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Interferon research abs 1 || Hemoglobin research abs || Stem cell research abs || Nucleic acid research abs || Herpes research abs || Bronchitis research abs || Schizophrenia research abs || Tuberculosis research abs || Pneumonia research abs || Constipation research abs || Laxative research abs || hair research abs || hair related research references || testosterone related research references

J Chromatogr A. 2002 Apr 19;954(1-2):199-206.
Artifact formation due to ethyl thio-incorporation into silylated steroid structures as determined in doping analysis.

van de Kerkhof DH, van Ooijen RD, de Boer D, Fokkens RH, Nibbering NM, Zwikker JW, Thijssen JH, Maes RA.

Department of Human Toxicology, Utrecht Institute of Pharmaceutical Sciences (UIPS), University of Utrecht, The Netherlands. d.h.vandekerkhoharm.uu.nl

Trimethylsilylation of target substances in a mixture of N-methyl-N-trimethylsilyltrifluoroacetamide (MSTFA), ammonium iodide and ethanethiol is frequently applied for the application of gas chromatography-mass spectrometry (GC-MS) in steroid analysis. However, artifacts were formed when using this mixture to silylate the steroids androsterone and etiocholanolone obtained from a urine matrix. The artifacts were identified as ethyl thio-containing products of the respective trimethylsilyl derivatives. The conversion of the studied products increased slowly as a function of time, was dependent on the presence of the urine matrix and was significantly accelerated by adding diethyl disulfide to the reagent before incubation. Also ethyl thio-incorporation into testosterone and epitestosterone was established. A mechanism for ethyl thio-incorporation is proposed. The conversion achieved after 120-h sample storage at room temperature was insufficient to significantly influence the analysis of androsterone and etiocholanolone under the studied conditions. However, the results provide fundamental insight into the mechanism of silylation and the occurring side-reactions. Moreover, when investigating the formation of new metabolites, the ethyl thio-incorporation can lead to misinterpretation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12058904&dopt=Abstract

Andrologia. 2002 Jun;34(3):172-6.
Distribution and function of FSH receptor genetic variants in normal men.

Asatiani K, Gromoll J, Eckardstein SV, Zitzmann M, Nieschlag E, Simoni M.

Institute of Reproductive Medicine of the University, Munster, Germany.

Follicle stimulating hormone (FSH) plays a key role in the maintenance of qualitatively and quantitatively normal spermatogenesis. It controls gamete development through Sertoli cells, via binding to its receptor. The influence and importance of FSH receptor (FSHR) variants on Sertoli cell function is not completely understood and remains to be investigated. In this retrospective study, we explored the impact and action of two distinct FSHR isoforms, Thr307/Asn680 and Ala307/Ser680, in a large group of men. This investigation includes 288 normal healthy men, 86 of whom were proven fathers previously studied, and 202 were newly recruited subjects. The FSHR polymorphism at position 680 was analyzed in the whole group, while position 307 was investigated in 150 subjects, both of them by single-stranded conformation polymorphism (SSCP) gel electrophoresis. The distribution frequency for position 680 was 29% for the Asn/Asn, 52% for the Asn-Ser, 19% for the Ser-Ser variant, and for position 307, 27% for the Thr-Thr, 55% for the Ala-Thr, 18% for the Ala-Ala, respectively. Polymorphism combinations that were different from Thr307/Asn680 - Ala307/Ser680 were found in four subjects. When subjects were grouped according to genotype at position 680, no significant differences between basal FSH, testosterone, inhibin B levels and semen parameters were found. This clinical finding demonstrates that, differently from females, in whom a significant correlation between FSHR polymorphism and basal FSH levels was found, the FSHR genotype has no influence on clinical parameters in males.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12059813&dopt=Abstract

Andrologia. 2002 Jun;34(3):180-7.
Primary culture of the rat epididymal epithelial cells as a source of oestrogen.

Wiszniewska B.

Department of Histology and Embryology, Pomeranian Academy of Medicine, 72 Powstancow Wlkp. St., 70-111 Szczecin, Poland. barbwisci.pam.szczecin.pl

Studies were performed on the rat epithelial cells of the caput and cauda epididymidis cultured in a full medium enriched with foetal calf serum without or with exogenous testosterone. After 3 days of culture, the cells formed a monolayer. The cytoplasm of epididymal epithelial cells cultured with testosterone was rich in lipid droplets, glycogen and PAS-positive substances, while their content was decreased in the cytoplasm of cells cultured without testosterone. The activity of 3beta-hydroxysteroid dehydrogenase was observed both in the cytoplasm of cultured epididymal epithelial cells and epithelial cells of epididymal sections. Hormone assays showed very low levels of dehydroepiandrosterone, androstenedione and testosterone, and the absence of progesterone in the media of cells cultured without testosterone and higher testosterone concentrations when the cells were cultured with exogenous testosterone. However, the concentration of 17beta-oestradiol found in the medium of cells was high, and exceeded many-fold its levels in the control media. Lentaron (Formestan), steroidal inhibitor of cytochrome P450 aromatase added to the culture decreased the secretion of oestradiol. RT-PCR analysis yielded cDNA products of 333 bp in length when primers were chosen to amplify a highly conserved sequence in the 3' region of the cytochrome P450 aromatase gene. This study demonstrates the ability of epididymal epithelial cells in vitro to synthesize androgens and mRNA for cytochrome P450 aromatase in the cultured epididymal epithelial cells of the rat as well as the ability to aromatise the synthesized androgen to 17beta-oestradiol.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12059815&dopt=Abstract

Andrologia. 2002 Jun;34(3):188-93.
Dexamethasone reduces acrosin activity of ram spermatozoa.

Tsantarliotou MP, Taitzoglou IA, Goulas P, Kokolis NA.

Department of Physiology, Faculty of Veterinary Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.

The aim of this study was to investigate the effect of dexamethasone on acrosin activity of spermatozoa in Chios rams during autumn (breeding season for sheep in Greece), in correlation with possible changes in blood testosterone. Dexamethasone was administered in four equal consecutive intramuscular injections, one every four hours (total dose: 3 mg kg(-1)). Total acrosin activity was determined in semen samples collected 48 h before and on the 4th and 7th day and thereafter once every week until the 77th day after dexamethasone administration. Blood samples for testosterone radioimmunoassays were collected 24 h before, during dexamethasone administration and on the 4th, 7th, 14th and 21st day after administration. Total acrosin activity in spermatozoa was reduced between days 7-28 after dexamethasone administration. Dexamethasone also induced a reduction in mean value and basal level of blood testosterone and inhibited its episodic secretion between 1 and 4 days after administration. As the reduction of acrosin activity appeared relatively soon after dexamethasone administration (7th day), it is likely that the increased amount of dexamethasone did not influence the synthesis of proacrosin in the late spermatids. As glucocorticoid receptors exist in the epididymis and accessory glands in various species, dexamethasone may have a direct influence on the synthesis and/or release of acrosin inhibitors in epididymal fluid or seminal plasma. These changes in acrosin activity in ovine spermatozoa mediated by dexamethasone may be of importance regarding the role of stress in the reduction of sperm fertilizing ability.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12059816&dopt=Abstract

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