A tissue culture model for studying ethanol toxicity on embryonic heart cells

A tissue system in which fibroblasts and myocytes from chick embryonic hearts were separately maintained was used to study the toxicity of ethanol. To reproduce the teratogenic effects of acute, high concentrations of ethanol typical of "binge" drinking, an open tissue culture system was e...

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Bibliographic Details
Published in:Cell biology and toxicology 1992-01, Vol.8 (1), p.1-11
Main Authors: Ni, Y, Feng-Chen, K C, Hsu, L
Format: Article
Language:English
Subjects:
Alcoholism and acute alcohol poisoning
Animals
Biological and medical sciences
Cell Count - drug effects
Cells, Cultured
Chick Embryo
Disease Models, Animal
Ethanol - toxicity
Fetal Alcohol Spectrum Disorders - embryology
Fetal Alcohol Spectrum Disorders - pathology
Fibroblasts - drug effects
Heart - drug effects
Heart - embryology
Medical sciences
Myocardium - cytology
Toxicology
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Summary:A tissue system in which fibroblasts and myocytes from chick embryonic hearts were separately maintained was used to study the toxicity of ethanol. To reproduce the teratogenic effects of acute, high concentrations of ethanol typical of "binge" drinking, an open tissue culture system was employed. With open cultures, the cells were initially exposed to peak alcohol levels for approximately 6 hr and were exposed to decreasing concentrations of ethanol for the remainder of each 24 hr period. After the first day of ethanol exposure, there was substantial cell loss in both fibroblast and myocyte cultures. Alcohol-induced cell loss was dose-dependent. Despite decreased cell density after the first day of ethanol exposure, the surviving cells differentiated into monolayers of fibroblasts or beating cardiac muscle fibers. However, both ethanol-exposed fibroblasts and myocytes appeared atrophic, that is, smaller and shrunken. Electrophoretic analysis or these ethanol-exposed fibroblast and myocyte cultures revealed specific reduction in the cellular contents of alpha-actinin, myosin, and actin. These decreases in cytoskeletal proteins may be responsible for the morphological abnormalities noted in these cells.
ISSN:0742-2091
1573-6822
DOI:10.1007/BF00119291