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Altered Development of Brain by Neonatal Ethanol Exposure: Zinc Levels during and after Exposure
Author(s) -
Samson Herman H.,
Diaz Jaime
Publication year - 1981
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1981.tb05362.x
Subject(s) - zinc , zinc deficiency (plant disorder) , ethanol , endocrinology , medicine , microcephaly , fetal alcohol syndrome , alcohol , brain damage , brain development , fetus , pregnancy , biology , chemistry , biochemistry , neuroscience , genetics , organic chemistry
Neonatal rats, exposed to ethanol by use of an artificial rearing technique during the first postnatal week, have been shown to have a 20% reduction in brain weight compared to littermate controls. The mechanisms responsible for this deficit remain to be determined. One hypothesis, which has been suggested that could be responsible for the microcephaly observed in the Fetal Alcohol Syndrome is that human alcoholics have decreased serum zinc levels. It is well documented that zinc deficiency in rats results in microcephaly. Thus, ethanol administered in the diet could result in lowered zinc levels in serum and brain, and hence be the underlying factor for the brain growth deficiency reported. In these studies, serum and brain zinc levels were determined for animals exposed to ethanol using the artificial rearing procedure, and for their littermate controls, artificially reared on the same formula without ethanol. No differences at any time were found in either serum or brain zinc levels. This would suggest that zinc availability could not account for the effects found on brain growth.