Due to the important role of glial cells in brain maturation and repor
ts on delayed astroglial proliferation following ethanol exposition, i
t was of great interest to examine the effects of the primary metaboli
te of ethanol - acetaldehyde - on astroglial cell growth. This was car
ried our by examining biochemical parameters of astroglial cells cocul
tured with Chinese hamster ovary cell line (CHO) transfected with alco
hol dehydrogenase (ADH), able to generate acetaldehyde from ethanol. A
cetaldehyde generated from ethanol by ADH-transfected CHO cells had an
inhibitory effect on the growth of astroglial cells as assessed by me
asuring marker enzyme activities and culture protein levels. Moreover,
both acetaldehyde and ethanol altered cell cycle and increased astrog
lial superoxide dismutase activity. Additionally, acetaldehyde, but no
t ethanol, increased malondialdehyde levels in cultured astroglia. The
se results clearly show that acetaldehyde may participate in the devel
opment of the Fetal Alcohol Syndrome.