Abstract
Fetal alcohol syndrome affects the development of the cardiac tissue in children, causing ventral septal defects and ventricular hypertrophy. Initial ultrastructural studies using rodents revealed mitochondria as the primary organelle affected by ethanol. Mitochondria from these animals displayed the classic pattern of mitochondrial degradation: condensation, crystolysis, and vacuolization. However an inherent problem existed in these models: the rodent heart is still immature at birth and full cardiac development does not occur until 18 days post-partem. This study uses the primate Macaca nemestrina in order to more closely parallel the cardiac development of a human infant.Furthermore, alcohol was administered in periodic doses to simulate binge drinking.Mothers were given weekly doses of one of the following isocaloric treatments: 0.0, 0.3, 0.6. 1.2, 1.8. or 4.1 g ethanol per kg body weight of the dam from week one of pregnancy until full-term. At birth the animals were removed from their mothers and hand-reared with appropriate peer contact.
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Schedule a callMore From: Proceedings, annual meeting, Electron Microscopy Society of America
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