Using proteomics, q-PCR and biochemical methods complementing as a multiapproach to elicit the crucial responses of zebrafish liver exposed to neonicotinoid pesticide

Kızılkaya, Şeyma Tartar; Akpınar, Gürler; Sesal, Nüzhet Cenk; Kasap, Murat; Gökalsın, Barış; Kayhan, Figen Esin

doi:10.1016/j.cbd.2023.101103

Cited by 2 publications

(2 citation statements)

References 70 publications

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“…CAT was significantly inhibited in both the BTH (p < 0.001) and BTON groups (p = 0.04). Downregulation of CAT expression levels led to an increase in CAT enzyme activity [62]. These observations are consistent with our measurement results.…”

Section: Discussionsupporting

confidence: 92%

Comparing the Developmental Toxicity Delay and Neurotoxicity of Benzothiazole and Its Derivatives (BTHs) in Juvenile Zebrafish

Yin,

Wang,

Mao

2024

Toxics

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In this study, a semi-static water exposure method was employed to investigate the early developmental and neurotoxic effects of four benzothiazole substances (BTHs), namely benzothiazole (BTH), 2-mercaptobenzothiazole (MBT), 2-hydroxybenzothiazole (BTON), and 2-aminobenzothiazole (2-ABTH), on zebrafish at an equimolar concentration of 10 μM. The findings revealed that all four BTHs exerted certain impacts on early development in zebrafish. MBT stimulated spontaneous movement in juvenile zebrafish, whereas BTON inhibited such movements. Moreover, all four BTHs hindered the hatching process of zebrafish larvae, with MBT exhibiting the strongest inhibition at 24 h post-fertilization (hpf). Notably, MBT acted as a melanin inhibitor by suppressing melanin production in juvenile zebrafish eyes and weakening phototaxis. Additionally, both BTH and BTON exhibited significantly lower speeds than the control group and other test groups under conditions without bright field stimulation; however, their speeds increased to average levels after percussion stimulation, indicating no significant alteration in motor ability among experimental zebrafish groups. Short-term exposure to these four types of BTHs induced oxidative damage in zebrafish larvae; specifically, BTH-, MBT-, and BTON-exposed groups displayed abnormal expression patterns of genes related to oxidative damage. Exposure to both BTH and MBT led to reduced fluorescence intensity in transgenic zebrafish labeled with central nervous system markers, suggesting inhibition of central nervous system development. Furthermore, real-time quantitative PCR results demonstrated abnormal gene expression associated with neural development. However, no significant changes were observed in 2-ABTH gene expression at this concentration. Overall findings indicate that short-term exposure to BTHs stimulates neurodevelopmental gene expression accompanied by oxidative damage.

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Section: Discussionsupporting

confidence: 92%

Comparing the Developmental Toxicity Delay and Neurotoxicity of Benzothiazole and Its Derivatives (BTHs) in Juvenile Zebrafish

Yin,

Wang,

Mao

2024

Toxics

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“…However, other locomotory behaviors altered by exposure to neonicotinoids have been reported ( Crosby et al, 2015 ; Robinson et al, 2017 ; Liu et al, 2018 ) and neurotoxic potential has been established in several studies ( Topal et al, 2017 ; Tian et al, 2020 ; Zhang et al, 2021 ); therefore, the neurotoxicity of IM and TM still warrants further study. Mounting evidence suggests that neonicotinoid insecticides may cause toxicity through other modes of action in vertebrates independent of neurotoxicity, including alteration of the hypothalamic-pituitary-gonad and thyroid axes ( Zhu et al, 2019 ), general metabolism and corticosteroid pathways ( Veedu et al, 2022 ; Zhang et al, 2023 ), generalized oxidative stress ( Yan et al, 2016 ; Veedu et al, 2022 ), or by disrupting the immune system ( Mason and Sample Organization, 2013 ; Morrissey et al, 2015b ; Gibbons et al, 2015 ; Hong et al, 2018b ; Kizilkaya et al, 2023 ). A better understanding of the sublethal responses to neonicotinoids and their impacts on non-target fish species would enable us to better monitor the impacts of agricultural insecticides on aquatic ecosystems.…”

Section: Discussionmentioning

confidence: 99%

Binary mixtures of imidacloprid and thiamethoxam do not appear to cause additive toxicity in fathead minnow larvae (Pimephales promelas)

Jeninga,

Kooij,

Harrahy

et al. 2023

Front. Toxicol.

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Introduction: Considerable use of neonicotinoid insecticides has resulted in their detection in surface waters globally, with imidacloprid (IM) and thiamethoxam (TM) frequently found together. Neonicotinoids are selective agonists for invertebrate nicotinic acetylcholine receptors (nAChR) leading to paralysis and death. While not overtly toxic to vertebrates, growing evidence suggests that chronic exposure to individual neonicotinoids can cause adverse health effects in fish. This work examined whether chronic exposure to binary mixtures of imidacloprid (IM) and thiamethoxam (TM) would be more toxic to fathead minnow (Pimephales promelas) larvae than either insecticide alone.Materials and Methods: Embryos were exposed to a 1:1 mixture of IM and TM (0.2, 2, 20, 200 or 2,000 μg/L of each pesticide) or a 1:5, 1:10, or 1:20 mixture of IM and TM (0.02 μg/L of IM with 0.1, 0.2, or 0.4 μg/L of TM) for a total of 8 days. Survival, developmental toxicity, embryonic motor activity, and startle escape responses were quantified.Results: Survival and growth were reduced, and hatching induced by exposure to a 1:1 mixture containing > 2 μg/L of each insecticide, but not following exposure to mixtures containing environmentally-relevant concentrations. Acute exposure to a 1:1 mixture did not alter embryonic motor activity; however, chronic exposure to these mixtures resulted in a slight but significant decrease in embryonic movements. Only 1:1 mixtures of high concentrations of IM and TM altered the startle escape response by increasing latency of response; however, a significant proportion of fish exposed to 1:1 mixtures had altered latency and burst speed. Taken together, these behavioral indicators of nAChR activation suggest that in mixtures, neonicotinoids could interfere with nAChR signaling despite their low affinity for the nAChR.Conclusion: Our findings suggest that toxicity of binary mixtures of IM and TM is primarily driven by IM, and that mixtures of IM with TM do not appear to cause significant additive toxicity when compared with our previous studies evaluating each neonicotinoid alone. Given the limited toxicological data available for mixtures of neonicotinoid insecticides in fish, further study is required to better understand the ecological risks these insecticides may pose to aquatic ecosystems.

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Using proteomics, q-PCR and biochemical methods complementing as a multiapproach to elicit the crucial responses of zebrafish liver exposed to neonicotinoid pesticide

Cited by 2 publications

References 70 publications

Comparing the Developmental Toxicity Delay and Neurotoxicity of Benzothiazole and Its Derivatives (BTHs) in Juvenile Zebrafish

Comparing the Developmental Toxicity Delay and Neurotoxicity of Benzothiazole and Its Derivatives (BTHs) in Juvenile Zebrafish

Binary mixtures of imidacloprid and thiamethoxam do not appear to cause additive toxicity in fathead minnow larvae (Pimephales promelas)

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