Sean Studstill, Weber State University
Life Sciences
Imidacloprid is a popular systemic insecticide that has been applied to our staple crops for two decades. According to the EPA, it is persistent in the environment and at risk of effecting non-targeted organisms. Imidacloprid is an insect neurotoxin; however it is also known to be toxic to various aquatic species in concentrations as low as 37 ppb. Ingestion of imidacloprid causes paralysis in organisms through the blockage of postsynaptic nicotinic cholinergic receptors. We sought to find out how toxic imidacloprid is to brine shrimp and what kinds of physiological reactions occur upon exposure.
Acute exposure was tested by placing roughly thirty larva or adults in seawater solutions with imidacloprid in concentrations of 0.73 ppb to 0.0073%. The source of imidacloprid was Bayer Advanced Complete Insect Killer, a commercial product containing 0.73% imidacloprid. Each larval acute condition was replicated three times per experiment, while adult shrimp had only one replication per condition per experiment. After each acute experiment, mortality and physiological states were analyzed. The responses of heat shock proteins (hsp) 90, 70 and 22 to increasing imidacloprid exposure were analyzed using SDS PAGE and Western blots.
Mortality rates for the shrimp in acute conditions were surprisingly low; however in the lowest concentration, inhibition of the motor capabilities of the shrimp could clearly be seen. Interestingly, acute mortality peaked at 7.3 ppm, rather than increasing with the concentration of the chemical as would be expected. Our western blots showed bands for hsp70 only for shrimp exposed to the chemical up to a concentration of 7.3 ppm.
Acute data suggests that imidacloprid is less lethal than expected, however it has considerable potential to paralyze at low concentrations. Western blot results indicate that concentrations of the compound higher than 7.3 ppm might actually interfere with the mechanisms of hsp70 regulation.