METABOLIC AND MITOTIC CHANGES ASSOCIATED WITH THE FETAL ALCOHOL SYNDROME

In the USA, fetal alcohol syndrome (FAS) is the leading known cause of mental retardation. FAS is estimated to affect 4000 infants yearly in the USA with an additional 7000 children suffering various forms of f etal alcohol effects in the absence of the full syndrome. A comparable incidence would be expected in other industrialized countries, but es sentially no data are available from either developing or third world countries. An understanding of the biochemical causes of FAS has been slow to develop, bur progress has been made toward a molecular causati on theory of FAS. This paper summarizes much of the current work as to the effects of fetal ethanol exposure on mitotic and metabolic parame ters as well as ethanol's effect on the cellular signalling pathways t hought to regulate these processes. Based upon these studies, it is ap parent that exposure of embryonic tissue to ethanol results in decreas ed growth and that alcohol adversely affects a multitude of cellular f unctions critical for the growth of the developing organism, including inhibition of protein and DNA synthesis. In addition, ethanol alters the uptake of critical nutrients such as glucose and amino acids and c auses changes in several kinase-mediated signal transduction pathways that regulate these biochemical processes.