Ethal odor dose, respectively. b Meals aversion induced by 1 l ccBA of naive and ccBA-preconditioned (1 l for 4 h) animals at distinctive time points. c Food aversion induced by 4 l of ccDA of naive and ccDA-preconditioned (4 l for 4 h) animals at diverse time points. d Survival of naive and ccBA-preconditioned worms 14 h immediately after a 3-h exposure to eight l ccBA. e Survival of naive and ccDA-preconditioned worms 14 h right after a 3-h exposure to 16 l ccDA. Information are Bak custom synthesis expressed as imply SEM. N, number of independent experiments. p values were obtained by one-way ANOVA with Fisher’s LSD post hoc test. n.s., not significant; p 0.05; p 0.01; p 0.Hajdet al. BMC Biology(2021) 19:Web page 6 ofsurvival decline on ccDA (Fig. 2d, e), representing a protective (hormetic) impact of ccBA plus a debilitating (distressing) effect of ccDA preconditioning. Hormesis and distress are well-known phenomena in strain biology and suggest efficient or insufficient physiological responses for the stress induced by ccBA or ccDA exposures, respectively [17]. These findings are consistent with those on Fig. 1, i.e., related survival rates of animals around the respective odors, displaying a recovery of ccBA-exposed worms from a transient early paralysis compared to the progressive decline right after modest initial paralysis of ccDA-exposed worms (cf. Fig. 1e , two h of exposure). Thus, ccBA preconditioning induces behavioral and physiological anxiety tolerance, while ccDA preconditioning induces behavioral sensitization and physiological distress. These final results recommend that nematodes can mount efficient physiological protection against ccBA, but can only engage extra alert behavioral defense through sensitization against ccDA.Undiluted benzaldehyde, but not diacetyl, activates specific systemic cytoprotective responsesRNAi, although that of gst-4 was abolished by skn-1 RNAi (Fig. 3c, d). Importantly, ccBA did not activate numerous other stress reporters, such as the HSF-1 and DAF-16 target hsp-16.2, the HSF-1 target and endoplasmic reticulum unfolded protein response (UPR) reporter hsp-4, the SKN-1-dependent gcs-1, as well as the DAF-16dependent sod-3 reporter (Added File 1: Fig. S3c). These findings demonstrate that a precise tension and detoxification response involving a subset of DAF-16- and SKN-1-activated genes participate in the molecular defense against ccBA toxicity. In contrast, no apparent anxiety responses had been detected upon ccDA exposure.ccBA-induced cytoprotective responses confer behavioral tolerance to ccBA, but not to ccDANext, we asked in the event the effective vs. insufficient physiological protection against ccBA and ccDA exposure may possibly be reflected in the differential mobilization of cellular defense responses to the respective toxic stresses. In agreement with our findings around the toxicity of ccBA, preceding research demonstrated that BA induced oxidative tension [26]. Therefore, we tested various oxidative stress response pathways that may be involved inside the physiological adaptation to ccBA. Using the TJ356 strain expressing MAO-A drug GFP-tagged DAF-16, we observed that exactly the same ccBA dose utilised for preconditioning induced a strong nuclear translocation of DAF-16 after 30 min, comparable to that induced by heat tension. However, DAF-16 remained cytosolic in response to ccDA (Fig. 3a and Additional File 1: Fig. S3a). The shift in DAF-16 localization exhibited a clear BA dose dependence (Additional File 1: Fig. S3b). These congruent ccBA dosedependent adjustments in DAF-16 translocation and food avoidance (cf.