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J Mol Biol. 2002 May 3;318(3):621-6.
Resolution of a disordered region at the entrance of the human sex hormone-binding globulin steroid-binding site.

Grishkovskaya I, Avvakumov GV, Hammond GL, Muller YA.

Forschungsgruppe Kristallographie, Max-Delbruck-Centrum fur Molekulare Medizin, 13092 Berlin, Germany.

The crystal structure of human sex hormone-binding globulin (SHBG) has revealed how 5alpha-dihydrotestosterone intercalates between the two seven-stranded beta-sheets of its amino-terminal laminin G-like domain. However, a region of disorder (residues 130 to 135 of SHBG) was identified together with a zinc-binding site in immediate proximity to the steroid. It has been important to resolve the structure of this region because previous studies have suggested that these residues may contribute to steroid binding directly. Here, we present the 2.35 A and 1.7 A crystal structures of the amino-terminal LG domain of SHBG obtained from a tetragonal crystal form and by EDTA-soaking of a trigonal crystal form, respectively. In both of these new structures, residues Pro130 to Arg135 are now clearly visible. Substitution of the two residues (Leu131Gly and Lys134Ala) pointing towards the steroid has shown that only Leu131 contributes significantly to steroid binding. Rather than covering the steroid-binding pocket in an extended conformation, a 3(10) helical turn is formed by residues Leu131 to Lys134 in this segment. Unfolding of this secondary structure element can either facilitate the entry of the steroids into the binding site or modulate the important contribution that Leu131 makes to steroid binding. A comparison with previous structures supports the concept that zinc binding re-orients the side-chain of His136, and this residue serves as a lever causing disorder within the loop structure between Pro130 and Arg135. (c) 2002 Elsevier Science Ltd.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12054810&dopt=Abstract

J Mol Cell Cardiol. 2002 Jun;34(6):679-88.
Epiandrosterone, a metabolite of testosterone precursor, blocks L-type calcium channels of ventricular myocytes and inhibits myocardial contractility.

Gupte SA, Tateyama M, Okada T, Oka M, Ochi R.

Department of Physiology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8412, Japan. sachin_guptahoo.com

The dehydroepiandrosterone metabolite epiandrosterone (EPI) inhibits the pentose phosphate pathway (PPP) and dilates isolated blood vessels pre-contracted by partial depolarization. We found that EPI (10-100 microM) also dose-dependently decreases left-ventricular developed pressure (LVDP), the rate of myocardial contraction (+d p /d t), and the pressure rate product (PRP); at 100 microM EPI, LVDP (131+/-9 vs 34+/-7 mmHg), +d p /dt (1515+/-94 vs 542+/-185 mmHg/s), and PRP (37870+/-2471 vs 9498+/-2375 HR x mmHg/min) were all significantly (P<0.05) reduced. EPI also elevated CPP in isolated hearts, decreased levels of myocardial NADPH and nitrite, and dose-dependently relaxed rat aortic rings pre-contracted with KCl. Electrophysiological analysis of single ventricular myocytes using whole cell clamp showed EPI to dose-dependently (100 n M-100 microM) and reversibly inhibit L-type channel currents carried by Ba2+ (IBa) (IC50=42+/-6 microM) by as much as 50%. At 30 microM, EPI shifted the steady-state inactivation curve to more negative potentials (V50=-26.6 mV vs -38.0 mV), thereby accelerating the decay of IBa during depolarization. These results suggest that EPI may act as a L-type Ca2+ channel antagonist with properties similar to those of 1,4-dihydropyridine (DHP) Ca2+ channel blockers. 2002 Elsevier Science Ltd. All rights reserved.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12054855&dopt=Abstract [PubMed - in process]

Prostaglandins Leukot Essent Fatty Acids. 2002 Apr;66(4):419-25.
Effect of fatty acids on estradiol and testosterone binding to whole DU-145 prostate cells.

Prinsloo SE, van Aswegen CH.

Wolmarans Research Laboratory, Department of Urology, University of Pretoria, Pretoria, South Africa. smulleoshllion.up.ac.za

Cancer of the prostate is one of the leading causes of cancer related deaths in men. An important role in the development of prostate cancer is played by androgens and androgen ablation is therefore currently used in cancer treatment. In the past, estrogens were widely used in treatment of prostate cancer, but there are indications that estrogens could also be involved in carcinogenesis. Lately, much research has been done on the modulation of the binding of steroid hormones to their receptors by polyunsaturated fatty acids (PUFAs), which could interfere with the steroid hormone's message. Therefore, the aim of this study was to determine in whole DU-145 human prostate cells the effect of EFAs and their metabolites on the binding and affinity of the estrogen receptor (ER) and androgen receptor (AR) to estradiol (E(2)) and testosterone (T), respectively. Fatty acids were dissolved in ethanol and added to the cell culture in a final ethanol concentration of 0.2% on the fourth day of incubation. The results showed that the PUFAs under investigation inhibited the AR's capacity, in contrast to the ER's capacity which was stimulated. However, the dissociation constants (K(d)) of the AR and ER complexes in the presence of the PUFAs, were as follows. Except for eicosapentaenoic acid (EPA) which decreased the AR dissociation constant and EPA and alpha-linolenic acid (ALA) which increased the ER dissociation constant, the remaining FAs had no significant effect on the K(d) values of both the AR and ER complexes. According to these priliminary results it is postulated that men should benefit with a diet rich in certain essential polyunsaturated fatty acids although its function remains to be clarified. 2002 Elsevier Science Ltd. All rights reserved.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12054912&dopt=Abstract

Nutr Metab Cardiovasc Dis. 2001 Dec;11(6):388-93.
Adrenal C19 steroids and serum lipoprotein levels in healthy men.

Vatalas IA, Dionyssiou-Asteriou A.

Department of Biological Chemistry Medical School, Athens University, Greece. jvatabn.gr

BACKGROUND AND AIM: It has become apparent that dehydroepiandrosterone (DHEA) plays a protective role in atherosclerosis, but its influence on serum lipids has not yet been clarified. The aim of this study was to evaluate the association of endogenous adrenal C19 steroid hormones [(DHEA) and androstenedione (ASD)] and serum lipoprotein levels. METHODS AND RESULTS: The serum concentrations of dehydroepiandrosterone sulphate (DHEA-S), ASD, total and free testosterone, estradiol, total cholesterol, LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C), triglycerides, apolipoprotein AI (ApoAI) and apolipoprotein B100 (ApoB100) were measured in a sample of 88 healthy men. Statistical analysis using Spearman's correlation coefficient showed a positive correlation between DHEA-S levels and ApoAI (p = 0.034), a negative correlation between ASD and triglycerides (p = 0.005), a positive correlation between ASD and LDL-C (p = 0.005), and a negative correlation between estradiol and HDL-C (p = 0.042). Multiple regression analysis revealed that DHEA-S is an independent factor for ApoAI, ASD an independent factor for triglycerides and LDL-C, and age an independent factor for ApoB100; estradiol was found to be a suggestive factor for HDL. CONCLUSIONS: The results suggest that the plasma levels of DHEA-S and ASD (adrenal C19 steroid hormones) correlate with the plasma lipid profiles of healthy men. It remains to be seen whether this profile is favourable.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12055703&dopt=Abstract

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DHEA is a natural hormone, and it is produced in our body by the adrenal glands. DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells. Our bodies produce decreasing amount of DHEA as we get older. various health benefits: To deter aging, improve sexual function/erectile dysfunction, treat cognitive decline, enhance athletic performance, facilitate weight loss, improve strength, prevent osteoporosis, enhance immunomodulation for rheumatic conditions, and treat depression.

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