The purpose of this lab was to observe how exposure to ethanol impacts early chick development. We also aimed to determine whether a dose dependence exists between exposure and manifestation of FAS. Chick eggs were injected with ethanol at different concentrations: 0%, 5%, 10% and 15% and development was terminated after 14 days. We found ethanol concentration had a significant effect on chick head diameter (tab.1), and the linear relationship can be seen in figure 2; as ethanol concentration increased head diameter decreased. However, we found no significant effect of ethanol concentration on the chicks total body mass or beak length (tab.1). Figure 1 and figure 3 depict the linear relationship between concentration of ethanol and total body
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We determined that some of the eggs had not been properly sterilized, likely some bacteria or fungus was introduced into the egg yolk and caused the embryos to die and later decompose. For future experiments proper aseptic technique to avoid contamination must be followed. Further, the data collected for table 1 was made by approximating the developmental stage of the chick embryos instead of using the Hamburger and Hamilton table, this left us with data that was unreliable and we were unable to use because the factors we used to data the chicks such as size, are largely impacted by genetics and not good markers for developmental staging. We would need to repeat this experiment and use a larger sample size in order to determine whether we would observe similar results, ideally we would see a decrease in both body mass and beak lenght as well as retarded development according to the Normal Table of Hamburger and Hamilton (Hamburger and Hamilton, 1951) and results that are more in line with the available …show more content…
The nature of these cells and the features that derive from them explains why we observed decreased head diameter in the chicks that were exposed to the highest concentration of ethanol; the ethanol induced apoptosis among this cell population leading to cells not migrating to their destinations. Further there were several anomalies that were observed in the chicks that were exposued to 15% ethanol; figure 6 depicts chick embryo with Spina bifida, there is a clear protrusion on the dorsal posterior region on the embryo is caused by incomplete closing of the spinal cord and surrounding membranes; figure 7 depicts a chick that did not have skull formation, the brain is not covered with bone only with membrane; and figure 8 depicts a chick with severly retarded growth and abnormal limb and beak development. All of these anomolies are results of apoptosis of the NCCs. It is widely accepted therefore, that the teratogenic effects of ethanol can be explained, at least in part, because ethanol targets these migrating cells and induces apoptosis within these cell populations (Oyedele and Kramer
We determined that some of the eggs had not been properly sterilized, likely some bacteria or fungus was introduced into the egg yolk and caused the embryos to die and later decompose. For future experiments proper aseptic technique to avoid contamination must be followed. Further, the data collected for table 1 was made by approximating the developmental stage of the chick embryos instead of using the Hamburger and Hamilton table, this left us with data that was unreliable and we were unable to use because the factors we used to data the chicks such as size, are largely impacted by genetics and not good markers for developmental staging. We would need to repeat this experiment and use a larger sample size in order to determine whether we would observe similar results, ideally we would see a decrease in both body mass and beak lenght as well as retarded development according to the Normal Table of Hamburger and Hamilton (Hamburger and Hamilton, 1951) and results that are more in line with the available …show more content…
The nature of these cells and the features that derive from them explains why we observed decreased head diameter in the chicks that were exposed to the highest concentration of ethanol; the ethanol induced apoptosis among this cell population leading to cells not migrating to their destinations. Further there were several anomalies that were observed in the chicks that were exposued to 15% ethanol; figure 6 depicts chick embryo with Spina bifida, there is a clear protrusion on the dorsal posterior region on the embryo is caused by incomplete closing of the spinal cord and surrounding membranes; figure 7 depicts a chick that did not have skull formation, the brain is not covered with bone only with membrane; and figure 8 depicts a chick with severly retarded growth and abnormal limb and beak development. All of these anomolies are results of apoptosis of the NCCs. It is widely accepted therefore, that the teratogenic effects of ethanol can be explained, at least in part, because ethanol targets these migrating cells and induces apoptosis within these cell populations (Oyedele and Kramer