Melatonin-induced increase in cytoplasmic estrogen receptor activity in hamster uteri

D. N. Danforth, L. Tamarkin, R. Do, Marc E Lippman

Research output: Contribution to journalArticle

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Abstract

The pineal gland hormone, melatonin, has been shown to influence the growth and metabolism of uterine tissue in the Syrian hamster. Because the uterus is an estrogen-responsive target tissue, we studied the effect of melatonin on the unoccupied estrogen receptor (ER) activity of immature hamster uteri in vivo and in vitro. A single sc injection of 2.5 melatonin increased the ER activity of uterine cytosol (R(c) 30% within 60 min [from 147.4 ± 14.1 (SE), to 191.8 ± 18.5 fmol/mg protein]. Scatchard analysis showed the induced population of receptor to be homogenous and of high affinity, with an equilibrium dissociation constant (K(d) = 0.08 nM) similar to that for uteri for vehicle-treated animals. The induction of R(c) by melatonin persisted for 90 min, but R(c) returned to control levels by 2 h after injection. Scatchard analysis of unoccupied nuclear receptor showed no significant differences either in the quantity of receptor (vehicle = 379.7 ± 46.7, melatonin = 396.9 ± 76.7 fmol/mg protein) or in the K(d) vehicle = 0.75 nM, melatonin = 0.60 nM) between these two groups. In vitro incubation of fresh whole uteri for 60 min in media containing 10-5 M melatonin increased R(c) by 83% (from 41.3 ± 10.7 to 75.4 ± 11.0 fmol/mg protein), supporting a direct effect of melatonin on uterine tissue. The R(c) induced by melatonin both in vivo in vitro was sensitive to the degree of homogenization used in preparation of the cytosol. Whereas conservative homogenization (two 10-sec bursts with an intermittent 40-sec cooling period) of uteri from melatonin-treated animals was associated with a significant increase in R(c), homogenization for 60 sec without intermittent cooling showed a significant decrease (from 251.1 ± 17.4 to 182.7 ± 5.8 fmol/mg protein) as compared with uteri from vehicle-treated animals. Whole organ analysis of uteri from animals injected with melatonin followed by [3H]estradiol, in which no homogenization was used, demonstrated a 26% increase in R(c) specific binding, confirming induction as the primary response to melatonin. These findings demonstrate the ability of melatonin to modulate ER activity in hamster uteri, and may help explain the effects of melatonin on uterine growth and metabolism.

Original languageEnglish
Pages (from-to)81-85
Number of pages5
JournalEndocrinology
Volume113
Issue number1
StatePublished - Jan 1 1983
Externally publishedYes

Fingerprint

Melatonin
Cytoplasmic and Nuclear Receptors
Cricetinae
Estrogen Receptors
Uterus
Cytosol
Proteins
Injections
Pineal Gland
Mesocricetus
Growth
Estradiol
Estrogens

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Danforth, D. N., Tamarkin, L., Do, R., & Lippman, M. E. (1983). Melatonin-induced increase in cytoplasmic estrogen receptor activity in hamster uteri. Endocrinology, 113(1), 81-85.

Melatonin-induced increase in cytoplasmic estrogen receptor activity in hamster uteri. / Danforth, D. N.; Tamarkin, L.; Do, R.; Lippman, Marc E.

In: Endocrinology, Vol. 113, No. 1, 01.01.1983, p. 81-85.

Research output: Contribution to journalArticle

Danforth, DN, Tamarkin, L, Do, R & Lippman, ME 1983, 'Melatonin-induced increase in cytoplasmic estrogen receptor activity in hamster uteri', Endocrinology, vol. 113, no. 1, pp. 81-85.
Danforth DN, Tamarkin L, Do R, Lippman ME. Melatonin-induced increase in cytoplasmic estrogen receptor activity in hamster uteri. Endocrinology. 1983 Jan 1;113(1):81-85.
Danforth, D. N. ; Tamarkin, L. ; Do, R. ; Lippman, Marc E. / Melatonin-induced increase in cytoplasmic estrogen receptor activity in hamster uteri. In: Endocrinology. 1983 ; Vol. 113, No. 1. pp. 81-85.
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abstract = "The pineal gland hormone, melatonin, has been shown to influence the growth and metabolism of uterine tissue in the Syrian hamster. Because the uterus is an estrogen-responsive target tissue, we studied the effect of melatonin on the unoccupied estrogen receptor (ER) activity of immature hamster uteri in vivo and in vitro. A single sc injection of 2.5 melatonin increased the ER activity of uterine cytosol (R(c) 30{\%} within 60 min [from 147.4 ± 14.1 (SE), to 191.8 ± 18.5 fmol/mg protein]. Scatchard analysis showed the induced population of receptor to be homogenous and of high affinity, with an equilibrium dissociation constant (K(d) = 0.08 nM) similar to that for uteri for vehicle-treated animals. The induction of R(c) by melatonin persisted for 90 min, but R(c) returned to control levels by 2 h after injection. Scatchard analysis of unoccupied nuclear receptor showed no significant differences either in the quantity of receptor (vehicle = 379.7 ± 46.7, melatonin = 396.9 ± 76.7 fmol/mg protein) or in the K(d) vehicle = 0.75 nM, melatonin = 0.60 nM) between these two groups. In vitro incubation of fresh whole uteri for 60 min in media containing 10-5 M melatonin increased R(c) by 83{\%} (from 41.3 ± 10.7 to 75.4 ± 11.0 fmol/mg protein), supporting a direct effect of melatonin on uterine tissue. The R(c) induced by melatonin both in vivo in vitro was sensitive to the degree of homogenization used in preparation of the cytosol. Whereas conservative homogenization (two 10-sec bursts with an intermittent 40-sec cooling period) of uteri from melatonin-treated animals was associated with a significant increase in R(c), homogenization for 60 sec without intermittent cooling showed a significant decrease (from 251.1 ± 17.4 to 182.7 ± 5.8 fmol/mg protein) as compared with uteri from vehicle-treated animals. Whole organ analysis of uteri from animals injected with melatonin followed by [3H]estradiol, in which no homogenization was used, demonstrated a 26{\%} increase in R(c) specific binding, confirming induction as the primary response to melatonin. These findings demonstrate the ability of melatonin to modulate ER activity in hamster uteri, and may help explain the effects of melatonin on uterine growth and metabolism.",
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N2 - The pineal gland hormone, melatonin, has been shown to influence the growth and metabolism of uterine tissue in the Syrian hamster. Because the uterus is an estrogen-responsive target tissue, we studied the effect of melatonin on the unoccupied estrogen receptor (ER) activity of immature hamster uteri in vivo and in vitro. A single sc injection of 2.5 melatonin increased the ER activity of uterine cytosol (R(c) 30% within 60 min [from 147.4 ± 14.1 (SE), to 191.8 ± 18.5 fmol/mg protein]. Scatchard analysis showed the induced population of receptor to be homogenous and of high affinity, with an equilibrium dissociation constant (K(d) = 0.08 nM) similar to that for uteri for vehicle-treated animals. The induction of R(c) by melatonin persisted for 90 min, but R(c) returned to control levels by 2 h after injection. Scatchard analysis of unoccupied nuclear receptor showed no significant differences either in the quantity of receptor (vehicle = 379.7 ± 46.7, melatonin = 396.9 ± 76.7 fmol/mg protein) or in the K(d) vehicle = 0.75 nM, melatonin = 0.60 nM) between these two groups. In vitro incubation of fresh whole uteri for 60 min in media containing 10-5 M melatonin increased R(c) by 83% (from 41.3 ± 10.7 to 75.4 ± 11.0 fmol/mg protein), supporting a direct effect of melatonin on uterine tissue. The R(c) induced by melatonin both in vivo in vitro was sensitive to the degree of homogenization used in preparation of the cytosol. Whereas conservative homogenization (two 10-sec bursts with an intermittent 40-sec cooling period) of uteri from melatonin-treated animals was associated with a significant increase in R(c), homogenization for 60 sec without intermittent cooling showed a significant decrease (from 251.1 ± 17.4 to 182.7 ± 5.8 fmol/mg protein) as compared with uteri from vehicle-treated animals. Whole organ analysis of uteri from animals injected with melatonin followed by [3H]estradiol, in which no homogenization was used, demonstrated a 26% increase in R(c) specific binding, confirming induction as the primary response to melatonin. These findings demonstrate the ability of melatonin to modulate ER activity in hamster uteri, and may help explain the effects of melatonin on uterine growth and metabolism.

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