Cardioteratogenic dose of ethanol reduces both lactic dehydrogenase and succinic dehydrogenase activity in the bulbar ridges of the embryonic chick heart

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Abstract
It has been established previously that the chick embryo is an appropriate model for studying the pathogenesis of ethanol‐induced ventricular septal defect and that the growth and fusion of the proximal bulbar ridges are critical to ventricular septation within the embryonic heart. To determine whether enzyme activity was altered significantly in bulbar ridges in response to a cardioteratogenic dose of ethanol, we injected 0.32 ml of 50% ethanol in chick Ringer's saline (CRS) into the air cells of 3‐day‐old chick embryos (72–84 h incubation, Hamburger‐Hamilton stages 18–19, Dekalb Delta strain). Embryos were harvested 48–60 h after treatment (stages 26–27). Hearts were removed, frozen and sectioned, and the tissues were processed for enzyme histochemical demonstrations of lactic and succinic dehydrogenase. Twelve ethanol‐treated embryos and 12 CRS‐treated controls were compared for lactic dehydrogenase (LDH) levels. Fourteen ethanol‐treated embryos and 14 controls were compared for succinic dehydrogenase (SDH) levels. Formazan deposits were quantified by means of computer‐assisted microdensitometry. Our results showed that ethanol decreased the mean LDH activity level by 36.3% (P = 0.05) and the mean SDH level by 40.8% (P < 0.02). Furthermore, ethanol significantly reduced LDH activity in 41.7% of the matched embryo pairs and significantly reduced SDH activity in 57.1% of the matched embryo pairs. Although some investigators have proposed that a disturbance in neural crest cell migration plays a major role in the pathogenesis of ethanol‐induced cardiac malformations, this study provides evidence that the bulbar ridges of the embryonic heart are also potential target tissues for ethanol.