Abstract
In spite of extensive research and persistent arguments, the mechanism of aluminum (Al) toxicity is still obscure. It is firmly established that aluminum is a potent neurotoxicant. So, the aim based on is aluminum damage chicken heart, as well as the vitelline circulation. In the first 3 days of incubation (D0-D2), 1.0, 2.0, or 4.0 mg aluminum chloride/0.3 ml avian saline was injected into the center of each viable fertilized egg yolk (AL1, AL2, and AL3 groups, respectively). Control eggs were either uninjected (AL0) or injected (ALS, 0.3 ml saline). Crown rump length was significantly decreased, while, embryonic mortalities, growth delay, as well as congenital heart defects were increased in the eggs injected 2.0 or 4.0 mg of Al. Although no relationship is clear about the embryonic mortality induced by Al in chicken embryos to the dose concentration, the higher mortality occurs in early developmental stages in developing chick embryos. Furthermore, chick embryos exposed to 4.0 mg/Al showed a high incidence of defects of ventricular septation and ventricular myocardium. Configuration and density of branched vitelline vessels were also significantly deteriorated after injection with 4.0 mg/Al. It concluded that Al is a cardiac teratogen for a chick in a dose-dependent way. These data highlight a novel approach for aluminum in congenital cardiovascular defects. Therefore, further research is needed to explain the teratogenicity of Al on the embryonic heart development.