Counteracting the negative effects of Imidacloprid using autophagy-inducing mechanisms

• In Event: Poster Presentation and Judging for: Biomedical; Cell & Molecular Biology; Chemistry & Biochemistry; Marine Science; Systematics & Evolutionary Biology.
  In Poster Session: Biomedical Sciences Poster Session

Abstract

Imidacloprid is a neonicitinoid that binds to the post-synaptic nicotinic acetylcholine receptors (nAChRs) of organisms. This binding blocks nAChRs and prevents acetylcholine-dependent neurotransmission, which eventually desensitizes the receptor, leads to paralysis and ultimately death. The concern with this widely-used pesticide is that it affects non-target organisms, such as humans, and can negatively impact the environment. Autophagy is a regulated cellular mechanism that removes unwanted toxins and dysfunctional organelles under inducible conditions. The compound, rapamycin, and hypoxia preconditioning (<1% O2) were shown to induce autophagy. Thus, we hypothesize that autophagy may protect organisms from the toxic actions of imidacloprid. To test this hypothesis, Caenorhabditis elegans nematode behavior was studied under four conditions: (1) DMSO, LB agar with Escherichia coli OP50 (bacterial food strain, LB-OP50), nematode growth medium (NGM), (2) rapamycin, DMSO, imidacloprid (3) NGM, LB-OP50, hypoxia preconditioning, and (4) NGM, imidacloprid, hypoxia preconditioning. Our results demonstrated that hypoxia preconditioning on its own had positive effects on C. elegans, however, it did not alleviate the negative effects of imidacloprid. DMSO and rapamycin treatments both showed similar results for all assays. DMSO with and without rapamycin decreased motility. Future plans include having a control group of C. elegans affected purely by imidacloprid, in order to compare the results. Also, further research as to why hypoxia preconditioning proved to be ineffective in regards to imidacloprid is needed.

Authors

• Astrid Romero, St. Edwards University

• Garrett Tauras, School of natural sciences