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Vol. 297, Issue 2, 774-779, May 2001
Section on Developmental and Molecular Pharmacology, Laboratory of
Developmental Neurobiology, National Institute of Child Health and
Human Development, National Institutes of Health, Bethesda, Maryland
(C.Y.S., D.T.A., D.E.B., J.M.H.); and Department of Clinical
Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel
Aviv, Israel (I.G.)
Two peptides [NAPVSIPQ (NAP) and SALLRSIPA (ADNF-9)], that are
associated with novel glial proteins regulated by vasoactive intestinal
peptide, are shown now to provide protective intervention in a model of
fetal alcohol syndrome. Fetal demise and growth restrictions were
produced after intraperitoneal injection of ethanol to pregnant mice
during midgestation (E8). Death and growth abnormalities elicited by
alcohol treatment during development are believed to be associated, in
part, with severe oxidative damage. NAP and ADNF-9 have been shown to
exhibit antioxidative and antiapoptotic actions in vitro. Pretreatment
with an equimolar combination of the peptides prevented the
alcohol-induced fetal death and growth abnormalities. Pretreatment with
NAP alone resulted in a significant decrease in alcohol-associated
fetal death; whereas ADNF-9 alone had no detectable effect on fetal
survival after alcohol exposure, indicating a pharmacological
distinction between the peptides. Biochemical assessment of the fetuses
indicated that the combination peptide treatment prevented the
alcohol-induced decreases in reduced glutathione. Peptide efficacy was
evident with either 30-min pretreatment or with 1-h post-alcohol
administration. Bioavailability studies with [3H]NAPVSIPQ
indicated that 39% of the total radioactivity comigrated with intact
peptide in the fetus 60 min after administration. These studies
demonstrate that fetal death and growth restriction associated with
prenatal alcohol exposure were prevented by combinatorial peptide
treatment and suggest that this therapeutic strategy be explored in
other models/diseases associated with oxidative stress.
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