Disease relevance of equilin

• Finally, preliminary studies conducted with the human breast tumor cell line MCF-7 demonstrated that the cytotoxic effects of the catechol estrogens from estrone, equilin, and 2-hydroxyequilenin were similar, whereas 4-hydroxyequilenin was a much more potent cytotoxin ( approximately 30-fold) [1].

High impact information on equilin

• The result demonstrates that binding of equilin at the active site of 17beta-HSD1 is the basis for inhibition of E1-to-E2 reduction by this equine estrogen in vitro [2].
• 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 [3].
• Real-time quantitative PCR revealed that retinaldehyde dehydrogenase (RALDH) 2, a critical enzyme in RA biosynthesis, was induced 4-fold by estrogen replacement therapy with either Premarin or a mixture of estrone and equilin sulfates for 3 months [4].
• These results indicate that 17 beta-EqS is cleared twice as fast as equilin sulfate (MCR, 176 L/day.m2), whereas the more potent estrogen 17 beta-Eq is cleared 2 times slower than equilin [5].
• Metabolic clearance rate of equilin sulfate and its conversion to plasma equilin, conjugated and unconjugated equilenin, 17 beta-dihydroequilin, and 17 beta-dihydroequilenin in normal postmenopausal women and men under steady state conditions [6].

Biological context of equilin

• The crystal structure determined at 3.0-A resolution reveals that the equilin molecule is bound at the active site in a mode similar to the binding of substrate [2].
• Pharmacokinetics of equilin and equilin sulfate in normal postmenopausal women and men [7].
• If equilin is added before hydrolysis, variable destruction takes place [8].
• Although equilin increased in later gestation, oestrone remained the major product [9].

Anatomical context of equilin

• A fetal gonad--placental system is proposed for equilin production, 3 beta-hydroxy-5,7-pregnadien-20-one being a precursor for 3 beta-hydroxy-5,7-androstadien-17-one in the fetal gonad and the latter being the precursor of equilin in the placenta [10].
• Equilin induced highly significant increases in the growth of both the macro and micro features of cortical nerve cell morphology [11].
• Analysis of the regional selectivity of equilin-induced neurotrophism in the cerebral cortex demonstrated that equilin significantly increased the growth of neurons from the frontal, temporal, and occipital regions, with neurons from the parietal region also influenced, though more modestly [11].
• In the human endometrium, equilin is metabolized to 2-hydroxy and 4-hydroxy equilin, with 2-hydroxylation being predominant [12].
• Unlike endogenous catechol estrogens, both equilin and equilenin were primarily converted by rat liver microsomes to 4-hydroxylated rather than 2-hydroxylated o-quinone GSH conjugates [1].

Associations of equilin with other chemical compounds

• In this communication we have shown that equine estrogens (especially equilin) exhibit higher antioxidant potency (as measured by fatty acids and sterols oxidation) when compared to estrone and estradiol-17 beta [13].
• In contrast with Eq and E1, only the low affinity binding sites were found (apparent Ka congruent to 1 X 10(4) M-1) [14].
• The two-state excited-state proton-transfer process for d-equilenin [d-3-hydroxyestra-1,3,-5(10),6,8-pentaen-17-one] and dihydroequilenin is found to depend both on pH and on proton acceptor concentration [15].

Gene context of equilin

• Mixtures of estradiol and six equine estrogens, including equilin, equilenin, 8,9-dehydroestrone, and their 17beta-hydroxyl derivatives, were assayed simultaneously to determine their relative binding to human ER-alpha and ER-beta [16].
• The half-life of equilin was approximately 19-27 min, and the MCR of equilin was calculated to be 1982 liters/day/m2 in the normal man and 3300 liters/day/m2 in the normal postmenopausal woman [7].
• EST/ISH cells were approximately 3-10-fold less sensitive to the equine estrogens equilin and 17-equilin as compared to control cells [17].
• 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 [18].

Analytical, diagnostic and therapeutic context of equilin

• A radioimmunoassay for equilin in equine pregnancy plasma [19].
• Effect of temperature on separation of estradiol stereoisomers and equilin by liquid chromatography using mobile phases modified with beta-cyclodextrin [20].
• A high-performance liquid chromatographic (HPLC) method with fluorescence detection (lambda(ex) = 280 nm; lambda(em) = 410 and 312 nm) in combination with a post-column on-line photochemical derivatization is described for the determination of equilin and equilenin in urine from normal postmenopausal women after therapy with conjugated oestrogens [21].
• A radioimmunoassay for equilin in post-menopausal plasma: plasma levels of equilin determined after oral administration of conjugated equine oestrogens (premarin) [22].

References