TY - JOUR
T1 - Antioxidants and fetal protection against ethanol teratogenicity
T2 - I. Review of the experimental data and implications to humans
AU - Cohen-Kerem, Raanan
AU - Koren, Gideon
N1 - Funding Information:
GK is a Senior Scientist of the Canadian Institutes for Health Research (CIHR), Supported by a NET (New Emerging Team) grant from CIHR and by the Research Leadership in Better Pharmacotherapy during Pregnancy and Lactation.
Funding Information:
RCK is supported by a Research Training Fellowship from the HSC Research Institute.
PY - 2003
Y1 - 2003
N2 - Ethanol is the most common human teratogen, and heavy drinking during pregnancy can result in serious adverse outcomes to the fetus. The cellular mechanisms by which ethanol induces damage in utero are not well understood, while induction of oxidative stress is believed to be one putative mechanism. Our objective is to review the data of antioxidant effects in experimental models of fetal alcohol syndrome. Prior to the description of the available experimental data, we will briefly review the mechanisms leading to ethanol-induced oxidative stress. Ethanol-induced oxidative damage to the fetus could be attenuated by a variety of antioxidants as was documented in whole animal and tissue culture studies. Experiments, retrieved from the literature search, are described and criticized. Although experimental data are still limited, the application of a treatment strategy that includes antioxidants is justified since antioxidant treatment in human pregnancy for pre-eclampsia was demonstrated to be safe and effective. The available experimental evidence and the safety of vitamins C and E in pregnancy suggest that experimental use of antioxidants in alcohol-consuming mothers should be seriously considered to reduce fetal alcohol damage.
AB - Ethanol is the most common human teratogen, and heavy drinking during pregnancy can result in serious adverse outcomes to the fetus. The cellular mechanisms by which ethanol induces damage in utero are not well understood, while induction of oxidative stress is believed to be one putative mechanism. Our objective is to review the data of antioxidant effects in experimental models of fetal alcohol syndrome. Prior to the description of the available experimental data, we will briefly review the mechanisms leading to ethanol-induced oxidative stress. Ethanol-induced oxidative damage to the fetus could be attenuated by a variety of antioxidants as was documented in whole animal and tissue culture studies. Experiments, retrieved from the literature search, are described and criticized. Although experimental data are still limited, the application of a treatment strategy that includes antioxidants is justified since antioxidant treatment in human pregnancy for pre-eclampsia was demonstrated to be safe and effective. The available experimental evidence and the safety of vitamins C and E in pregnancy suggest that experimental use of antioxidants in alcohol-consuming mothers should be seriously considered to reduce fetal alcohol damage.
KW - Antioxidant
KW - Ethanol
KW - Teratogenicity
UR - http://www.scopus.com/inward/record.url?scp=0037221722&partnerID=8YFLogxK
U2 - 10.1016/S0892-0362(02)00324-0
DO - 10.1016/S0892-0362(02)00324-0
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C2 - 12633732
AN - SCOPUS:0037221722
SN - 0892-0362
VL - 25
SP - 1
EP - 9
JO - Neurotoxicology and Teratology
JF - Neurotoxicology and Teratology
IS - 1
ER -