Anthocyanins: Are they beneficial in treating ethanol neurotoxicity?

Gang Chen, Jia Luo

Research output: Contribution to journalReview articlepeer-review

40 Scopus citations

Abstract

Heavy alcohol exposure produces profound damage to the developing central nervous system (CNS) as well as the adult brain. Children with fetal alcohol spectrum disorders (FASD) have a variety of cognitive, behavioral, and neurological impairments. FASD currently represents the leading cause of mental retardation. Excessive alcohol consumption is associated with Wernicke-Korsakoff syndrome (WKS) and neurodegeneration in the adult brain. Although the cellular/molecular mechanism underlying ethanol's neurotoxicity has not been fully understood, it is generally believed that oxidative stress plays an important role. Identification of neuroprotective agents that can ameliorate ethanol neurotoxicity is an important step for developing preventive/therapeutic strategies. Targeting ethanol-induced oxidative stress using natural antioxidants is an attractive approach. Anthocyanins, a large subgroup of flavonoids present in many vegetables and fruits, are safe and potent antioxidants. They exhibit diverse potential health benefits including cardioprotection, anti-atherosclerotic activity, anti-cancer, antidiabetic, and anti-inflammation properties. Anthocyanins can cross the blood-brain barrier and distribute in the CNS. Recent studies indicate that anthocyanins represent novel neuroprotective agents and may be beneficial in ameliorating ethanol neurotoxicity. In this review, we discuss the evidence and potential of anthocyanins in alleviating ethanol-induced damage to the CNS. Furthermore, we discuss possible underlying mechanisms as well as future research approaches necessary to establish the therapeutic role of anthocyanins.

Original languageEnglish
Pages (from-to)91-101
Number of pages11
JournalNeurotoxicity Research
Volume17
Issue number1
DOIs
StatePublished - Jan 2010

Bibliographical note

Funding Information:
Acknowledgment We thank Kimberly Bower for reading this manuscript. This research was supported by grants from the National Institutes of Health (AA015407 and AA017226).

Keywords

  • Antioxidants
  • Brain
  • Cell death
  • Cyanidin glucosides
  • Neuroprotection
  • Reactive oxygen species

ASJC Scopus subject areas

  • Neuroscience (all)
  • Toxicology

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