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LH (S-type) Rat ELISA

  • Regulatory status:RUO
  • Type:Sandwich ELISA, Biotin-labelled antibody
  • Other names:Luteinizing hormone, Lutropin, Lutrophin
  • Species:Rat
Cat. No. Size Price


630-23929 96 wells (1 kit)
PubMed Product Details
Technical Data

Cat # changed from RSHAKRLH-010SR to 630-23929

Type

Sandwich ELISA, Biotin-labelled antibody

Applications

Serum, Plasma

Sample Requirements

10 µl/well

Shipping

At ambient temperature. Upon receipt, store the product at the temperature recommended below.

Storage/Expiration

Store the complete kit at 2–8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).

Calibration Curve

Calibration Range

0.313–10 ng/ml

Limit of Detection

31.3 pg/ml

Summary

Research topic

Reproduction, Animal studies

Summary

Luteinizing hormone (LH) is produced in both men and women from the anterior pituitary gland in response to luteinizing hormone-releasing hormone (LH-RH or Gn-RH), which is released by the hypothalamus. LH, also called interstitial cell-stimulating hormone (ICSH) in men, is a glycoprotein with a molecular weight of approximately 30.000 daltons. It is composed of two non covalently associated dissimilar amino acid chains, alpha and beta. The alpha chain is similar to that found in human thyroid-stimulating hormone (TSH), follicle stimulating hormone (FSH), and human chorionic gonadotropin (hCG). The difference between these hormones lie in the amino acid composition of their beta subunits, which account for their immunological differentiation. The basal secretion of LH in men is episodic and has the primary function of stimulating the interstitial cells (Leydig cells) to produce testosterone. The variation in LH concentrations in women is subject to the complex ovulatory cycle of healthy menstruating women, and depends upon a sequence of hormonal events along the gonado-hypothalamic-pituitary axis. The decrease in progesterone and estradiol levels from the preceeding ovulation initiates each menstrual cycle. As a result of the decrease in hormone levels, the hypothalamus increases the secretion of gonadotropin-releasing factors (GnRF), which in turn stimulates the pituitary to increase FSH production and secretion. The rising FSH levels stimulate several follicles during the follicular phase, one of these will mature to contain the egg. As the follicle develops, estradiol is secreted, slowly at first, but by day 12 or 13 of a normal cycle increasing rapidly. LH is released as a result of this rapid estradiol rise because of direct stimulation of the pituitary and increasing GnRF and FSH levels. These events constitute the preovulatory phase. Ovulation occurs approximately 12 to 18 hours after the LH reaches a maximum level. After the egg is released, corpus luteum is formed which secretes progesterone and estrogen – two feedback regulators of LH. The luteal phase rapidly follows this ovulatory phase, and is characterized by high progesterone levels, a second estradiol increase, and low LH and FSH levels. Low LH and FSH levels are the result of the negative feedback effects of estradiol and progesterone on the hypotalamic-pituitary axis. After conception, the developing embryo produces hCG, which causes the corpus luteum to continue producing progesterone and estradiol. The corpus luteum regresses if pregnancy does not occur, and the corresponding drop in progesterone and estradiol levels results in menstruation. The hypothalamus initiates the menstrual cycle again as a result of these low hormone levels. Patients suffering from hypogonadism show increased concentrations of serum LH. A decrease in steroid hormone production in females is a result of immature ovaries, primary ovarian failure, polycystic ovary disease, or menopause; in these cases, LH secretion is not regulated. A similar loss of regulatory hormones occurs in males when the testes develop abnormally or anorchia exists. High concentrations of LH may also be found in primary testicular failure and Klinefelter syndrome, although LH levels will not necessarily be elevated if the secretion of androgens continues. Increased concentrations of LH are also present during renal failure, cirrhosis, hyperthyroidism, and severe starvation. A lack of secretion by the anterior pituitary may cause lower LH levels. As may be expected, low levels may result in infertility in both males and females. Low levels of LH may also be due to the decreased secretion of GnRH by the hypothalamus, although the same effect may be seen by a failure of the anterior pituitary to respond to GnRH stimulation. Low LH values may therefore indicate some dysfunction of the pituitary or hypothalamus, but the actual source of the problem must be confirmed by other tests. In the differential diagnosis of h

Product References (5)

References

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Summary References (22)

References to LH

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  • Boyar R, Finkelstein J, Roffwarg H, Kapen S, Weitzman E, Hellman L. Synchronization of augmented luteinizing hormone secretion with sleep during puberty. N Engl J Med. 1972 Sep 21;287 (12):582-6
  • Cohen KL. Metabolic, endocrine, and drug-induced interference with pituitary function tests: a review. Metabolism. 1977 Oct;26 (10):1165-77
  • Cumming DC, Reid RL, Quigley ME, Rebar RW, Yen SS. Evidence for decreased endogenous dopamine and opioid inhibitory influences on LH secretion in polycystic ovary syndrome. Clin Endocrinol (Oxf). 1984 Jun;20 (6):643-8
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  • Ferin M, Van Vugt D, Wardlaw S. The hypothalamic control of the menstrual cycle and the role of endogenous opioid peptides. Recent Prog Horm Res. 1984;40:441-85
  • Harris GW, Naftolin F. The hypothalamus and control of ovulation. Br Med Bull. 1970 Jan;26 (1):3-9
  • Hoff JD, Quigley ME, Yen SS. Hormonal dynamics at midcycle: a reevaluation. J Clin Endocrinol Metab. 1983 Oct;57 (4):792-6
  • Hoff JD, Quigley ME, Yen SS. Hormonal dynamics at midcycle: a reevaluation. J Clin Endocrinol Metab. 1983 Oct;57 (4):792-6
  • Hosseinian AH, Kim MH. Predetermination of ovulation timing by luteinizing hormone assay. Fertil Steril. 1976 Apr;27 (4):369-74
  • Jeffcoate SL. The control of testicular function in the adult. Clin Endocrinol Metab. 1975 Nov;4 (3):521-43
  • Knobil E. The neuroendocrine control of the menstrual cycle. Recent Prog Horm Res. 1980;36:53-88
  • Krieger DT. Placenta as a source of 'brain' and 'pituitary' hormones. Biol Reprod. 1982 Feb;26 (1):55-71
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  • Pierce JG, Parsons TF. Glycoprotein hormones: structure and function. Annu Rev Biochem. 1981;50:465-95
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  • Ross GT, VandeWeile RL, Frantz AG. Chapter 7 in "The Ovaries and the Breasts" in "Textbook of Endocrinology" (R. H. Williams, Ed.), W.B. Saunders Co. 1981;
  • Shome B, Parlow AF. Human follicle stimulating hormone (hFSH): first proposal for the amino acid sequence of the alpha-subunit (hFSHa) and first demonstration of its identity with the alpha-subunit of human luteinizing hormone (hLHa). J Clin Endocrinol Metab. 1974 Jul;39 (1):199-202
  • Simpson ER, MacDonald PC. Endocrine physiology of the placenta. Annu Rev Physiol. 1981;43:163-88
  • Uotila M, Ruoslahti E, Engvall E. Two-site sandwich enzyme immunoassay with monoclonal antibodies to human alpha-fetoprotein. J Immunol Methods. 1981;42 (1):11-5
  • Whitley RJ, Keutmann HT, Ryan RJ. Studies on the isolation and chemical-physical properties of porcine follicle-stimulating hormone. Endocrinology. 1978 Jun;102 (6):1874-86
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