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Dehydroepiandrosterone (DHEA) ELISA

Catalog no.RE52221
Regulatory Status
RUO
Kit size
12 x 8
Method
ELISA
Incubation time
1 x 1 h; 1 x 30 min
Standard range
0.37 - 30 ng/mL
Specimen / Volumes
20 µL Serum
Substrate / isotope
TMB 450 nm
instructions for usecertificate

Dehydroepiandrosterone (DHEA) ELISA Enzyme immunoassay for the quantitative determination of Dehydroepiandrosterone (DHEA) in human serum. Dehydroepiandrosterone (DHEA; androstenolone; 3b-hydroxy-5-androsten-17-one) is a C19 steroid produced in the adrenal cortex and, to a lesser extent, gonads. DHEA serves as a precursor in testosterone and estrogen synthesis. Due to the presence of a 17-oxo (rather than hydroxyl) group, DHEA has relatively weak androgenic activity, which has been estimated at ~10 % that of testosterone. However in neonates, peripubertal children and in adult women, circulating DHEA levels may be several-fold higher than testosterone concentrations, and rapid peripheral tissue conversion to more potent androgens (androstenedione and testosterone) and estrogens may occur. Moreover, DHEA has relatively low affinity for sex-hormone binding globulin. These factors may enhance the physiologic biopotency of DHEA. The physiologic role of DHEA has not been conclusively defined. A variety of in vitro effects, including antiproliferative effects in different cell lines and effects on enzyme-mediated cell metabolism, have been reported. In vivo studies suggest that DHEA may affect cholesterol and lipid metabolism, insulin sensitivity and secretion and immune function.

For concrete data please consult the Instruction for Use in the download box on the top right side.

(1) Kroboth, P. D., Salek, F. S., Pittenger, A. L., Fabian, T. J., & Frye, R. F. DHEA and DHEA‐S: A Review. J. Clin. Pharmacol. 1999, 39 (4),), 327-348. (2) Flier, J. S., & Foster, D. W. Eating Disorders: Obesity, Anorexia Nervosa, and Bulimia Nervosa. Williams Textbook of Endocrinology. Williams Textb. Endocrinol. Eat. Disord. obesity, Anorex. Nerv. Bulim. Nerv. Saunders, Philadelphia, PA. 1998. (3) Baulieu, E. E.; Robel, P. Dehydroepiandrosterone (DHEA) and Dehydroepiandrosterone Sulfate (DHEAS) as Neuroactive Neurosteroids. Proc. Natl. Acad. Sci. U. S. A. 1998, 95 (8), 4089–4091. https://doi.org/10.1073/pnas.95.8.4089. (4) Heaney, J. L. J.; Phillips, A. C.; Carroll, D. Ageing, Physical Function, and the Diurnal Rhythms of Cortisol and Dehydroepiandrosterone. Psychoneuroendocrinology 2012, 37 (3), 341–349. https://doi.org/10.1016/j.psyneuen.2011.07.001. (5) Al-Turk, W., & Al-Dujaili, E. A. Effect of Age, Gender and Exercise on Salivary Dehydroepiandrosterone Circadian Rhythm Profile in Human Volunteers. Steroids, 2016, 106, 19–25. (6) Guilliams, T. The Role of Stress and the HPA Axis in Chronic Disease Management. Point Inst. 2018, 80. (7) Guilliams, T. G.; Edwards, L. Chronic Stress and the HPA Axis: Clinical Assessment and Therapeutic Considerations. Stand. 2010, 9 (2), 1–12. (8) Shoback, D., & Gardner, D. G. (Eds. ). Greenspan’s Basic & Clinical Endocrinology. McGraw-Hill Educ. 2018. (9) El-Gharib, M.; El-Din Hazaa, S. Salivary versus Serum Approaches in Assessment of Biochemical Hyperandrogenemia. J. Basic Clin. Reprod. Sci. 2014, 3 (1), 54. https://doi.org/10.4103/2278-960x.129283. (10) Berg, G.; Wagner-Doebler, I.; Maree Burke, C.; Lindheim, L.; Bashir, M.; Münzker, J.; Trummer, C.; Zachhuber, V.; Pieber, T. R.; Gorkiewicz, G.; Obermayer-Pietsch, B. The Salivary Microbiome in Polycystic Ovary Syndrome (PCOS) and Its Association with Disease-Related Parameters: A Pilot Study. Front. Microbiol. | www.frontiersin.org 2016, 1, 1270. https://doi.org/10.3389/fmicb.2016.01270. (11) Tock, L.; Carneiro, G.; Pereira, A. Z.; Tufik, S.; Zanella, M. T. Adrenocortical Production Is Associated with Higher Levels of Luteinizing Hormone in Nonobese Women with Polycystic Ovary Syndrome. Int. J. Endocrinol. 2014, 2014. https://doi.org/10.1155/2014/620605. (12) King, J. A.; Wisniewski, A. B.; Bankowski, B. J.; Carson, K. A.; Zacur, H. A.; Migeon, C. J. Long-Term Corticosteroid Replacement and Bone Mineral Density in Adult Women with Classical Congenital Adrenal Hyperplasia. J. Clin. Endocrinol. Metab. 2006, 91 (3), 865–869. https://doi.org/10.1210/jc.2005-0745. (13) Migeon CJ, W. A. Congenital Adrenal Hyperplasia Owing to 21-Hydroxylase Deficiency. Endocrinol Metab Clin North Am 2001, 30:, 193–206.

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