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At least 217 records · Page 12Linked to original sources
PubMed1993

Adrenal steroid receptors in the PVN: studies with steroid antagonists in relation to macronutrient intake.

These studies tested the impact of steroid receptor antagonists on food intake induced by steroid agonists implanted into the paraventricular nucleus (PVN) and also on feeding that naturally occurs at the onset of the active (dark) period in the rat. Implants of corticosterone (CORT) or the selective type II agonist RU28362 in the PVN stimulated feeding in adrenalectomized (ADX) rats, specifically by enhancing carbohydrate ingestion. This feeding response induced by CORT or RU28362 was blocked by PVN implants of the type II antagonist RU486 but was unaffected by the type I antagonist RU28318. In contrast, the type I agonist aldosterone (ALDO) in the PVN stimulated feeding in both sham and ADX rats by preferentially enhancing fat ingestion, which could be inhibited by the type I antagonist RU28318 but not by the type II antagonist RU486. These results indicate that the feeding elicited by CORT at dark onset is dependent upon the functional integrity of type II glucocorticoid receptors within the PVN, in contrast to the feeding elicited by ALDO which is dependent upon endogenous type I steroid receptor activation within this nucleus. Test results with these antagonists alone in freely feeding animals support a functional role for these PVN steroid receptors in adrenal steroid control of natural food intake. Specifically, blockade of PVN type II receptors with RU486 in intact rats selectively suppressed spontaneous carbohydrate feeding at dark onset, while PVN implants of the type I receptor antagonist RU28318 caused a suppression of spontaneous fat intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1996

[Acute cervical necrotizing fasciitis of pharyngeal origin: possible role of steroidal and non-steroidal anti-inflammatory agents. Apropos of 5 cases].

Within 20 cases of cervical acute necrotizing fasciitis treated in the intensive care unit and hyperbaric oxygen therapy department between 1986 and 1995, the authors report five cases of pharyngeal origin. 4 have been initially treated with anti-inflammatory drugs: non steroidal (1 case), steroidal (2 cases), non steroidal and steroidal (1 case). The five patients have been operated. They needed at least 30 days of endotracheal intubation and hyperbaric oxygen therapy. No death outcome but a important morbidity is reported. The immunosuppressive features of the two type of anti inflammatory drugs are exposed. Different publications suggesting the possible association between non steroidal anti inflammatory drugs and non cervical necrotizing fasciitis are reported. It is not possible to prove a direct link because of the number of our cases, because of the wide number of pharyngitis treated in the area, and because the absence of precise data about the use of anti inflammatory drugs in the initial treatment of this pharyngitis. Existence of other type of antalgic and non immunosuppressive drugs make the use of anti inflammatory drugs not justify.

Acute Disease↗
PubMed2003

Expression of steroid receptor coactivators and corepressors in human endometrial hyperplasia and carcinoma with relevance to steroid receptors and Ki-67 expression.

BACKGROUND: To examine the steroid hormone dependent growth mechanism of human endometrial hyperplasia and carcinoma, expression levels of steroid receptor cofactors, such as coactivators (steroid receptor coactivator 1 [SRC-1] and p300/cyclic AMP-response element-binding protein (p300/CBP]) and corepressors (nuclear receptor corepressor [NCoR] and silencing mediator for retinoid and thyroid-hormone receptors [SMRT]), were investigated. METHODS: The expression levels of cofactors were examined immunohistochemically using 20 samples of normal endometria, 36 samples of hyperplastic endometria, and 58 of malignant endometria and were compared with the expression levels of estrogen receptor (ER), progesterone receptor (PR), and a proliferation marker, Ki-67. RESULTS: In samples of normal endometria, the expression of coactivators was observed diffusely in glandular cells in the proliferative phase, with a mean positivity index (PI) of 81.8 for SRC-1 and 91.3 for p300/CBP, whereas expression levels decreased in endometrial hyperplasia (PI: SRC-1, 58.9; p300/CBP, 83.8) and endometrial carcinoma (PI: SRC-1, 45.0; p300/CBP, 55.4). In endometrial hyperplasia, there was a significant correlation between the expression of ER and SRC-1 or p300/CBP. In contrast, there were no significant statistical or topologic correlations between the expression of coactivators and the expression of ER/PR in endometrial carcinoma. The expression of corepressors generally was limited, except for elevated expression of NCoR in endometrial hyperplasia (PI, 23.8). CONCLUSIONS: The current study showed that expression levels of the steroid receptor coactivators SRC-1 and p300/CBP were reduced in endometrial carcinoma compared with normal and hyperplastic endometrium. In addition, topologic coexpression of both coactivators and ER/PR was lost in endometrial carcinoma. Accordingly, limited response to sex steroids in patients with endometrial carcinoma may be ascribed to the dissociation of cofactors and ER/PR.

Carcinoma↗
PubMed1996

Direct evidence for the localization of the steroid-binding site of the plasma sex steroid-binding protein (SBP or SHBG) at the interface between the subunits.

Complete dissociation of dimeric plasma sex steroid-binding protein (SBP or SHBG) was obtained in 6 M urea at 10 degrees C. Removal of urea resulted in the refolding of monomers, followed by reformation of dimeric SBP, which migrates with the same mobility as the native protein. Dimerization does not require Ca+2 or steroid. Renatured monomers yield dimers with dissociation constants for 5 alpha-dihydrotesterone (DHT) and 17 beta-estradiol (E2) indistinguishable from those of native human SBP. This phenomenon was also demonstrated by mixing human and rabbit SBPs that, upon renaturation, form a hybrid dimer composed of one human subunit and one rabbit subunit. The hybrid binds both DHT and E2 in contrast to rSBP, which only binds the androgen. Therefore, we conclude that (1) docking of the two subunits creates an asymmetric steroid-binding site located at the interface between the subunits, and (2) only one face of the dimer defines the specificity for binding E2 by encompassing portion of a structural motif that recognizes the flat ring A of E2. The remaining portion, which recognizes the saturated ring A of DHT, is shared by both faces of the dimer. Because native monomers do not exist alone, the often-asked question of whether the SBP monomer binds steroid can be considered meaningless; steroid-binding activity is expressed only in the dimeric state. Finally, formation of the hybrid indicates that SBP dimerization represents a conserved event during the molecular evolution of SBP, suggesting that the structural elements responsible for dimerization will be homologous in SBPs from other species.

Animals↗
PubMed1993

In vitro steroid secretion during early development of mono-sex rainbow trout: sex differences, onset of pituitary control, and effects of dietary steroid treatment.

Sex differentiation in many teleost species can be controlled by treatment with steroids. To investigate the development of steroidogenesis during both natural and controlled sex differentiation, the production of androstenedione, testosterone, and estradiol were determined in tissues from populations of all-female and all-male rainbow trout (Oncorhynchus mykiss). At various times from hatching through gonadal sex differentiation, explants of steroidogenic tissues were incubated in vitro alone or in the presence of partly purified salmon gonadotropin and the resulting media were assayed for steroids. Androstenedione and testosterone were produced at higher levels in media from testes than from ovaries within 2 weeks of the onset of feeding (before any dramatic gonadal differentiation). Gonadal estradiol secretion was nondetectable until about 1 month after the onset of feeding when females produced more than males. Gonadotropin stimulated gonadal steroid production only after differentiation, but stimulated anterior kidney (interrenal) production of androstenedione much earlier in development. Dietary treatment of rainbow trout with either estradiol or 17 alpha-methyltestosterone (MT) inhibited in vitro gonadal steroid production and this effect persisted in MT-fed fish even after withdrawal of dietary steroids.

Aging↗
PubMed1979

Steroidal modulation of steroid secretion in vitro: an experimental approach to intra-follicular regulatory mechanisms.

Studies in vitro and in vivo indicate that steroid secretion by granulosa cells of the developing follicle is modulated in part by steroid hormones themselves. Androgens stimulate progestin synthesis in vitro by granulosa cells of all developmental stages independently of their role as an estrogen precursor; generally, the action of estradiol results in suppression of progesterone secretion. The nature of the relationship between steroid secretion by granulosa cells and the physiological processes of follicular development or atresia remains to be investigated in greater detail. The cellular mechanism(s) of steroidal modulation of steroid secretion is unknown but apparently does not involve changes in the number of granulosa cell LH receptors per se.

Androgen Antagonists↗
PubMed1994

Sodium dodecyl sulphate polyacrylamide gel electrophoresis of urinary proteins in steroid-responsive and steroid-resistant nephrotic syndrome in children.

Sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS PAGE) of urinary proteins was performed in 56 children with nephrotic syndrome during relapse, of whom 31 had their urines tested within 2 months of the onset of disease. The urines of all 32 steroid-sensitive [presumed minimal change nephrotic syndrome (MCNS)] patients revealed albumin and transferrin bands only; whereas 19 steroid-resistant children with focal glomerular sclerosis showed additional excretion of IgG and low molecular weight proteins (lysozyme, beta 2-microglobulin). This mixed pattern of proteinuria was also detected in 5 other steroid-resistant patients, 3 of whom were Africans with MCNS on biopsy and 2 who were Indians and not biopsied. Findings in patients studied within 2 months of presentation were identical to those investigated later in the course of the disease. SDS PAGE analysis of urine, which appears to distinguish steroid-responsive from steroid-resistant patients may provide a valuable adjunct to the management of childhood nephrotic syndrome.

Adolescent↗
PubMed1976

Simultaneous estimation of urinary steroids by semi-automated gas chromatography. Investigation of neo-natal infants and children with abnormal steroid synthesis.

Development of a method for multicomponent analysis of urinary steroids on open-tubular columns is described. The urinary steroid conjugates were hydrolysed enzymatically, extracted on Amberlite XAD-2 columns, purified on columns of Sephadex LH-20, then analysed as methyloxime trimethylsilyl ethers on a gas chromatograph on which up to 24 samples may be automatically injected. All major urinary steroids from 17-oxosteroids to cortisol metabolites were analysed and these were quantified relative to internal standards, 5alpha-androstane-3alpha, 17alpha-diol and cholesteryl butyrate added to the samples prior to derivatisation. The precision of the full technique and reproducibility of repetitive automatic solid injection was found to be acceptable for the purpose of profile analysis. Examples of urinary steroid profiles in normal infants and infants with disorders of adrenal steroid production and excretion are given.

Adrenal Gland Neoplasms↗
PubMed1983

Steroid binding to synaptic plasma membrane: differential binding of glucocorticoids and gonadal steroids.

The specific binding of [3H]-corticosterone, [3H]-17 beta-estradiol, [3H]-testosterone, and [3H]-progesterone to synaptic plasma membrane (SPM) prepared from rat brain has been characterized. The dissociation constant is estimated as on the order of 1 x 10(-7) M for corticosterone and 1 x 10(-8) M for the other three steroids. In a competition experiment, none of the 3H-steroids was displaced by the other steroids at 500-fold excess, indicating the presence of specific binding sites on the membrane for each type of steroid. Moreover, pre-incubation of the SPM with phospholipase A2 or phospholipase C totally destroys the membrane binding of corticosterone and testosterone, but the binding of estradiol and progesterone remains intact. Since the SPM prepared from brain tissue is derived from many different neuronal cell types, it is possible that the membrane binding sites for glucocorticoids and for gonadal steroids are present in different neurons.

Adrenalectomy↗
PubMed1992

Steroids and "the pill": early steroid research at Searle.

The announcement from the Mayo Clinic in 1949 of the dramatic effectiveness of cortisone in the treatment of rheumatoid arthritis stimulated tremendous interest in steroid chemistry, endocrinology, and related areas of medicine. Shortly thereafter, G. D. Searle & Co. initiated a major effort in steroid research, the objective of which was to discover better steroid drugs than those available at that time or steroids that could be used for conditions for which no compounds were previously available. This effort was remarkably successful and resulted in the introduction of several important pioneering drugs. These included norethandrolone, marketed in 1956 as Nilevar, the first anabolic agent with a favorable separation between protein building and virilization, and spironolactone, introduced in 1959 as Aldactone, the first steroid antialdosterone antihypertensive agent. Of special importance was the research that culminated in the discovery of Enovid. This substance, a combination of the progestin norethynodrel and the estrogen mestranol was first approved in 1957 for the treatment of a variety of disorders associated with the menstrual cycle. The era of oral contraception began in May 1960, when Enovid was approved by the Food and Drug Administration for ovulation inhibition, and was immediately thereafter introduced for such use.

Contraceptives, Oral, Hormonal↗
PubMed1991

Analysis of coenzyme binding by human placental 3 beta-hydroxy-5-ene-steroid dehydrogenase and steroid 5----4-ene-isomerase using 5'-[p-(fluorosulfonyl)benzoyl]adenosine, an affinity labeling cofactor analog.

3 beta-Hydroxy-5-ene-steroid dehydrogenase and steroid 5----4-ene-isomerase copurify as a single, homogeneous protein from human placental microsomes. Affinity alkylation with 2 alpha-bromoacetoxyprogesterone suggests that the dehydrogenase and isomerase substrate steroids bind at different sites on the same protein. However, the coenzyme, NADH, completely abolishes the alkylation of both enzyme activities by the progestin analog [Thomas J .L., Myers R. P., Rosik L. O. and Strickler R. C., J. Steroid Biochem. 36 (1990) 117-123]. Unlike bacterial 3-keto-5-ene-steroid isomerase, the human isomerase reaction is stimulated by diphosphopyridine nucleotides (NADH, NAD+). The affinity labeling nucleotide analog, 5'-[p-(fluorosulfonyl)benzoyl]adenosine (FSA), inactivates the dehydrogenase and isomerase activities at similar rates in an irreversible manner which follows first order kinetics with respect to both time and alkylator concentration (0.2-0.6 mM). FSA is a cofactor site-directed reagent that binds with similar affinity as a competitive inhibitor of NAD+ reduction by dehydrogenase (Ki = 162 microM) or as a stimulator of isomerase (Km = 153 microM). Parallel plots derived from Kitz and Wilson analysis indicate that FSA inactivates the two enzyme activities with equal alkylation efficiency (k3/Ki = 1/slope = 0.51/mol-s for both). The 3 beta-hydroxysteroid substrate, pregnenolone, protects isomerase as well as dehydrogenase from inactivation by FSA. These observations are evidence for a single cofactor binding region which services both enzyme activities.

3-Hydroxysteroid Dehydrogenases↗
PubMed1992

Studies on anabolic steroids--11. 18-hydroxylated metabolites of mesterolone, methenolone and stenbolone: new steroids isolated from human urine.

New metabolites of mesterolone, methenolone and stenbolone bearing a C18 hydroxyl group were isolated from the steroid glucuronide fraction of urine specimens collected after administration of single 50 mg doses of these steroids to human subjects. Mesterolone gave rise to four metabolites which were identified by gas chromatography/mass spectrometry as 18-hydroxy-1 alpha-methyl-5 alpha-androstan-3,17-dione 1, 3 alpha,18-dihydroxy-1 alpha-methyl-5 alpha-androstan-17-one 2, 3 beta,18-dihydroxy-1-alpha-methyl-5 alpha-androstan-17-one 3 and 3 alpha,6 xi,18-trihydroxy-1 alpha-methyl-5 alpha-androstan-17-one 4. These data suggest that mesterolone itself was not hydroxylated at C18, but rather 1 alpha-methyl-5 alpha-androstan-3,17-dione, an intermediate metabolite which results from oxidation of mesterolone 17-hydroxyl group. In addition to hydroxylation at C18, reduction of the 3-keto group and further hydroxylation at C6 were other reactions that led to the formation of these metabolites. It is of interest to note that in the case of both methenolone and stenbolone, only one 18-hydroxylated urinary metabolite namely 18-hydroxy-1-methyl-5 alpha-androst-1-ene-3,17-dione 5 and 18-hydroxy-1-methyl-5 alpha-androst-1-ene-3,17-dione 6 were both detected in post-administration urine specimens. These data indicate that the presence of a methyl group at the C1 or C2 positions in the steroids studied is a structural feature that seems to favor interaction of hepatic 18-hydroxylases with these steroids. These data provide further evidence that 18-hydroxylation of endogenous steroids can also occur in extra-adrenal sites in man.

Androstenols↗
PubMed2005

Effects of sub-lethal levels of dichlorodiphenyltrichloroethane and dichlorodiphenyldichloroethylene on in vitro steroid biosynthesis by ovarian follicles or steroid metabolism by embryos of rainbow trout (Oncorhynchus mykiss).

This study examined the possibility that DDT and DDE, at sub-lethal exposure levels, exert direct effects on the biotransformation of gonadal steroids by rainbow trout (Oncorhynchus mykiss) ovarian follicles and embryos. Ovarian follicles were co-incubated with DDT or DDE at 0.01 or 1 mg l-1 to examine effects of the pesticides on basal or cAMP-activated steroidogenesis. Ovarian preparations were incubated with radiolabelled [3H]pregnenolone ([3H]P5), and the tritiated metabolites of [3H]P5 metabolism were separated using high-performance liquid chromatography (HPLC). Testosterone (T) and 17beta-estradiol (E2) production were also measured using radioimmunoassay (RIA). Embryos were either exposed to the pesticides in ovo, or co-incubated in vitro with the pesticides. The effect of the pesticides on embryo steroid biotransformation was examined using a range of radioactively labelled substrates, including [3H]P5, [3H]progesterone ([3H]P4), [3H]T and [3H]E2. At the concentrations used, the pesticides had no significant effect on the relative amounts of unconjugated radiolabelled steroids formed by the biotransformation of [3H]P5 under conditions of basal or cAMP-stimulated ovarian steroidogenesis. However, DDT and DDE appeared to reduce the basal accumulation of androgen as a product of P5 biotransformation by ovarian follicles. Basal or cAMP-stimulated total estrogen production was not affected. In addition, DDT at 1 mg l-1 and DDE at 0.01 mg l-1 significantly increased and decreased cAMP-stimulated T accumulation, respectively. Also DDT at 0.01 mg l-1 and DDE at 1 mg l-1 significantly increased and decreased basal E2 accumulation, respectively. The steroid metabolites synthesized from the different substrates by embryos were essentially similar in both controls and pesticide-exposed groups, and the survival of embryos to hatch was not significantly affected by pesticide exposure, in ovo, with an approximately 90% hatchability in all treatment groups. This study suggests that although DDT and DDE may affect ovarian androgen synthesis under some conditions, under the conditions of the present study, they do not impact on overall rates of gonadal estrogen synthesis. Similarly, the pesticides do not appear to directly affect steroid biotransformation by embryos.

Animals↗
PubMed1984

Reversed-phase high-performance liquid chromatography of steroid 3-sulfates and the corresponding unconjugated steroids.

Simultaneous separation of steroid 3-sulfates and the corresponding free steroids has been accomplished by reversed-phase high-performance liquid chromatography (RP-HPLC). Addition of ammonium sulfate to the aqueous component of the mobile phase results in retention of the steroid sulfates to octadecyl silica packings by an apparent ion-pairing mechanism without affecting the retention of the free steroids. The retention time of steroid sulfates was dependent on the ammonium sulfate concentration in the mobile phase. Biologically important C19 delta 5, 3beta-hydroxysteroids and corresponding 3-sulfate conjugates or estrogen and estrogen 3-sulfates have been resolved with this RP-HPLC system.

Ammonium Sulfate↗
PubMed1997

Natural steroids counteracting some actions of putative depressogenic steroids on the central nervous system: potential therapeutic benefits.

Psychological similarities in the symptomatology of Cushing's and depressive diseases led to repeated attempts of treatment of the affective disease by suppression of adrenocortical secretion. While successful in many patients, all drugs employed-metyrapone, ketoconazole and aminoglutethimide-carry the danger of inducing adrenal insufficiency. In addition, their undesirable side effects were also a main reason for treatment suspension. In our 1990 proposal for the treatment of depression through control of adrenal steroid levels, we set as one of the goals the identification of steroids which can antagonize each other on their effects on the central nervous system. Specifically, we looked first at steroids that could counter each other's effects on long-term potentiation, a putative memory mechanism in the central nervous system. One reason for this was the consensus that memory mechanisms are affected in both Cushing's and depressive patients. Another was the fact that cortisol-type hormones which underlie, at least in part, the depressogenic actions of adrenal steroids also have inhibitory effects on LTP. We conjectured, then, that a steroid with opposite effects, one that could enhance long-term potentiation and, further, that could counter the depressant effects of corticosterone on long-term potentiation, could be of use in the treatment of depression. Dehydroepiandrosterone sulfate increases long-term potentiation in a dose-related manner, and preliminary data suggest that it also counteracts the depressant effects of corticosterone on long-term potentiation when injected simultaneously on experimental animals. Potentially at least, rather than resort to total suppression of adrenocortical activity, it may be possible to treat depression just by counteracting some of the effects of cortisol-like hormone actions in the central nervous system. Further, both in clinical trials as well as in experimental animals, dehydroepiandro-sterone sulfate has been shown to enhance performance in memory-requiring tasks.

Adrenal Cortex Hormones↗
PubMed1986

Profiling steroid hormones and urinary steroids.

This paper reviews techniques utilized in the profiling of steroids in body fluids and tissues. Methods for profiling plasma unconjugated steroids and urinary steroid metabolites are focused on. Concentrations or levels of excretion of a variety of steroids have been documented and reviewed. The importance of profiling techniques in the study of normal and pathophysiology of hormonal steroids is discussed.

Animals↗
PubMed1986

Detection of a transient enzyme-steroid complex during active-site-directed irreversible inhibition of 3-oxo-delta 5-steroid isomerase.

The reaction of the active-site-directed irreversible inhibitor (17S)-spiro[estra-1,3,5(10),6,8-pentaene-17,2'-oxiran]-3-ol (5 beta) with 3-oxo-delta 5-steroid isomerase has been monitored by repetitive scanning ultraviolet spectroscopy of a solution of 5 beta plus isomerase against a blank containing only 5 beta. Upon initial mixing of 5 beta with the isomerase an absorbance maximum at ca. 250 nm appears. With time, this peak decreases and is replaced with a new peak near 280 nm. These results directly demonstrate the existence of a transient enzyme-steroid intermediate in the inactivation reaction. The ultraviolet spectrum suggests that the steroid in the transient complex resembles the ionized phenol, while the phenolic group in the irreversibly bound complex is un-ionized. These spectral studies support our previous proposal that there are two enzyme-steroid complexes that are related by a 180 degree rotation about an axis perpendicular to the plane of the steroid nucleus. This hypothesis offers an explanation for the reaction of 17 beta-oxiranes with the same residue (Asp-38) that is thought to be involved in the catalytic mechanism. Two new oxiranes, (17S)-spiro[estra-1,3,5(10)-triene-17,2'-oxiran]-3 beta-ol (6 beta) and (17S)-spiro[5 alpha-androstane-17,2'-oxiran]-3-one (8 beta), were also found to be potent active-site-directed irreversible inhibitors of the isomerase (k3/KI = 31 M-1 s-1 and 340 M-1 s-1, respectively). The relationship of these results to the nature of the active site of the isomerase is discussed.

Binding Sites↗
PubMed1992

Photoaffinity labelling of steroid-hormone-binding glutathione S-transferases with [3H]methyltrienolone. Inhibition of steroid-binding activity by the anticarcinogen indole-3-carbinol.

The identification and characterization of steroid-hormone-binding glutathione S-transferases (GST) were undertaken using photoaffinity-labelling techniques. Irradiation of mouse liver cytosol, in the presence of 50 nM-[3H]methyltrienolone, resulted in the specific affinity labelling of five proteins. One of these proteins, designated MBP27, had an approximate molecular mass of 27 kDa under denaturing conditions and was induced by treatment of mice with either 2(3)-t-butyl-4-hydroxyanisole (BHA) or phenobarbital (PB). An additional affinity-labelled protein, MBP25, which was not detected in untreated mouse cytosol, was induced in the liver cytosols from BHA- and PB-treated mice. The molecular masses of these proteins and their induction by BHA and PB suggested that they may be steroid-hormone-binding GST subunits. Irradiation of mouse liver cytosol in the presence of [3H]methyltrienolone, followed by immunoprecipitation using GST-specific antibodies established that both GST mu and GST alpha bind [3H]methyltrienolone and both contribute to the affinity-labelled protein designated MBP27. GST Ya1 Ya1, an alpha class GST that is not expressed in untreated mouse liver but is induced by BHA and PB, was also found to bind [3H]methyltrienolone and is identical with the affinity-labelled protein designated MBP25. Experiments were undertaken next to assess the effects of the anticarcinogenic plant compound indole-3-carbinol (I3C) on GST-mediated steroid hormone-binding using the photoaffinity labelling techniques. Treatment of mice with I3C resulted in the induction of immunoreactive GST mu and GST Ya1 Ya1. However, the steroid-binding activity of these proteins in vitro was severely inhibited by the acid-condensation products of I3C that are generated in the stomach after ingestion. These results suggest that I3C may inhibit GST-mediated steroid-binding activity which could contribute to the anticarcinogenic activity of this compound.

Affinity Labels↗