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Insecticides are widely used in crop protection against insects and frequently detected in aquatic environment. Photolysis kinetics are directly related with exposure assessment and risk assessment. However, the photolysis mechanism of neonicotinoid insecticides with different structures has not been studied and compared systematically in the literature. In this paper, the photolysis rate constants in water were determined for eleven insecticides under irradiation of simulated sunlight. At the same time, the photolysis mechanism and effect of dissolved organic matter (DOM) on their photolysis were studied. The results showed that photolysis rates of eleven insecticides vary in a large range. The photolysis rates of nitro-substituted neonicotinoids and butenolide insecticide are much faster than that of cyanoimino-substituted neonicotinoids and sulfoximine insecticide. The ROS scavenging activity assays reveal that direct photolysis dominates the degradation of seven insecticides and, on the other hand, self-sensitized photolysis dominates four insecticides. The shading-effect from DOM can reduce the direct photolysis rates, on the other hand, ROSs generated by triplet-state DOM ( 3 DOM*) can also accelerate photolysis of insecticides. According to the photolytic products identified from HPLC-MS, these eleven insecticides have different photolysis pathways. Six insecticides are degraded from the removal of nitro group from their parent compounds and four insecticides are degraded through ·OH reaction or singlet oxygen ( 1 O 2 ) reaction. QSAR (quantitative structure-activity relationship) analysis showed that photolysis rate was directly related to the energy gap between the highest occupied molecular orbital to the lowest unfilled molecular orbital (E gap  = E LUMO -E HOMO ) and dipole moment (δ). These two descriptors reflect the chemical stability and reactivity of insecticides. The pathways developed from identified products and the molecular descriptors of QSAR models can well verify the photolysis mechanisms of eleven insecticides., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Neonicotinoids have been often detected in aquatic environment with high concentrations; however, little is known about their risk and fate to/in fish. This study systematically investigated the bio-uptake, tissue distribution and metabolism of neonicotinoids in zebrafish, taking clothianidin (CLO) as an example. The results revealed the uptake and elimination kinetics of CLO in whole fish and different tissues was very similar, and its bioconcentration factor (<1) indicates the low bioaccumulation potential in zebrafish. The highest accumulative tissues for CLO were found to be intestine and liver. Eight biotransformation products were identified in intestine and liver, and the metabolic pathways were found to be N-demethylation and nitro-reduction. The metabolic kinetics of two products (desmethyl clothianidin and clothianidin urea) revealed the metabolism of CLO mainly occurred in liver and intestine. This suggested that the hepatobiliary system played an important role in the metabolism and elimination of CLO. This study provides a comprehensive evaluation of the toxicokinetics of CLO in zebrafish, and these results can contribute to its ecological risk assessment., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

• A significant interspecies correlation equation has been developed between tadpole and worm toxicities. • A theoretical equation has been developed to explain the QSAR models. • Insecticides and fungicides can be classified as specifically-acting compounds to both tadpoles and worms. • Worms are more sensitive than tadpoles for reactive compounds because of their polar property. • Ionic compounds exhibit low toxicity to tadpoles and worms because of their poor bio-uptake potential. Insecticides, fungicides, dinitrobenzenes, resorcinols, phenols and anilines are widely used in agricultural and industrial productions. However, their modes of toxic action are unclear in some nontarget organisms, such as worms and tadpoles. In this study, acute toxicity data was experimentally collected for Limnodrilus hoffmeisteri worms and Rana chensinensis tadpoles, respectively. Interspecies correlation and excess toxicity were calculated to determine modes of action (MOAs) between the two species for class-based compounds. The result showed that, although the interspecies correlation of toxicity between the tadpoles and worms is significant with a coefficient of determination (R2) of 0.83, tadpoles are more sensitive than the worms and toxicity values between these two species are not identical with an overall 0.43 log unit difference. Regression analysis revealed that the toxicity of nonpolar narcotics or baseline compounds is linearly related to hydrophobicity for both the tadpoles and worms and the two baseline models are parallel, suggesting that these nonpolar narcotics share the same MOA between the two species. The difference of baseline toxicities between the two species is attributed to differences in bioconcentration factors. Analysis of the excess toxicity calculated from the toxicity ratio (TR) suggested that phenols and anilines can be classified as polar narcotics, not only to fish, but also to the tadpoles and worms. These compounds are more toxic than the baseline compounds and quantitative structure-activity relationship (QSAR) models show that their toxicity is linearly related to chemical hydrophobicity and polarity. Analysis of the excess toxicity reveals that aminophenols and resorcinols can be classified as reactive compounds, and insecticides and fungicides can be classified as specifically-acting compounds for both species. These compounds exhibited significantly greater toxic effect to both the tadpoles and worms. QSAR models have been developed to describe the toxic mechanisms for nonpolar narcotics, polar narcotics, reactive chemicals and specifically-acting compounds, and a theoretical equation has been derived to explain the effect of bio-uptake and interaction of the chemical with target receptors for both tadpole and worm toxicity. Our study reveals that tadpole toxicity can be estimated from worm toxicity data and the two species can serve as surrogates for each other in the safety evaluation of organic pollutants. [ABSTRACT FROM AUTHOR]

Mitochondria are significant targets in cells for many environmental chemicals. Mitochondrial damage and dysfunction can lead to apoptosis and death of fish. The objectives of this study were to compare the modes of action (MOAs) between fish, cell and mitochondrial toxicity. To achieve the goal, toxicity correlation, excess toxicity and quantitative structure–activity relationship (QSAR) were investigated between these three toxicity endpoints for a wide range of compounds. Results showed that fish toxicity is well correlated to cytotoxicity, but overall fish toxicity is relatively greater than the cytotoxicity. On the other hand, fish or cell toxicity is poorly related to mitochondrial toxicity, suggesting some compounds share same toxic mechanism but some not. The excess toxicity calculated from toxicity ratio (TR) shows that specifically-acting compounds in cytotoxicity, such as insecticides, fungicides, herbicides, dyes and medications used to treat cancer, depression, heart failure and blood pressure, are active compounds in mitochondrial toxicity. However, the less inert compounds identified in fish and cell toxicity exhibit greatly mitochondrial toxicity. QSAR models reveal that fish or cell toxicity is closely related to the chemical hydrophobicity, ionization, energy of lowest unoccupied molecular orbital, hydrogen bonding potential and stability. These descriptors reflect chemical bio-uptake, reactivity and interaction with target receptors. On the other hand, binomial model reveals that mitochondrial toxicity is closely related to the chemical hydrophobicity and polarizability/dipolarity, indicating bio-uptake and Van der Waals interaction play key roles in mitochondrial toxicity. Theoretical equations have been used to explain the toxicity correlation, excess toxicity and QSAR for fish, cell and mitochondrial toxicity. Above results suggest that cytotoxicity can serve as a surrogate for fish toxicity and be used in the safety evaluation of organic pollutants in aqueous environment, but not mitochondrial toxicity, although some compounds share same modes of action between fish or cell toxicity and mitochondrial toxicity. [Display omitted] • Fish toxicity is closely related to cytotoxicity, but not mitochondrial toxicity. • QSAR or binomial models are developed for fish, cell and mitochondrial toxicity. • Many pesticides and medications exhibit excess toxicity to fish, cell and mitochondria. • Phenols and anilines exhibit significant toxicity to mitochondria, but not to fish and cells. • Theoretical equations can well explain toxicity correlation, excess toxicity and QSAR. [ABSTRACT FROM AUTHOR]