6.1. Oxidative Stress
Alterations in the redox status in the CNS was supported by studies demonstrating ethanol—
mediated changes in the production and/or activity of endogenous antioxidants in various organs,
including the cerebellum and placenta [26,60,61].
Ethanol can induce oxidative stress directly by formation of free radicals which react with different
cellular compounds, or indirectly by reducing intracellular antioxidant capacity, such as decreased
glutathione peroxidase levels. A significant increase in oxidative stress was demonstrated in placental
villous tissue following two hours of ethanol perfusion, primarily involving the nitric oxide pathway in
the trophoblast and DNA damage in the villous stromal cells [61]. Alcohol-induced oxidative stress
was also found to increase lipid peroxidation and damage protein and DNA. However, there is lack of
data from human clinical studies. No significant different in urine 2,3-dinor-6-keto-prostaglandin F1α,
or 11-dehydro-thromboxane B2 8-isoprostane F2α an oxidative stress markers was found between
pregnant women who drank heavily and those who abstained [62].
6.2. Disturbed Prostaglandin Synthesis
Alcohol is known to affect prostaglandins, hence, influencing fetal development and parturition.
When mice were treated with aspirin (a prostaglandin synthesis inhibitor) prior to alcohol exposure,
the alcohol-induced malformations were reduced by 50% in comparison to mice treated with aspirin
after alcohol exposure [63]. Urinary 6-keto-PGF1alpha and 2,3-dinor-6 keto PG F1 alpha were higher
in heavily drinking mothers and infants who suffered from FAS compare to abstinent mothers and
infants. High levels of thromboxane B2 in urine were also found in the infants of the drinking mothers
but without correlation to FAS [64].