Abstract

Due to the important role of glial cells in brain maturation and reports on delayed astroglial proliferation following ethanol exposition, it was of great interest to examine the effects of the primary metabolite of ethanol-acetaldehyde-on astroglial cell growth. This was carried out by examining biochemical parameters of astroglial cells cocultured with Chinese hamster ovary cell line (CHO) transfected with alcohol dehydrogenase (ADH), able to generate acetaldehyde from ethanol. Acetaldehyde generated from ethanol by ADH-transfected CHO cells had an inhibitory effect on the growth of astroglial cells as assessed by measuring marker enzyme activities and culture protein levels. Moreover, both acetaldehyde and ethanol altered cell cycle and increased astroglial superoxide dismutase activity. Additionally, acetaldehyde, but not ethanol, increased malondialdehyde levels in cultured astroglia. These results clearly show that acetaldehyde may participate in the development of the Fetal Alcohol Syndrome.

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