If you don't remember your password, you can reset it by entering your email address and clicking the Reset Password button. You will then receive an email that contains a secure link for resetting your password
If the address matches a valid account an email will be sent to __email__ with instructions for resetting your password
Fetal alcohol syndrome (FAS) is the most common non genetic cause of mental retardation. Oxygen consumption in the brain results in generation of free radicals and this effect is magnified in response to alcohol. Antioxidative enzymes like superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) function to prevent the cellular damage produced by free radicals. Our objective was to evaluate the effect of prenatal alcohol on antioxidant enzyme expression.
A well-characterized FAS model was used (Webster, 1980). Timed, pregnant C57BL6/J mice were treated on gestational day 8 (E8) with intraperitoneal injection of saline (control) or alcohol (0.03 mL/g). Pups were harvested on gestational day 18 (E18), their brains extracted and homogenized. Each fetal brain was analyzed individually for mRNA expression of SOD, GPx and CAT using real-time PCR with 18S for internal control. Student t test was used for statistical analysis (significance: p<0.05).
25 pups from 4 litters in the alcohol group and 23 pups from 5 litters in the saline group were analyzed. There was no difference in maternal or pup weight between the two groups. SOD, GPx and CAT mRNA expression was significantly lower in the alcohol group compared to controls (Figure, p<0.001).
Prenatal alcohol exposure inhibits SOD, GPx and CAT expression. The reduction in these antioxidant enzymes promotes an oxidant environment and contributes to the cytotoxicity associated with FAS. The antioxidant system may be a novel pathway to target for prevention of the long term morbidity of FAS.