OXIDATIVE STRESS AND THE FETOTOXICITY OF ALCOHOL-CONSUMPTION DURING PREGNANCY

Pregnant Quackenbush Special mice were exposed to ethanol under semiac ute (3.0 g/kg body weight intragastrically, days 7 to 12 of pregnancy) , and chronic conditions (15% ethanol in drinking water for 5 weeks be fore and during pregnancy) to assess whether embryo-fetotoxic actions of the drug involve oxidative stress effects. Effects were monitored b oth in the maternal system and embryo. Alcohol compromised the materna l system by increasing the generation of lipid peroxides in the liver. It also decreased glutathione and vitamin E levels, and glutathione p eroxidase and superoxide dismutase activities in this organ. Glutathio ne peroxidase activity in the maternal blood decreased. Only minor alc ohol-induced changes occurred in the uterine endometrium, including de creased xanthine oxidase and increased gamma-glutamyl transpeptidase. Similarly, only few changes were induced in day-12 embryos by alcohol. In this case, glutathione content and xanthine oxidase activity decre ased while glutathione reductase activity increased following exposure to the chronic regime. With the possible exception of the maternal li ver where evidence of oxidative damage was detected, these results do not reflect substantial changes in the antioxidant defences of either the pregnant mouse or embryo. However, the changes may contribute to t he growth retarding and other fetotoxic effects of alcohol when they a re totalled into the multifactorial actions of the drug.