ETHANOL-INDUCED OXIDATIVE STRESS AND ENZYMATIC DEFENSES IN CULTURED FETAL-RAT HEPATOCYTES

Previously, we have documented an ethanol (E)-induced oxidative stress (OS) in cultured fetal rat hepatocytes (FRH). The cause of this is un certain, but an inhibition of kev antioxidant enzymes could be a/the f actor. OS was also observed in fetal liver (FL) during in utero E expo sure, but not in maternal liver. a difference that might be related to selectively lower enzymatic defenses in the fetus. Here, we record ef fects of E on activities of catalase (Cat), superoxide dismutase (Cu, Zn SOD and Mn SOD), glutathione peroxidase (GPX), and glutathione-S-tr ansferase (GST) in FRH isolated from 20-day-old fetuses and exposed to E (2 mg/ml) for up to 24 h and we compare these to adult rat liver da ta. E treatment decreased fetal liver reduced glutathione (GSH) pools by 23% (p <0.05) and increased malondialdehyde (MDA) by 14% (P <0.05) within 24 h of E exposure. E caused an increase in fetal liver Cat by 18%, 32%, and 47% by 3, 6, and 24 h of E, respectively (p <0.05). A 24 -h E exposure increased Cu, Zn SOD by 22% (p <0.05) and Mn SOD by 21% (p <0.05). A 24 h E treatment increased GPX by 18% (p <0.05) and GST b y 17% (p <0.05). Cat in whole FL was 26% of adult (p <0.05) whereas Cu , Zn SOD and Mn SOD in whole FL were 12% and 11% of adult levels (p <0 .05). GPX and GST in FL were 11% and 28% of adult values (p <0.05). It is concluded that in FRH, E-induced OS is not caused by impaired acti vities of these enzymes, but their low basal activities (vs. adult) ma y predispose the fetus to OS.