Background information and purpose of the study
Many studies have obtained inconsistent findings vis-a-vis the effects of atrazine on vertebrates. To elucidate the effects of the chemical on humans, researchers utilize vertebrate model systems. It has been suggested that the herbicide could have potential effects on morphological features and hormonal pathways, implying that the normal biological events that are critical for normal functions are altered. Xenopus laevis is an amphibian that is widely applied in invertebrate assays to assess the impacts of exposures to harmful substances that are naturally found in the surroundings and/or are released by man into the environment.
Previous studies have demonstrated that some effects of certain chemicals are dependent on the stages of both animal and human development. For example, tadpoles show relatively high rates of sensitivity and mortality when they are exposed to carbaryl or atrazine. On the other hand, they show relatively low rates of sensitivity and mortality when they are subjected to the chemicals at the initial stages of embryonic growth. Based on the species of tadpoles, when they begin feeding, they would show different response rates in relation to very small amounts of atrazine. Generally, different species exhibit relatively high levels of responses at early and/or late larval phases.
Previous research has demonstrated that acute exposures to the chemical just before feeding is commenced are likely to result in altered developmental processes of the heart and kidney. The most sensitive phase of growth in most vertebrates is during organ morphogenesis. For instance, during the process of organ enlargement in zebrafish, exposure to the herbicide has the highest level of sensitivity. In addition, even being exposed to the chemical for very a short period could have many effects on various developmental events.
The researchers based their statement of the problem on the fact that molecular events that were observed in previous studies were not described, but they were responsible for malformations. The study aimed at achieving two goals/purposes. First, it focused on describing the impacts of the herbicide both at the tissue and at molecular levels. Second, it aimed at identifying the RA pathway members, which were responsible for altering the normal growth of intestines in animals that were subjected to atrazine.
Data
In Table 1, the data displayed are used to show PCR conditions that were important in amplifying genes examined in the study. It is vital to state that the primers, temperatures, and cycles adopted could enable amplification of the genes. The graph in Figure 2A shows the expression levels of both MMP9TH and MMP18. When all the tadpoles in the experiment were subjected to relatively high levels of atrazine, the results indicate that MMP18 increased remarkably. The graph in Figure 2B demonstrates that there were no major changes in the amounts of MMP9TH, MMP11, and MMP18, but the amount of MMP18 increased outstandingly in comparison with tadpoles that were not exposed to the chemical.
Personal conclusions about the data
The authors of the article presented the data in a very organized manner. Based on the findings, the data presented support the initial hypothesis that was adopted in the study. From my assessment, I cannot find any missing data or questions that were left unanswered.
The authors’ conclusions
I agree with the authors’ conclusions because they used good laboratory methods and procedures to obtain their findings, which are systematically presented in the article. In addition, the findings have important implications for researchers and the public because they have demonstrated that atrazine could disrupt molecular and hormonal pathways that are involved in the development of organs. Finally, I agree with the conclusions because references were used in relation to previous research that focused on the impacts of the herbicide.
Reference
Lenkowski, Jenny, and Kelly McLaughlin. “Acute atrazine exposure disrupts matrix metalloproteinases and retinoid signaling during organ morphogenesis in Xenopus laevis.” Journal of Applied Toxicology 30.6 (2010): 582-589.