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. Author manuscript; available in PMC: 2018 Mar 1.
Published in final edited form as: Neurotoxicol Teratol. 2016 Oct 29;60:40–49. doi: 10.1016/j.ntt.2016.10.012

Figure 1.

Figure 1

A,C,E,G,I. Chemotaxis indices (CIs) in adults after exposure to isoflurane as L1 larvae. Unexposed animals (solid fill), exposed animals (angled hatching). For all graphs, error bars denote SEM values, N>300 animals for each value. B,D,F,H,J Differences in CIs (ΔCI) between exposed and unexposed animals. Difference between ΔCI of N2 (19.5 +/− 3.7) and each mutant was compared to determine if the mutant affected AIN. ** = ΔCI different from N2, p<0.01, ***= ΔCI different from N2, p<0.005. A,B. Mitochondrial mutants. Chemotaxis in unexposed mitochondrial mutants (gas-1, nuo-6, mev-1, isp-1) was not worsened by isoflurane exposure. The exception was clk-1 which had a ΔCI similar to that of N2. C,D. ROS scavengers/ ER Stress. The effects of defects in ROS scavenging on AIN in C. elegans. CIs of five superoxide disumutatse mutants and hsp-4 (loss of the ER-specific heat shock protein HSP-4). E,F. DAF-2 dependent pathway. The effects of the daf-2 stress pathway on AIN. Loss of DAF-2 removed the AIN effect. The daf-16 mutation removed the effect of daf-2 on AIN. G,H. Kinases. Effects of 5 kinases on neurotoxicity. Loss of cmk-1 and gcn-2, both involved in innate immunity and ER-related stress, eliminated AIN. Loss of ire-1 also eliminated AIN and is discussed later. I,J. Transcription factors. The transcription factors skn-1, hif-1 and xpb-1 all eliminated AIN.