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Sci Total Environ
2023 Apr 15;869:161794. doi: 10.1016/j.scitotenv.2023.161794.
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Characterization of imidacloprid-induced hepatotoxicity and its mechanisms based on a metabolomic approach in Xenopus laevis.
Zhou X
,
Ming R
,
Guo M
,
Jiao H
,
Cui H
,
Hu D
,
Lu P
.
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The toxic effects of imidacloprid are attracting increased concern because of its widespread use in agriculture and its persistence in the aquatic environment. Imidacloprid bioaccumulates and triggers various morphological and behavioral responses in amphibians, but the toxic effects and mechanism of imidacloprid in amphibians remain uncertain. In this study, the acute toxicity and chronic effects of imidacloprid on Xenopus laevis were studied. Acute toxicity for 96 h revealed that imidacloprid had an LC50 value of 74.18 mg/L. After exposure for 28 d under 1/10 and 1/100 LC50, liver samples from X. laevis were employed for biochemical analyses, pathological studies, and nontargeted metabolomics to systematically assess the toxic effects and mechanisms of imidacloprid. The results showed that oxidative stress and hepatic tissue morphology changes were observed in treated X. laevis liver. Twelve metabolites involved in metabolic pathway were altered between the control and high exposure groups and twenty-one metabolites were altered between the control and low exposure group. Eight metabolic pathways exposed to high levels and nine metabolic pathways exposed to low level of imidacloprid were disturbed. These pathways were primarily related to amino acid metabolism, lipid metabolism, and nucleotide metabolism. Our research provides essential information to evaluate the potential toxicity of imidacloprid to nontarget aquatic organisms.
Fig. 1. SOD (A), CAT (B), and GST (C) levels and MDA(D) activity in X. laevis exposed to a high concentration (7.40 mg/L) and low concentration (0.74 mg/L) of imidacloprid. Each column represents the average of three samples, and SD is represented with an error bar. Significant changes among the experimental groups are indicted at p < 0.05.
Fig. 2. OPLS-DA plot in positive (A) and negative (B) ion modes in the 7.40 mg/L imidacloprid group. The corresponding validation plots (C) in positive and negative ion modes (D) based on 200 permutation tests at high exposures.
Fig. 3. OPLS-DA plot in positive (A) and negative (B) ion modes in the 0.74 mg/L imidacloprid group. The corresponding validation plots (C) in positive and negative (D) ion modes based on 200 times of permutation tests at low exposures.
Fig. 4. Heatmap generated by the most variable differential metabolites whose concentrations changed between the control and 7.40 mg/L group in positive(A) and negative mode(C). concentrations changed between the control and 0.74 mg/L group in positive(B) and negative mode(D). Red represents upregulated metabolites, and blue represents downregulated metabolites.
Fig. 5. Venn diagram presenting the overlapped metabolites that significantly vary from the comparisons of control–high exposure and control–low exposure to imidacloprid. (A). Pathway analysis of the overlapped metabolites of high and low exposure. (B). Analysis of pathways for differential metabolites between control and high exposure (C) and between control and low dose exposure (D).
Fig. 6. Schematic diagram of significant metabolic pathways affected by imidacloprid in X. laevis liver. The up-regulated metabolites were labeled with red and down-regulated with blue, respectively. The blue arrow represents high exposure to imidacloprid. and the purple arrow represents low concentration to imidacloprid.
Fig. S1. Concentrations of imidacloprid in exposure solutions at different stages, 7.40 mg/L (1/10 LC50) group; 0.74 mg/L (1/100 LC50) group
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Fig. S2. Histopathology of the liver after imidacloprid exposure. Control (A), liver exposed to 0.74 mg/L of imidacloprid for 28 d (B). The liver exposed to 7.40 mg/L of imidacloprid for 28 d (C). Red arrows represent inflammatory cell infiltration, black arrows represent hepatocyte necrosis, yellow arrows represent tissue congestion.
Fig. S3. PCA in positive (A) and in negative ion mode (B).
Fig. S4. Classification of different metabolites in high exposure group (A) and in low exposure group (B).
