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Transcriptional effects of dietary chlorpyrifos‑methyl exposure in Atlantic salmon (Salmo salar) brain and liver
- Olsvik, P.A., Berntssen, M.H.G., Søfteland, L., Sanden, M.
- Comparative biochemistry and physiology 2019 v.29 pp. 43-54
- Salmo salar, acetylcholinesterase, brain, chlorpyrifos-methyl, dietary exposure, enzyme activity, enzyme inhibition, feeds, fish, genes, juveniles, lipid metabolism, liver, neurons, protein degradation, proteins, sequence analysis, toxicity, transcription (genetics)
- Elevated levels of chlorpyrifos‑methyl have been detected in plant-based Atlantic salmon feeds. To evaluate the potential negative effects of long-term and continuous dietary exposure to chlorpyrifos‑methyl in fish, we fed juvenile Atlantic salmon three concentrations (0.1, 1.0 and 8.0 mg/kg) of the pesticide for about two months. Brain and liver tissues were collected after 30 and 67 days of exposure. Homogenized brain tissue was examined for effects on acetylcholinesterase, and brain and liver tissue from fish exposed to 8.0 mg/kg were used for transcriptional analysis (RNA-seq). The results showed a transient accumulation of chlorpyrifos‑methyl in the brain with lower levels after 67 days of exposure compared to after 30 days of exposure. In contrast, the liver showed a time-dependent accumulation pattern. No effect on acetylcholinesterase activity, the primary target of chlorpyrifos‑methyl, was seen in the brain. However, after 30 days of exposure, 98 significantly differentially expressed genes (DEGs) were found in brain tissue and 239 DEGs in liver tissue. After 67 days of exposure, two and 258 DEGs were found in brain and liver tissue, respectively. Continuous dietary exposure of chlorpyrifos‑methyl most profoundly affected mechanisms associated with protein degradation and lipid metabolism in both brain and liver. Specific for the brain, many of the significant DEGs encode proteins involved in neuron function. In conclusion, this study shows that chlorpyrifos‑methyl affects the transcription of genes involved in neurological function in Atlantic salmon brain, even at exposure concentrations below the threshold for systemic toxicity as seen from brain acetylcholinesterase inhibition.