Key Features and Values
- Same sample type can be used across all assays to simplify inclusion into routine serology work-up
- Ready to use reagents reduces hands-on time for assay preparation
- Long shelf life cost-effective solution by reducing wastage due to expired kits
- Suitable for inclusion on automated plate systems simplifies scale-up of test volume
- Supported by a complete panel of assays for supporting treatment monitoring of several forms of hormonal dysfunctions
FSH ELISA kit is a direct solid phase immunoassay for the quantitative determination of Follicle-Stimulating Hormone (FSH) in human serum or plasma. FSH ELISA kit is intended for laboratory use only.
Follicle Stimulating Hormone (FSH) is a glycoprotein consisting of two subunits with an approximate molecular mass of 35,500 daltons. The α- subunit is similar to other pituitary hormones [luteinising stimulating hormone (LH), thyroid stimulating hormone (TSH) and chorionic gonadotropin (hCG)] while the β-subunit is unique. The β- subunit confers the biological activity to the molecule. Stimulation by gonadotropin-releasing hormone (GnRH) causes release of FSH, as well as LH, from the pituitary and is transported by the blood to their sites of action, the testes or ovary.
In men, FSH acts on the Sertoli cells of the testis, stimulating the synthesis of inhibin, which appears to specifically inhibit further FSH secretion and androgen-binding protein. Thus, it indirectly supports spermatogenesis. In women, FSH acts on the granulosa cells of the ovary, stimulatin steroidogensis. All ovulatory menstrual cycles have a characteristic pattern of FSH, as well as LH, secretion. The menstrual cycle is divided into a follicular phase and a luteal phase by the midcycle surge of the gonadotropins (LH and FSH). As the follicular phase progresses, FSH concentration decreases. Near the time ovulation occurs, about midcycle, FSH peaks (lesser in magnitude than LH) to its highest level. The clinical usefulness of the measurement of Follicle Stimulating Hormone (FSH) in ascertaining the homeostasis of fertility regulation via the hypothalamic – pituitary – gonadal axis has been well established1-2.
1. Odell, W.D., Parlow, A.F., et al, J Clin Invest, 47, 2551 (1981).
2. Saxema, B.B., Demura, H.M., et al, J Clin Endocrinol Metab., 28, 59 (1968).
3. Wennink JM, Delemarre-van de Waal HA, Schoemaker R, Schoemaker H, Schoemaker J. 1990 Luteinizing hormone and follicle stimulating hormone secretion patterns in girls throughout puberty measured using highly sensitive immunoradiometric assays. Clin Endocrinol (Oxf). 33:333–344.
4. Winter JS, Faiman C. 1973 The development of cyclic pituitarygonadal function in adolescent females. J Clin Endocrinol Metab. 37:714–718.
5. Simoni M, Gromoll J, Nieschlag E 1997 The follicle stimulating hormone receptor: biochemistry, molecular biology, physiology and pathophysiology. Endocr Rev 18:739–773.
6.Vitt UA, Kloosterboer HJ, Rose UM, Mulders JW, Kiesel PS, Bete S, Nayudu PL 1998 Isoforms of human recombinant folliclestimulating hormone:comparison of effects on murine follicle development in vitro. Biol Reprod 59:854–861.
7. Layman LC, Lee EJ, Peak DB, Namnoum AB, Vu KV, van Lingen BL, Gray MR, McDonough PG, Reindollar RH, Jameson JL 1997 Delayed puberty and hypogonadism caused by mutations in the follicle stimulating hormone ß subunit gene. N Engl J Med 337:607–611.
8. Robertson DR 1991 Circulating half-lives of follicle stimulating hormones and luteinizing hormone in pituitary extracts and isoform fractions of ovariectomized and intact ewes. Endocrinology 129:1805– 1813.
9. Wide L 1981 Electrophoretic and gel chromatographic analyses of follicle stimulating hormone in human serum. Ups J Med Sci 86:249–258.
10. Berger P, Bidart JM, Delves PS, Dirnhofer S, Hoermann R, Isaacs N,Jackson A, Klonisch T, Lapthorn A, Lund T, Mann K, Roitt I, SchwarzS, Wick G 1996 Immunochemical mapping of gonadotropins. Mol Cell Endocrinol 125:33–43.