Toxicity of nonylphenol and nonylphenol ethoxylate on Caenorhabditis elegans.

Among the most used chemicals in the world are nonionic surfactants. One of these environmental pollutants is nonylphenol ethoxylate (NP-9), also known as Tergitol, and its degradation product, nonylphenol (NP). The objective of this work was to determine the toxicity of NP and NP-9 in Caenorhabditis elegans. Wild-type L4 larvae were exposed to different concentrations of the surfactants to measure functional endpoints. Mutant strains were employed to promote the activation of toxicity signaling pathways related to mtl-2, gst-1, gpx-4, gpx-6, sod-4, hsp-70 and hsp-4. Additionally, stress response was also assessed using a daf-16::GFP transgenic strain. The lethality was concentration dependent, with 24-h LC50 of 122 μM and 3215 μM for NP and NP-9, respectively. Both compounds inhibited nematode growth, although NP was more potent; and at non-lethal concentrations, nematode locomotion was reduced. The increase in the expression of tested genes was significant at 10 μM for NP-9 and 0.001 μM for NP, implying a likely role for the activation of oxidative and cellular stress, as well as metabolism pathways. With the exception of glutathione peroxidase, which has a bimodal concentration-response curve for NP, typical of endocrine disruption, the other curves for this xenobiotic in the strains evaluated were almost flat for most concentrations, until reaching 50-100 μM, where the effect peaked. NP and NP-9 induced the activation and nuclear translocation of DAF-16, suggesting that transcription of stress-response genes may be mediated by the insulin/IGF-1 signaling pathway. In contrast, NP-9 induced a concentration-dependent response for the sod-4 and hsp-4 mutants, with greater fluorescence induction than NP at similar levels. In short, NP and NP-9 affect the physiology of C. elegans and modulate gene expression related to ROS production, cellular stress and metabolism of xenobiotics.