Combined Toxicity of Nitro-Substituted Benzenes and Zinc to Photobacterium Phosphoreum: Evaluation and QSAR Analysis

Abstract

The single toxicity (IC50) of zinc (Zn) and 11 nitro-substituted benzenes to Photobacterium phosphoreum were determined, respectively. On basis of single toxicity, the joint toxicity of binary mixtures of Zn and 11 nitro-substituted benzenes at different Zn concentrations of 0.2 IC50, 0.5 IC50, and 0.8 IC50 were measured. The joint toxicity was evaluated by toxic unit (TU) and additive index (AI) methods. The results indicated that the joint toxicity was not only depending on the Zn concentrations but also on the substituted groups of nitro-substituted benzenes. The quantitative structure-activity relation (QSAR) equations were developed and the results showed that the toxicity of nitro-substituted benzenes has different joint effect at the different Zn concentrations. At the Zn concentration of 0.2 IC50, the binary joint effects were mainly antagonism and the joint toxicity was negatively related to descriptors called VE2_B(p) and TIC3. At the Zn concentration of 0.5 IC50 and 0.8 IC50, the binary joint effects were mainly antagonism and simple addition, and the joint toxicity was related to the same descriptor Eig06_ AEA(dm). It indicated that the joint toxic actions were similar when combined at the medium and high concentrations of Zn.

Mixture toxicity of zinc oxide nanoparticle and chemicals with different mode of action upon Vibrio fischeri

“…Similar results were obtained for the joint effects of nZnO combined with propiconazole by Hackenberger et al [41]. Zhang et al [42] also found that the binary joint effects of Zn 2+ and 11 nitrosubstituted benzenes to Photobacterium phosphoreum were mainly antagonism.…”

Mathematical Modeling Approaches for Assessing the Joint Toxicity of Chemical Mixtures Based on Luminescent Bacteria: A Systematic Review

“…Likewise, the joint toxicities of Cu (low, medium and high levels) with 11 nitroaromatic compounds (nitrobenzene, o -dinitrobenzene, m -nitrobromobenzene, p -nitrobromobenzene, o -nitroaniline, p -nitroaniline, p -nitrobenzoic acid, o -nitrophenol, m -nitrophenol, p -nitrophenol and 2,4-dinitrophenol) were studied by P. phosphoreum with developed QSAR analysis, there is a good agreement between the predicted values and experimental with R 2 = 0.764, P = 0.000, (Su et al, 2012 ). By drawing on the study of Su's, Zhang's, Su, Zhang, Li, Qin and Zhang ( 2019a ) work on the acute toxic effect of mixtures between metal Zn and above-mentioned 11 nitroaromatic compounds established robust QSAR models to predict the joint interaction when combined with Zn at low, medium, and high concentrations (Zhang et al, 2019a ). Not limited to heavy metals and organics, the joint toxicity of mixed organics can also be predicted by QSAR models.…”

“…Likewise, Jarque et al held the view that V. fishieri luminescence assay to evaluate the toxicity associated with sediments from the Morava River and its tributary Drevnice River followed seasonal patterns (Jarque et al, 2016). Luminescent bacteria toxicity bioassay could also be carried out to evaluate the ecological risk of wastewater before and after diverse treatment processes, including ozonation, Fenton, UV, electrochemical degradation, biological process, and so on (De Schepper et al, 2012;Hamdi El Najjar et al, 2014;Lütke Eversloh et al, 2014;Wei et al, 2015;Nebout et al, 2016;Xu et al, 2018).…”

A review of quantitative structure-activity relationship modelling approaches to predict the toxicity of mixtures

“…Wang et al [77] were amongst the first to propose the use of binding energy descriptors in modelling mixture toxicityexamining the feasibility of substituting logK owmix with the molecular docking descriptor E binding , owing to the linear trend observed between the two. Zou et al [88] investigated both the acute and chronic toxicities of antibiotics from the sulfonamide family, alongside the sulfonamide potentiator trimethoprim. The study initially identified the receptors responsible for both their acute and chronic effects towards Aliivibrio fischeri; determining them to be luciferase, dihydropteroate synthase and dihydrofolate reductase.…”

“…Unlike previous extrapolation models, understanding of the differing toxic mechanisms between acute and chronic exposures was considered. In a variation from Zou et al [88], in which DHFR served as the sole mediator of TMP toxicity, the targets for the antibiotics reported in this study were represented by surrogate luciferase proteins. Due to a specific target not being considered and instead characterised by surrogates, the model demonstrated promise in predicting the toxicity chemicals for which mechanisms are unknown.…”