Alcohol withdrawal and brain injuries: Beyond classical mechanisms

Marianna E. Jung, Daniel B. Metzger

Research output: Contribution to journalReview articlepeer-review

34 Scopus citations


Unmanaged sudden withdrawal from the excessive consumption of alcohol (ethanol) adversely alters neuronal integrity in vulnerable brain regions such as the cerebellum, hippocampus, or cortex. In addition to well known hyperexcitatory neurotransmissions, ethanol withdrawal (EW) provokes the intense generation of reactive oxygen species (ROS) and the activation of stress-responding protein kinases, which are the focus of this review article. EW also inflicts mitochondrial membranes/membrane potential, perturbs redox balance, and suppresses mitochondrial enzymes, all of which impair a fundamental function of mitochondria. Moreover, EW acts as an age-provoking stressor. The vulnerable age to EW stress is not necessarily the oldest age and varies depending upon the target molecule of EW. A major female sex steroid, 17β-estradiol (E2), interferes with the EW-induced alteration of oxidative signaling pathways and thereby protects neurons, mitochondria, and behaviors. The current review attempts to provide integrated information at the levels of oxidative signaling mechanisms by which EW provokes brain injuries and E2 protects against it.

Original languageEnglish
Pages (from-to)4984-5011
Number of pages28
Issue number7
StatePublished - Jul 2010


  • 17β-estradiol
  • Antioxidant
  • Brain aging
  • Ethanol withdrawal
  • Mitochondria
  • Oxidative stress
  • Protein kinase
  • Protein oxidation


Dive into the research topics of 'Alcohol withdrawal and brain injuries: Beyond classical mechanisms'. Together they form a unique fingerprint.

Cite this