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Chronic estradiol exposure induces oxidative stress in the hypothalamus to decrease hypothalamic dopamine and cause

Sheba M J MohanKumar1, Badrinarayanan S Kasturi, Andrew C Shin

  • 1Neuroendocrine Research Laboratory, Dept. of Pathobiology and Diagnostic Investigation, College of Veterinary Medicine, Michigan State Univ., East Lansing, 48824, USA. mohankumar@cvm.msu.edu

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
|December 24, 2010
PubMed
Summary
This summary is machine-generated.

Chronic estrogen exposure causes oxidative stress in the hypothalamus, decreasing dopamine and leading to hyperprolactinemia. This research clarifies how prolonged estrogen impacts the tuberoinfundibular dopaminergic system.

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Area of Science:

  • Neuroendocrinology
  • Hormone Action
  • Oxidative Stress Research

Background:

  • Estrogens are known to induce hyperprolactinemia, likely via the tuberoinfundibular dopaminergic (TIDA) system.
  • Dopamine (DA) from TIDA neurons inhibits prolactin secretion; estrogens reduce DA to stimulate prolactin.
  • The precise mechanism of estrogen's effect on TIDA neurons remains unclear.

Purpose of the Study:

  • To investigate the hypothesis that chronic low-level estradiol-17β (E(2)) exposure induces oxidative stress in the hypothalamus.
  • To determine if this oxidative stress inhibits TIDA neuron function and causes hyperprolactinemia.
  • To elucidate the mechanism by which estrogens affect the TIDA system.

Main Methods:

  • Adult female rats received slow-release E(2) pellets for 30, 60, or 90 days.
  • Compared E(2)-exposed rats with old constant estrous (OCE) rats.
  • Measured glial fibrillary acidic protein, interleukin-1β (IL-1β), nitrate, and tyrosine hydroxylase (TH) nitration in the arcuate nucleus (AN) and median eminence (ME).
  • Assessed DA concentrations in the ME and prolactin levels.

Main Results:

  • Chronic E(2) exposure increased markers of oxidative stress (glial fibrillary acidic protein, IL-1β, nitrate) in the AN.
  • Increased TH nitration was observed in the ME, indicating impaired DA synthesis/transport.
  • DA concentrations in the ME decreased, and hyperprolactinemia was observed in an exposure-dependent manner.
  • These changes were comparable to those in OCE rats.

Conclusions:

  • Chronic low-level E(2) exposure induces oxidative stress in the arcuate nucleus.
  • This oxidative stress inhibits TIDA neuronal function, leading to decreased dopamine production.
  • The findings suggest a mechanism for estrogen-induced hyperprolactinemia via TIDA system inhibition.