Be the first to like this
Growing research has implicated Fipronil as a teratogen in the development of chordates. Fipronil is a pesticide that acts to disrupt and inhibit normal nerve activity. The result is excessive nerve stimulation caused by overstimulation of gamman-aminobuytric (GABA) gated chloride ion channels. Experiments using zebrafish (Danio rerio) indicate Fipronil is teratogenic at concentrations above 0.7 μM. In this study, the effect of increasing concentrations (0.7 μM, 1.1 μM, 2.3 μM) of Fipronil on neurological development were examined. Our results showed that within six hours of GABA-receptor expression (36 hours-high pec) there was neurological damage as indicated by an abnormal behavioral escape touch response (resembling the accordion class phenotype), abnormal morphology (ventrally curved long fin), and damage to neurological tissue (notochord damage concentrated in the dorsal area of the trunk-tail interface). Within 48 hours (long-pec) damage was more extreme as observed in behavior, long tail morphology, and damage to neurological tissue. Furthermore, distinct regions of necrotic tissue were visible, accompanied by aberrant circulation. This data demonstrates Fipronil teratogenicity increases with exposure and concentration and is correlated with increasing damage to the notochord during development. This vertebrate study may have implications for diseases such as fetal alcohol syndrome (FAS) and autism on the phenotypic impact of Fipronil on the development of GABAergic neural pathways.
Keywords: zebrafish, fipronil, teratogen, GABA channels, notochord, necrosis.