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Synthesis, Enzyme Localization, and Regulation of Neurosteroids
Published in Sheryl S. Smith, Neurosteroid Effects in the Central Nervous System, 2003
ovary, J. Clin. Endocrinol. Metab., 74, 994-998, 1992. Ukena, K., Kohchi, C., and Tsutsui, K., Expression and activity of 3beta-hydroxysteroid dehydrogenase/delta5-delta4-isomerase in the rat Purkinje neuron during neonatal life, Endocrinology, 140, 805-813, 1999.Coirini, H., Gouezou, M., Liere, P., Delespierre, B., Pianos, A., Eychenne, B., Schumacher, M., and Guennoun, R., 3 Beta-hydroxysteroid dehydrogenase expression in rat spinal cord, Neuroscience, 113, 883-891, 2002.Mensah-Nyagan, A.G., Feuilloley, M., Dupont, E., Do-Rego, J.L., Leboulenger, F., Pelletier, G., and Vaudry, H., Immunocytochemical localization and biological activity of 3 beta-hydroxysteroid dehydrogenase in the central nervous system of the frog, J. Neurosci., 14, 7306-7318, 1994.Mathieu, M., Mensah-Nyagan, A.G., Vallarino, M., Do-Rego, J.L., Beaujean, D., Luu-The, V., Pelletier, G., and Vaudry, H., Immunohistochemical localization of 3P-hydroxyseroid dehydrogenase and 5α reductase in the brain of the African lungfish Protopterus amnectens, J. Comp. Neurol., 2000, submitted.Sanne, J.L. and Krueger, K.E., Expression of cytochrome P450 side-chain cleavage enzyme and 3 beta-hydroxysteroid dehydrogenase in the rat central nervous system: a study by polymerase chain reaction and in situ hybridization, J. Neurochem., 65,
Oocyte Survival and Development during Follicle Formation and Folliculogenesis in Mice Lacking Aromatase
Published in Endocrine Research, 2022
Jessica M. Toothaker, Kristen Roosa, Alexandra Voss, Suzanne M. Getman, Melissa E. Pepling
There is some evidence supporting the idea that estrogen synthesized by fetal ovaries may play a role in maintaining oocytes in cysts. First, the fetal mouse ovary is capable of synthesizing its own estrogen. Estradiol was detected in the ovaries of fetal mice along with the enzymes aromatase and 3beta hydroxysteroid dehydrogenase (3βHSD), which are required for the biosynthesis of estradiol.19 Second, when fetal mouse ovaries were grown in culture in the absence of estrogen, cyst breakdown, and follicle formation were accelerated as compared to in vivo.17 In addition, if the estrogen that inhibits cyst breakdown is derived from the maternal circulation, one would expect the initiation of cyst breakdown to coincide with a decrease in circulating maternal estrogen. In mice, the initiation of cyst breakdown begins at 17.5 dpc, however a rapid decrease in maternal estrogen is not observed until the day of birth.19 Furthermore, the capacity for fetal ovaries to secrete estradiol has been observed in other species, such as cattle.20 However, when fetal ovaries were cultured during the time of cyst breakdown and follicle formation in the presence of letrozole, an aromatase inhibitor, to eliminate any production of estrogen by the fetal ovary, cyst breakdown and follicle formation was not affected.19 These findings indicate that a source of estrogen apart from the fetal ovary regulates follicle formation.
The Role of Genetic Variants in the Association between Dietary Acrylamide and Advanced Prostate Cancer in the Netherlands Cohort Study on Diet and Cancer
Published in Nutrition and Cancer, 2018
Andy Perloy, Leo J. Schouten, Piet A. van den Brandt, Roger Godschalk, Frederik-Jan van Schooten, Janneke G. F. Hogervorst
The SNPs (n = 60) we selected were in the following genes: aldo-keto reductase family 1, member C1 (AKR1C1), aldo-keto reductase family 1, member C2 (AKR1C2), catalase (CAT), catechol-O-methyltransferase (COMT), cytochrome P450 family 1 subfamily A member 1 (CYP1A1), cytochrome P450 family 1 subfamily A member 2 (CYP1A2), cytochrome P450 family 1 subfamily B member 1 (CYP1B1), cytochrome P450 family 11 subfamily A member 1 (CYP11A1), cytochrome P450 family 17 subfamily A member 1 (CYP17A1), cytochrome P450 family 19 subfamily A member 1 (CYP19A1), cytochrome P450 2E1 (CYP2E1), epoxide hydrolase 1 (EPHX1), estrogen receptor 1 (ESR1), estrogen receptor 2 (ESR2), glutathione peroxidase 1 (GPX1), glutathione S-transferase alpha 5 (GSTA5), glutathione S-transferase P1 (GSTP1), hydroxysteroid (17-beta) dehydrogenase 3 (HSD17B3), 3beta-hydroxysteroid dehydrogenase (HSD3B1/B2), MGC12965, mutY DNA glycosylase (MUTYH), nuclear factor kappa B subunit 1 (NFKB1), nitric oxide synthase 2 (NOS2), NAD(P)H quinone dehydrogenase 1 (NQO1), 8-oxoguanine DNA glycosylase 1 (OGG1), progesterone receptor (PGR), prostaglandin-endoperoxide synthase 2 (PTGS2), ribonucleotide reductase regulatory subunit M2 (RRM2), sex hormone binding globulin (SHBG), solute carrier family 7 (cationic amino acid transporter, y+ system), member 11 (SLC7A11), superoxide dismutase 1 (SOD1), superoxide dismutase 2 (SOD2), steroid 5 alpha-reductase 1 (SRD5A1), sulfotransferase family 1A member 1 (SULT1A1), sulfotransferase family 1E member 1 (SULT1E1), thioredoxin (TXN), UDP glucuronosyltransferase family 1 member A6-10 (UGT1A6-10), xeroderma pigmentosum, complementation group C (XPC), and x-ray repair complementing defective repair in Chinese hamster cells 1 (XRCC1).