for the reaction, when pregnenolone was used as substrate, was also linear up to 10 min at the optimum pH 8.0 but, in contrast to the reaction when DHA was the substrate, had an apparent Km of 20 mumol/l and was inhibited by pregnenolone sulphate, 5 alpha-androst-16-en-3 beta-yl sulphate, DHA and 5 alpha-androst-16-en-3 beta-ol, but not by DHA sulphate. 5 alpha-Androst-16-en-3 beta-yl sulphate inhibited the reaction non-competitively and to the same extent at concentrations over the range 11.3-45.2 mumol/l. These data suggest that DHA and pregnenolone may not be sulphoconjugated by the same sulphotransferase. With 5 alpha-androst-16-en-3 beta-ol as substrate, the time-course for its sulphate formation was linear up to 15 min, and this reaction could explain the quantities of 5 alpha-androst-16-en-3 beta-yl sulphate that are found endogenously in porcine testis. Our results further suggest that these quantities could well inhibit the sulphation of pregnenolone in porcine testis in vivo, and the possibility of control of sulphoconjugation in this tissue is discussed. Having regard to the smaller quantities of 5 alpha-androst-16-en-3 beta-yl sulphate present in porcine liver, our results suggest that the sulphation of DHA there may not be so much affected.

Androstenols↗