Abstract

Chronic ethanol ingestion, mostly in young adults, constitutes a frequent drug-abuse situation, which is associated to a wide variety of pathological disturbance affecting a number of organs, including liver, kidney, heart, pancreas and brain. The ethanol effects are more prominent when occurring at the perinatal period of life, generating, among other disabilities, brain developmental and functional impairments, as well as the so-called “fetal alcoholic syndrome”. However, low doses of ethanol, although not producing conspicuous signs of physiological impairment, may affect the developing organism, impairing the renal and cardiovascular system, among others. As a consequence of increased oxidative stress produced by ethanol intake and its subsequent oxidation, lipid peroxidation increases, enhancing reactive oxygen species formation, which is potentially injurious to the brain tissue. When occurring during gestation, lipid peroxidation may occur in the placenta, an event that would partially be responsible for fetal nutrition disturbance and consequently late physiological impairment. In this short review, data on ethanol effects on the nervous and cardiorenal structure and function are analyzed at the light of the most relevant hypotheses concerning ethanol mechanisms of action. Additionally, experimental data from the authors laboratories are presented and discussed, focusing particular attention to the possibility of differential neural and cardiorenal ethanol effects as a function of the dose used in distinct experimental models.

Keywords: Fetal development, ethanol, neural programming, cortical spreading depression, renal blood flow, blood pressure, oxidative stress