Preventing Alcohol Toxicity at the Molecular Level

Researchers have determined the mechanism by which the eight amino acid peptide NAP, an active fragment of the glial-derived activity-dependent neuroprotective protein, protects against alcohol-induced embryo toxicity and growth retardation in mice.

Investigators at Harvard Medical School (Boston, MA, USA) and the National Institute on Alcohol Abuse and Alcoholism (NIAAA, Bethesda, MD, USA; www. nih.gov) produced NAP derivatives with specific amino acid substitutions and screened the compounds in cultured rat neurons for their protection against cell toxins and in whole mouse embryos for their protection against alcohol.

Their study, published June 13, 2003, in the online edition of Science, revealed that NAP protected mouse embryos from alcohol toxicity by blocking its effects on the L1 cell adhesion molecule rather than by its broad neuroprotective actions. Fetal alcohol syndrome is the leading preventable cause of mental retardation in the United States, affecting about one in 1,000 U.S. infants and about 6% of children born to alcoholic women.

"This elegant study demonstrates that the protective effect of NAP against alcohol damage differs from that of NAP against neurotoxins,” said Ting-Kai Li, M.D., director, NIAAA. "Ethanol inhibition of L1 is now strongly implicated in the pathogenesis of fetal alcohol damage and a foremost target of medication development.”





Related Links:
Harvard Medical School
National Institute on Alcohol Abuse and Alcoholism