The increased global use of pyrethroids raises concern for non-target aquatic species. Bifenthrin, among the most predominantly detected pyrethroids in the environment, is frequently measured in water samples above concentrations reported to induce neuroendocrine and neurotoxic effects to several threatened and endangered fish species, such as the Chinook salmon and steelhead trout. To better characterize the neurotoxic effect of bifenthrin to salmonids, rainbow trout were treated with environmentally relevant concentrations of bifenthrin (15 and 30 ng/L) for two weeks and assessed for changes in transcriptomic profiles and histopathological alterations. The top bioinformatic pathways predicted to be impaired in bifenthrin-exposed trout were involved in gonadotropin releasing hormone signaling, the dysregulation of iron homeostasis, reduced extracellular matrix stability and adhesion, and cell death. Subsequent histopathological analysis showed a significant increase in TUNEL positive cells in the cerebellum and optic tectum of bifenthrin-treated trout, relative to controls (p < 0.05). These findings suggest that low, ng/L concentrations of bifenthrin are capable of dysregulating proper neuroendocrine function, impair the structural integrity of the extracellular matrix and cell signaling pathways in the brain, and induce apoptosis in neurons of juvenile salmonids following bifenthrin treatment, which is consistent with metabolomic profiles demonstrating a common target and mechanism.
Distribution of undulin, tenascin, and fibronectin in the human periodontal ligament and cementum: comparative immunoelectron microscopy with ultra-thin cryosections.