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Teratogenic Effects of Ethanol during Hyperplastic Growth in Cardiac Myocyte Cultures
Author(s) -
Adickes Edward D.,
Mollner Teresa J.,
Makoid Michael C.
Publication year - 1993
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.1530-0277.1993.tb05653.x
Subject(s) - ethanol , thymidine , cell growth , dna synthesis , myocyte , population , endocrinology , hyperplasia , medicine , biology , leucine , cell , in vitro , chemistry , biochemistry , amino acid , environmental health
Ethanol alters cellular growth and maturation, teratologic factors that are recognized as contributing to abnormal phenotypic expression. Cultured neonatal Sprague‐Dawley rat cardiac myocytes were utilized to determine how ethanol alters growth and development. Two ethanol exposure paradigms were studied: (1) constant, to cultures in closed chambers for 7 days at low (10 mM) and high (50 mM) concentrations; and (2) periodic (24‐hr) to cells during hyperplastic growth. In constantly exposed cultures, 10 and 50 ITIM ethanol concentrations depressed the rate of leucine incorporation and the rate of thymidine uptake during early hyperplastic growth (log phase growth). A resultant slower expansion of cell populations was noted. Although the period of maximum vulnerability appeared to be the hyperplastic growth phase, a second set of experiments using 10 and 50 mM ethanol were performed to assess the effects of short (24‐hr) exposures. DNA synthesis was depressed during early hyperplastic growth compared with controls (days 2‐4), reflected as a decrease in thymidine incorporation and smaller cell population. This study demonstrates that ethanol depresses both DNA and protein synthesis during hyperplastic growth resulting in an insufficient, protein‐deficient cell mass, incapable of participating in normal embryogenesis.