Assessing Oxidative Stress as a Molecular Mechanism for Nematicidal Activity of Chalcones 17, 25, and 30 in C. elegans

Overview

By 2050, food production must rise to meet the needs of a global population of over nine billion people. However, plant-parasitic nematodes (PPNs) are a leading cause of annual agricultural losses totaling $173 billion. Current methods like methyl bromide are toxic to humans and the environment. In 2011, Dr. Calderon-Urrea’s lab developed organic nematicides—Chalcones 17, 25, and 30—that kill nematodes within three hours at 0.001 M; however, their mode of action is unknown. Since most nematicides are known to kill nematodes by affecting the nervous system or inducing excessive production of reactive oxygen species (ROS), we hypothesized that Chalcones 17, 25, and 30 cause death to the nematodes by inducing ROS production. To investigate this hypothesis, Caenorhabditis elegans (synchronized to the same life stage) were placed in 96-well plates with M9 buffer serving as the negative control; 25 mM of H2O2, as the positive control. The worms were exposed to each chalcone at both 0.00001 M and 0.0001 M. H2DCFDA, a fluorescent probe, was added to monitor ROS production. An additional 96-well plate was used to conduct a lifespan assay to monitor worm viability. Our results suggest that Chalcones 17, 25, and 30 don’t induce ROS production in C. elegans, ruling out one of the two main mechanisms that many nematicides use. The fluorescent probe, H2DCFDA, although toxic, indicated no effect on the lifespan of C. elegans. Thus, chalcones have a different nematicidal mechanism than inducing oxidative stress, ruling out ROS production as the mode of action.

Competition history

• CSEF 2026 Biochemistry/ Molecular Biology (Senior Division) · Entry S-04-26

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