Publisher's Synopsis
The pathological and behavioral manifestations of alcoholism are caused by a number of biological factors, including genetic predisposition, metabolic alteration and cellular injury. In this issue, investigators explore novel mechanisms underlying alcohol-induced tissue injury, particularly in the liver and in the central nervous system. Special emphasis is placed on understanding ethanol's ability to enhance cellular signaling pathways and protein kinases, which are known to play an important role in mediating cellular damage. Topics discussed include ethanol's effect on cholesterol homeostasis in neural membranes and on cytokine-induced nitric oxide production in astrocytes. Ethanol is shown to enhance oxidative stress and increase the production of reactive oxygen species. Further studies focus on novel pharmacologic agents for preventing relapse and alleviating alcohol-mediated organ damage. Providing an excellent summary of recent progress in biomedical research on alcoholism, this issue is of interest not only to researchers in the alcohol field, but also to investigators in areas related to oxidative stress, tissue injury, signal transduction and neurodegeneration.
