Mechanisms of fetal toxicity to alcohol with special consideration to fetal zinc deficiency

Alcohol use in pregnancyis associated with a wide range ofadverse pregnancy outcomes and whilst the likelihood of these increases with heavy drinkingpatterns, morbidityto the fetus may nevertheless result from anacute episode of alcohol consumption (i.e. "binge-drinking"). Increased maternal age, genetic susceptibility to alcohol, low socio-economic status, tobacco smokingand illicit drug use have all been reported to contribute to increased risk from alcohol exposure in pregnancy. Fundamental to understanding the risks associated with alcohol consumption in pregnancy and to providing an insight into factors that may contribute to comorbidity, is a basic understanding of how alcohol causes fetotoxicity. In this chapter we will review the potential mechanisms causing alcohol-mediated damage to the fetus, including alteredretinoic acid metabolism, excess prostaglandins, oxidative stress and alterations in placental structure and function, with a particular focus on the accumulating evidence that fetal zinc deficiency may underpin many of events that interrupt developmental processes. This chapter also includes new findings in regard to zinc homeostasis, including the roles of the metal binding protein metallothionein and zinc transporters, and the regulation of these by inflammatory mediators. © 2012 by Nova Science Publishers, Inc. All rights reserved.P. Coyle, B. L. Summers-Pearce, C. J. Cowley, and A. M. Rof