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PubMed1979

Use of borohydride reduction in the separation of estrogen carbonyls.

The chromatographic behavior of the estrogen carbonyls, equilenin, equilin, and estrone, and their respective sodium borohydride reduction products has been studied. The separation of the 17 alpha-hydroxy reduced compounds is superior to the separations achieved for the parent carbonyls using both reversed-phase and normal-phase systems. The reductions appear quantitative by the chromatographic systems used but other work indicates that a small quantity of 17 alpha-hydroxy isomer is produced. The separations developed here have been used in the identification of 9-dehydroestrone, an impurity in estrone, and in the identification of the estrogens in a commercial aqueous suspension of estrogenic substances.

Borohydrides↗
PubMed1980

Application of dansyl derivatization to the high pressure liquid chromatographic identification of equine estrogens.

The HPLC qualitative analysis of conjugated estrogens is accomplished by a two-step procedure involving the formation of the corresponding dansyl derivatives. The first step involves the acid hydrolysis of the conjugated estrogens, followed by dansyl derivatization and HPLC separation of these derivatives on a liChrosorb Si-60 column with 50% (v/v) chloroform-n-heptane as the mobile phase. All of the dansyl estrogens are well separated except for the 17-keto estrogens, estrone, equilin, and equilenin. The second step, designed to detect the three 17-keto estrogens, begins with the selective sodium borohydride reduction of the conjugated 17-keto estrogens to the corresponding 17-hydroxyl compounds (the beta-epimer being formed in vast predominance over the alpha-epimer), followed by acid hydrolysis, dansyl derivatization, and HPLC separation of the derivatives as in the first step. Detection of the 17-keto estrogens is possible by determining differences in peak heights between the chromatograms of the first and second analyses. The The proposed method is sensitive, the dansyl derivatives stable, and nine different estrogens can be readily identified.

Animals↗
PubMedDate not supplied

Comparison of the antioxidant effects of equine estrogens, red wine components, vitamin E, and probucol on low-density lipoprotein oxidation in postmenopausal women.

OBJECTIVE: Oxidized low-density lipoprotein (LDL) seems to play an important role in the etiology of atherosclerosis. To further study this, we performed two studies: (1) we determined the ability of 10 estrogen components of the drug, conjugated equine estrogen (CEE), trans-resveratrol (t-resveratrol) and quercetin (red wine components), trolox (vitamin E analog), and probucol (a serum cholesterol-lowering drug) to delay or prevent the oxidation of plasma LDL isolated from untreated postmenopausal women, and (2) we assessed the effect of long-term (>1 year) estrogen replacement therapy and hormone replacement therapy on LDL oxidation by ex vivo methods. DESIGN: For the in vivo study, three groups of postmenopausal women were selected based on whether they were on long-term CEE therapy (group A: 0.625 mg CEE; n = 21), on combination CEE plus progestogen therapy (group B: 0.625 mg CEE + 5.0 mg medroxyprogesterone acetate, 10 days; n = 20), or not on any hormone therapy (group C; n = 37). For the in vitro study, only LDL samples obtained from group C were used. The kinetics of LDL oxidation were measured by continuously monitoring the formation of conjugated dienes followed by determination of the lag time. RESULTS: All compounds tested protected the LDL from oxidative damage. The relative antioxidant potency of estrogen components was generally greater than that of the other compounds. The minimum dose (nmoles) required to double the lag time from the control lag time of 57 +/- 2 min was 0.47 for 17beta-dihydroequilenin, 17alpha-dihydroequilenin, Delta 8 -estrone; 0.6 to 0.7 for Delta 8 -17beta-estradiol, equilenin, and quercetin; 0.9 for 17beta-dihydroequilin and 17alpha-dihydroequilin; 1.3 for equilin, estrone, 17beta-estradiol, 17alpha-estradiol; 1.4 for trolox; 1.9 for probucol; and 3.0 for t-resveratrol. The data from the in vivo study indicate that after long-term estrogen replacement therapy (group A) and hormone replacement therapy (group B), the LDL was significantly ( p < 0.01) protected (higher lag time) against oxidation compared with the control (group C). There was no difference between groups A and B. CONCLUSIONS: The oxidation of LDL isolated from postmenopausal women is inhibited differentially by various estrogens and other antioxidants. The unique ring B unsaturated estrogen components of CEE were the most potent, and t-resveratrol, the red wine component, was the least potent. Long-term CEE or CEE + medroxyprogesterone acetate administration to postmenopausal women protects the LDL against oxidation to the same extent. These combined data support the hypothesis that some of the cardioprotective benefits associated with CEE therapy and perhaps red wine consumption may be due to the ability of their components to protect LDL against oxidative modifications.

Antioxidants↗
PubMed1986

Structure-activity relationships of sex steroid analogs determined in vitro in a thyroid hormone-responsive membrane Ca2+-ATPase model.

Physiological concentrations of L-T4 were found previously to stimulate Ca2+-ATPase activity in vitro in reticulocyte membranes from female rabbits and to inhibit this enzyme in reticulocyte membranes from males. In these previous studies, preincubation of intact cells or ghosts with testosterone (5 X 10(-11) M) converted female-source reticulocyte membranes to male-type responsiveness to thyroid hormone (inhibition of Ca2+-ATPase activity). Preincubation of reticulocyte membranes with 17 beta-estradiol (5 X 10(-11) M) converted male-source membranes to female-type responsiveness (stimulation by L-T4 of membrane Ca2+-ATPase activity). Using this sex steroid-sensitive thyroid hormone-dependent membrane enzyme system, we investigated the structure-activity relationships of analogs of sex steroids and unrelated steroids. 5 beta-Androstanes were active compared to testosterone in assays using female-source membranes, while 5 alpha-androstanes were less active. Within the 5 beta-androstanes, activity was dependent on at least one hydroxyl group at the C3- or C17-position. Nongonadal steroids tested were less active, establishing specificity of the sex steroid effect in assays using female-source membranes. Assayed in male-source membranes, estrone and 3-hydroxy-1,3,5-(10)7-estratraen-17-one (equilin) were active compared for estrogen effect with 17 beta-estradiol, while estriol was less active. The activities of hydrocortisone and aldosterone were 76% and 71%, respectively, in this system. These structure-activity relationships are distinct from those described for gonadal steroid-cytoplasmic binding proteins or nuclear interactions, and represent a novel sex steroid-thyroid hormone effect on activity of a membrane enzyme.

Animals↗
PubMed1975

Formation of steroids by the pregnant mare. V. Metabolism of 14C-isopentenylpyrophosphate and 3H-dehydroisoandrosterone injected into the fetus.

A mixture of 1-14C-isopentenylpyrophosphate and 3H-dehydroisoandrosterone was injected into a horse fetus intramuscularly during laparotomy, after which maternal urine was collected for 4 days. Steroid conjugates in the urine were extracted with Amberlite XAD-2 resin, hydrolysed and separated into phenolic and neutral fractions. From the phenolic fraction estrone, 17alpha-estradiol, equilin and equilenin were isolated. Only estrone and 17alpha-estradiol contained both 3H and 14C, while the ring B unsaturated estrogens contained only 14C. From the neutral fraction 14C-labeled 3beta-hydroxy-5alpha-pregnan-20-one, 5alpha-pregnane-3beta,20beta-diol and 5alpha-pregnan-3beta, 20alpha-diol were isolated. These results demonstrate that the route of biosynthesis of both the ring B saturated and unsaturated estrogens is the same up to the stage of isopentenylpyrophosphate. Thus, the bifurcation in the classical pathway of steroid biosynthesis reported previously by us is occurring at a point after the formation of isopentenylpyrophosphate and prior to the formation of squalene.

17-Ketosteroids↗
PubMed1983

Effects of various replacement oestrogens on hepatic transcortin synthesis in climacteric women.

The influence of peri-menopausal oestrogen replacement therapy upon protein synthesis in the liver was investigated. Changes in the cortisol-binding capacity of transcortin (TC-BC) were utilized as an indicator of hepatic oestrogen sensitivity. Forty-two climacteric women were studied before and after treatment with various drugs at different doses (patients receiving identical compounds served as their own controls for the evaluation of dosage effects; duration of medication: 14 days at each dose). Oral administration of oestriol (1 and 2 mg daily; n = 6), oestriol (1 and 2 mg daily) + oestradiol-17 beta (2 and 4 mg daily; n = 8), oestradiol valerate (1, 2, 4 and 6 mg daily; n = 6), conjugated equine oestrogens (0.3 and 0.6 mg daily; n = 6), sodium oestrone sulphate (0.8 and 1.6 mg daily) + sodium equilin sulphate (0.2 and 0.4 mg daily; n = 6) and quinoestrol (25 micrograms daily; n = 6) failed to alter TC-BC. However, ingestion of higher doses of conjugated equine oestrogens (0.9 and 1.25 mg daily; n = 5) and quinoestrol (50 micrograms daily; n = 6) caused a significant rise (P less than 0.01). Ethinyloestradiol was given orally as a reference substance and elicited an elevation of expected magnitude. Vaginal administration of dienoestrol cream (1 mg daily; n = 4) did not change TC-BC. These data indicate that the hepatotrophic effects of replacement oestrogens vary depending on the preparation and dosage selected for treatment.

Climacteric↗
PubMed1983

Identification of 3 beta-hydroxy-5,7-pregnadien-20-one and 3 beta-hydroxy-5,7-androstadien-17-one as endogenous steroids in the fetal horse gonad.

The 5,7-dienes, 3 beta-hydroxy-5,7-pregnadien-20-one and 3 beta-hydroxy-5,7-androstadien-17-one were extracted from fetal horse gonads and purified by solvent partition, thin-layer chromatography and high performance liquid chromatography. The isolated steroids were identified by comparison with the synthetic steroids using ultraviolet and mass spectroscopy and by gas chromatography-mass spectroscopy. The identification of these compounds as endogenous steroids, together with the data on their biosynthesis reported previously, support the proposal that in the fetal horse gonad there is a 5,7-diene pathway biosynthesizing 3 beta-hydroxy-5,7-androstadien-17-one, which is the proposed precursor for equilin in the placenta.

Androstadienes↗
PubMed1985

Identification of 3 beta-hydroxy-5,7-androstadien-17-one as a secretory product of the fetal horse gonad in vivo and in vitro.

Isolation of 3 beta-hydroxy-5,7-androstadien-17-one, as a major component of steroids extracted from vein blood of the fetal gonads of the horse, supports the proposed role for the compound as a precursor for equilin formation in the placenta of the mare. The 5,7-diene was extracted from blood collected from gonadal veins of fetal ovaries and testes in situ, and from a fetal testis connected to an artery in the neck region of the mare. Perfusion of fetal gonads in the laboratory was carried out to allow longer periods of collection. In addition, isolated cell preparations from a fetal testis were incubated for 4-8 h in tissue culture to investigate steroid secretion in vitro. Final purification of neutral steroids in the extracts was carried out by high performance liquid chromatography, and identification was made by u.v. and mass spectrometry. The presence of 3 beta-hydroxy-5,7-androstadien-17-one in extracts from all sources provided evidence for its secretion in vivo and in vitro. Other 5,7-dienes, which were less polar than the C19 compound, were noted in extracts of media but not identified. These data support the view that a 5,7-diene pathway is involved in the biosynthesis of 3 beta-hydroxy-5,7-androstadien-17-one in the fetal horse gonad.

Androstadienes↗
PubMed2002

Interaction of endogenous compounds in human and rat urine with P-glycoprotein.

The effect of hydrophobic extracts of human and rat urine on in-vitro P-glycoprotein (P-gp) function was examined, in terms of intra-, inter-individual variations, and physiological states. Six urine samples out of 7, obtained from one male subject on different days, suppressed P-gp function with different potencies. Similarly, 11 samples out of 15 different individuals (8 males and 7 females) inhibited P-gp function. Among them, urine from one female, obtained 1 month after delivery, showed a potent inhibitory effect. Another urine from a pregnant female, obtained 1 week before delivery, showed further potent inhibition on P-gp function. In addition, urine from normal rats strongly inhibited P-gp function at much lower concentrations than human urine, and the inhibitory potencies varied in diseased states; control (without urine extract)=experimental acute renal failure<experimental acute hepatic failure<normal rat urine. When human urine extract was separated by a two-dimensional thin-layer chromatography, several spot fractions inhibited P-gp function, and equilin was identified in one fraction as an endogenous P-gp inhibitor. In conclusion, it was demonstrated that urine contains many endogenous P-gp inhibitors, and their inhibitory potencies on P-gp function vary with intra- and inter-individual variations, and under different physiological states.

Journal Article↗
PubMed1999

[Efficacy of hormone replacement therapy on hyperlipidemia].

In women, serum lipid levels and the incidence of myocardial ischemia increase after menopause. Deficiency of estrogen is believed to be the cause of these epidemiological phenomena. On the other hand, hormone replacement therapy(HRT), has prevailed in developed countries. Estrogen is replaced to ease climacteric disorders, and retard bone loss. Many clinical studies cleared the effect of HRT on lipids, in which total and LDL-C (cholesterol) decreased, and HDL-C increased. TG increased by conjugated equilin estrogen but not by transdermal estradiol. In our study, hepatic triglyceride lipase(HTGL) was suppressed by HRT, but lipoprotein lipase(LpL) was not suppressed. HRT decreases coronary artery diseases, but it is still controversial whether HRT is efficient in patients who already have heart disease.

Coronary Artery Disease↗
PubMed1999

Conjugated estrogens and breast cancer risk.

Available epidemiologic data suggest the possibility that the use of oral conjugated equine estrogens (CEE) 0.625 mg/day as a first-choice dose could be associated with a very limited (if any) breast cancer risk increase. Some biological peculiarities of oral CEE back the possibility of a limited detrimental effect on breast tissue, due to either direct or indirect actions. Direct actions. Some experimental findings suggest that the 17 alpha-dihydroderivatives of equilenin and equilin (15% of the CEE components) have a non-estrogenic or even an anti-estrogenic effect on breast tissue. This could partially counterbalance the stimulatory action of the other CEE components. Indirect actions. Oral estrogens, through their metabolic and hepatocellular effects (emphasized by the first liver passage) cause a sharp increase in sex hormone binding globulin (SHBG) level which is followed by a lower quantity of both estrogen and androgen in the free, bioavailable, form. More importantly, they cause a decrease in circulating insulin-like growth factor I (IGF-I) activity, due to both a reduction in IGF-I synthesis by the liver and an increase in IGF-binding protein-1 level. A strong relationship between breast cancer risk and the concentration of circulating IGF-I in premenopausal women has been recently found. Actually, estrogens and IGF-I have a synergistic effect on cell proliferation, and IGF-I is necessary for maximum estrogen-receptor activation in breast cancer cell lines. The possibility does exist that the SHBG level increase and the IGF-I bioavailability decrease, caused by oral CEE, balance the increased estrogen stimulation on breast tissue.

Adult↗
PubMed1990

17 beta-estradiol is the most active component of the conjugated estrogen mixture active on uremic bleeding by a receptor mechanism.

We have reported previously that a mixture of conjugated estrogens which is effective in shortening the prolonged bleeding time in uremic patients is also effective on bleeding time in a rat model of uremia. With the present study we took advantage from such a rat model of chronic uremia and decided to identify the component(s) of the conjugated estrogen mixture responsible for shortening the bleeding time. Moreover, we wanted to clarify whether estrogen effect on primary hemostasis is due to a receptor mechanism and can be neutralized by specific estrogen receptor antagonists such as tamoxifen or clomiphene. Both estrone sulfate and 17 beta-estradiol, but not equilin, were effective in shortening the prolonged bleeding time of uremic rats. 17 beta-Estradiol was the most active component of the mixture, reproducing the time course of bleeding time shortening of the entire mixture (effect lasting 48 hr). The effect of estrone sulfate injection lasted only 24 hr. Tamoxifen and clomiphene pretreatment prevented the shortening of bleeding time induced by conjugated estrogen mixture and its active components. These findings indicate that 17 beta-estradiol is the key compound of the conjugated estrogen mixture effective on bleeding time shortening and that the effect of estrogens on primary hemostasis is mediated by a receptor mechanism.

Animals↗
PubMed1985

Estrogen 2- and 4-hydroxylase activity, catechol estrogen formation, and implications for estrogen carcinogenesis in the hamster kidney.

Estrogen 2- and 4-hydroxylase (ESH), a microsomal enzyme which mediates the formation of catechol estrogens, has been studied in the kidneys of castrated male Syrian hamsters, a species uniquely susceptible to induction of renal carcinomas by both steroidal and stilbene estrogens. The apparent Km for estrone was 17.0 microM, and Vmax was 0.5 pmol per mg protein per min for ESH in renal microsomes derived from castrated hamsters. Different steroidal estrogen substrates exhibited decreasing catechol formation with hamster kidney microsomal preparations in the following order: estrone greater than d-equilenin greater than 17 beta-estradiol greater than equilin greater than ethynyl estradiol greater than estriol. Except for beta-dienestrol, the stilbene estrogens revealed levels of catechol formation that were similar to 17 beta-estradiol. These findings provide a rationale for the weak carcinogenic activity of ethynyl estradiol, estriol, and beta-dienestrol, since they were poor substrates for hamster renal ESH and for the relatively potent carcinogenic activity of the distal metabolite of diethylstilbestrol, indenestrol B/A, which exhibited substantial levels of o-hydroxylation when used as a substrate. Interestingly, ESH activity was significantly greater in the hamster kidney compared to corresponding rat tissue, and catechol estrogen formation was found to be 2.5- to 19-fold higher in the hamster kidney compared to the rat, using various steroidal and stilbene estrogen substrates. Moreover, the finding that a 3.5- to nearly 6-fold decrease, compared to untreated levels, in catechol formation in kidneys but not in livers of alpha-naphthoflavone-exposed hamsters, depending on the steroidal or stilbene estrogen substrate used, is consistent with the belief that the catechol estrogen pathway is pertinent to events leading to estrogen-induced renal tumorigenesis in the hamster.

Animals↗
PubMed1988

Interactions of putative estrogens with the intracellular receptor complex in mouse Leydig cells: relationship to preneoplastic hyperplasia.

The interaction of 14 steroidal and nonsteroidal estrogen agonists and antagonists with the intracellular estrogen receptor system was examined in cell suspensions prepared from the testes of mice that develop malignant Leydig cell tumors after prolonged estrogen administration. The ability of these substances to stimulate DNA synthesis in short-term (3-day) studies and to provoke Leydig cell hyperplasia with prolonged (3-mo) administration was also measured. Our data were consistent with the proposal that, in Leydig cells, the carcinogenic effects of estrogens are mediated through the intracellular receptor complex that results in a localization of hormone bound to chromatin and nuclear matrix. All tested compounds displaced 17 beta-[3H]estradiol from the cytosolic estrogen receptor, but to varying degrees; and there was no discernible relationship between their ability to compete for this receptor and their efficacy in stimulating DNA synthesis. The effect of the test compounds on the levels of estrogen receptor in cytosol and in nuclei was measured by [3H]estradiol exchange. 17 beta-Estradiol, equilin, 17 alpha-ethinylestradiol, diethylstilbestrol, hexestrol, dienestrol, coumestrol, and nafoxidine provoked a complete estrogen receptor response: acutely a decrease in the level of cytosolic estrogen receptor and an increase in the nuclear estrogen receptor. All of these substances acutely stimulated DNA synthesis. Tamoxifen, clomiphene, and nitromifene provoked a decrease in cytosolic receptor but no increase in demonstrable nuclear estrogen receptor. 17 alpha-Estradiol, mestranol, and estriol did not significantly alter the levels of estrogen receptor in cytosol or nuclei. Only those substances that increased measurable nuclear estrogen receptor also acutely stimulated DNA synthesis. Chronic (3-mo) treatment of 2-mo-old male BALB/c mice with diethylstilbestrol, 17 beta-estradiol, ethinylestradiol, and nafoxidine led to Leydig cell hyperplasia. Chronic mestranol treatment also provoked Leydig cell hyperplasia; this is most probably due to induction of liver metabolism of mestranol to ethinylestradiol. Chronic treatment with 17 alpha-estradiol, tamoxifen, and clomiphene failed to produce significant histologic al changes in the testes. Only chronic administration of those substances that exhibited a complete estrogen receptor response and acutely stimulated DNA synthesis produced Leydig cell hyperplasia.

Animals↗
PubMed1987

Steroid modulation of liver regeneration and hepatic microsomal enzymes in rats of either sex.

Rats of either sex as intact or partially hepatectomized (two-thirds liver removal) were injected s.c. daily for 7 days post-operatively with natural and synthetic estrogens, androgens or anabolic steroids, progesterone and adrenal cortical hormones and killed on day 10 at which time the livers were processed for microsomal analyses (protein, cytochrome P-450 and enzymes, aminopyrine demethylase and aromatic hydrocarbon or benzo[a]pyrene hydroxylase). Groups were also induced with phenobarbital injected i.p. on the last 3 days at 80 mg/kg each. With the intact males, hexestrol was the only estrogen which caused liver enlargement and at a daily dosage of 1.0 micrograms per rat as well as a decrease in the hydroxylase level. Estradiol benzoate (15 micrograms/rat daily) depressed cytochrome P-450 and the other steroids screened had little effect on the microsomal parameters except for a rise in demethylase with deoxycorticosterone acetate (1.0 mg). A greater sensitivity to estrogens and the other steroid types was noted with the partially hepatectomized males and in the direction of depressions in the microsomal elements, the respective data being expressed as percentages of the controls. Estrogens were better tolerated by the intact female and in general, liver enlargement was remarkable. Microsomal activity was elevated with estradiol benzoate or little affected by estrogens except for depressions in hydroxylase levels with equilin (15 micrograms) and the high dosages of hexestrol and diethylstilbestrol, the last agent also eliciting an increase in cytochrome P-450. No statistically significant effect on the microsomal parameters was observed with the intact female treated with 17-methyltestosterone and the anabolic steroids but decreases occurred on injection with testosterone propionate and the cortical hormones. As with the operated male, partially hepatectomized females exhibited no hepatotrophic response to estrogens and the microsomal changes were moderate with such agents as with the other steroid types and resembling the findings for intact males. Competitive inhibition was followed by Lineweaver-Burke analyses of aminopyrine demethylase in operated females treated with several of the steroids.

Animals↗
PubMed1995

Carcinogenic activities of various steroidal and nonsteroidal estrogens in the hamster kidney: relation to hormonal activity and cell proliferation.

The therapeutic use of estrogens has been associated with an increased risk of some of the most predominant, as well as less prevalent, cancers in women. The estrogen-induced renal tumor is one of the primary animal models to evaluate the carcinogenic properties of estrogens. Correlations were made with various estrogens by using parameters of estrogenicity end points such as competitive binding, progesterone receptor induction, and alterations in prolactin levels; in vitro renal proximal cell proliferation; and in vivo estrogen-induced carcinogenicity. The most potent estrogens were Moxestrol (MOX), diethylstilbestrol (DES), and 17 beta-estradiol, followed by indenestrol B, 16 alpha-hydroxyestrone, and 11 beta-methoxyestradiol with moderate estrogenic activities, whereas 11 beta-methylestradiol, 17 alpha-estradiol, indanestrol, and deoxoestrone were all relatively weaker. As expected, hydrolyzed Premarin (unconjugated estrogens) was strongly estrogenic. Of the estrogens tested, MOX was the most potent carcinogenic estrogen in the hamster kidney. Both 16 alpha-hydroxyestrone and 11 beta-methoxyestradiol induced intermediate tumor incidences with distinctly lower frequencies of renal tumor foci compared to the most potent carcinogenic estrogens. However, hamsters treated for 9.0 months with 11 beta-methylestradiol, 17 alpha-estradiol, deoxoestrone, and indanestrol exhibited no tumors. In contrast, treatment with estrone, equilin plus d-equilenin, and hydrolyzed Premarin for the same time period resulted in 100% renal tumor incidences and numerous tumor foci. Cell proliferation studies of cultured hamster kidney proximal tubule cells were carried out at varying estrogen concentrations (0.01-100 nM). Exposure to MOX resulted in consistently high renal cell proliferative response over a concentration range of 0.1-10 nM. Strongly carcinogenic estrogens such as estrone had a maximal renal cell proliferation response (2.4-fold above untreated control levels) between 0.1 and 10 nM, DES and 17 beta-estradiol responded at 1.0 nM, and 4-hydroxyestradiol responded at 10 nM. Interestingly, exposure to ethinylestradiol, a potent estrogen, at similar or higher doses as those used for DES and 17 beta-estradiol, yielded only a 10% renal tumor incidence and induced only a 1.7-fold increase in proximal tubule cell proliferation. In contrast, 17 alpha-estradiol, deoxoestrone, indanestrol, and 11 beta-methylestradiol, all weakly estrogenic and noncarcinogenic agents, had relatively little effect on tubule cell proliferation. The hydrolyzed Premarin exhibited a maximal 2.0-fold cell proliferative response at 10 nM. The present results provide clear evidence that, in the hamster kidney, the degree of carcinogenicity of a given estrogen correlates with its ability to induce proximal tubule cell proliferation in vitro.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1977

Determination of aqueous solubility and pKa values of estrogens.

Reported estrone pKa and solubility data show wide variation. Improved experimental procedures were designed and used to obtain reproducible results. The pKa values for several estrogens and related compounds also were determined to assess the effects of structural differences on ionization. No evidence was obtained for long-range D to A ring electronic transmission affecting pKa. Significant differences in pKa values resulted only when conjugated unsaturation was added into the B ring of estrone or estradiol. The aqueous solubilities of estrone and 17alpha-estradiol were 0.8 and 3.9 microgram/ml, respectively, at 25degrees.

Chemical Phenomena↗