The use of neonicotinoid insecticides (NEO) continues to increase in the United States but currently limited information is available on their effects on non-target aquatic organisms (e.g. amphibians). Several NEO have been implicated in Colony Collapse Disorder (a syndrome affecting honey bees, Apis mellifera), due to contact with NEO- treated plants. More recently, NEO have been detected in surface and ground waters throughout the USA.
The current understanding of the NEO mode of action is based on target-insects, such as aphids in the Aphididae. The NEO bind directly to nicotinic acetylcholine receptors (nAChR), thus mimicking the action of acetylcholine (ACh) as a selective agonist of nAChRs. Acetylcholinesterase (AChE) will then break down ACh, terminating signals from nAChR on neurons in the central nervous system. However, AChE does not degrade NEO, thus the NEO binding to the nAChR is irreversible. Animals can detoxify chemicals by the induction of cytochrome p450 (CYP), with recent results showing that NEO are broken down to non-toxic components by CYP gene-induced oxidative detoxification in insects. However, such information is not available for the non-target amphibians having all or major parts of their life cycles in aquatic ecosystems.
This study builds upon previous work that showed that Xenopus laevis tadpoles exposed during early development to sub-chronic concentrations of NEO had a significant reduction in growth and increase in mortality. Thus, this investigation examined the expression of target genes (encoding the nAChR, AChE, CYP) in brain and liver from the exposed or control treatment groups of African clawed tadpoles (Xenopus laevis) in order to decipher the NEO mode of action at the transcriptional level.
The results indicated that at the NEO concentrations chosen for tadpole exposures, neither the gene expression for nAChR or AChE was altered. This indicated that the observed reduction in tadpole growth is not directly related to interaction of the NEO at the receptor level. Conversely, CYP expression levels in tadpoles were consistently upregulated by 50%, suggesting a detoxification mechanism at work. Investigation of additional detoxification biomarkers, such as those encoding stress proteins, as well as increased metabolic action by way of the glycolysis pathway and amino acid metabolism will further elucidate the NEO mode of action.