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Normalizing Effects of Bioflavonoids on EtOH-induced Indices of Lipid Peroxidation in Rat Neonates and Dams

La Grange, L., Ding, Z., Houston, M., Klein, E.
Pharmaceutical biology 2003 v.41 no.3 pp. 188-193
brain, catechin, ethanol, fetal alcohol syndrome, fetal development, glutathione, lipid peroxidation, liquid diet, liver, malondialdehyde, mortality, neonates, oxidative stress, pups, quercetin, rats, silymarin, toxicity
Oxidative stress may be a factor in the development of fetal alcohol syndrome. In previous studies we have observed that the concomitant in utero administration of ethanol (EtOH) and the bioflavonoid silymarin ameliorated some of the toxic effects of EtOH exposure. We tested the capacity of three bioflavonoids, silybin (an active constituent of silymarin), (+)catechin, and quercetin to normalize indicators of lipid peroxidation in rat neonates exposed in utero to EtOH. Pregnant rats were randomly assigned to 6 treatment groups: rodent chow, liquid diet (pairfed), EtOH/liquid diet (35% EDC), EtOH/silybin, EtOH/quercetin, and EtOH/(+)catechin. At birth, dam and pup brains and livers were excised for malondialdehyde (MDA) and glutathione (GSH) determination. Birth mortality rates in the EtOH and EtOH/quercetin groups were significantly higher than those of the pairfed group. All of the bioflavonoids normalized the EtOH-induced increase in MDA production and decrease in GSH levels with the exception of pup brain GSH and MDA measures, for which there were no significant differences. In utero exposure is associated with indications of increased oxidative stress both to the mother and the fetus. When any of the three bioflavonoids was added to the 35% EDC, the indicators of oxidative stress were normalized.