An integrated approach, based on mass spectrometry, for the assessment of imidacloprid metabolism and penetration into mouse brain and fetus after oral treatment

Passoni, Alice; Mariani, Alessandro; Comolli, Davide; Fanelli, Roberto; Davoli, Enrico; Paola, Massimiliano De; Bagnati, Renzo

doi:10.1016/j.tox.2021.152935

Cited by 13 publications

(4 citation statements)

References 28 publications

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“…Imidacloprid concentration was measured according to previous report 23 . Plasma (50 μL) were mixed with 200 μL of acetonitrile.…”

Section: Methodsmentioning

confidence: 99%

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Decreases in the number of microglia and neural circuit dysfunction elicited by developmental exposure to neonicotinoid pesticides in mice

Namba,

Tominaga,

Ishihara

2024

Environmental Toxicology

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Neonicotinoids are insecticides widely used in the world. Although neonicotinoids are believed to be toxic only to insects, their developmental neurotoxicity in mammals is a concern. Therefore, we examined the effects of developmental exposure to neonicotinoids on immune system in the brain and post‐developmental behaviors in this study. Imidacloprid or clothianidin was orally administered to dams at a dosage of 0.1 mg/kg/day from embryonic day 11 to postnatal day 21. Imidacloprid decreased sociability, and both imidacloprid and clothianidin decreased locomotor activity and induced anxiety, depression and abnormal repetitive behaviors after the developmental period. There was no change in the number of neurons in the hippocampus of mice exposed to imidacloprid. However, the number and activity of microglia during development were significantly decreased by imidacloprid exposure. Imidacloprid also induced neural circuit dysfunction in the CA1 and CA3 regions of the hippocampus during the early postnatal period. Exposure to imidacloprid suppressed the expression of csf1r during development. Collectively, these results suggest that developmental exposure to imidacloprid decreases the number and activity of microglia, which can cause neural circuit dysfunction and abnormal behaviors after the developmental period. Care must be taken to avoid exposure to neonicotinoids, especially during development.

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“…Imidacloprid concentration was measured according to previous report 23 . Plasma (50 μL) were mixed with 200 μL of acetonitrile.…”

Section: Methodsmentioning

confidence: 99%

“…Imidacloprid concentration was measured according to previous report. 23 Plasma (50 μL) were mixed with 200 μL of acetonitrile. The mixtures were vortexed and centrifuged at 20 000 Â g for 10 min.…”

Section: Determination Of Imidacloprid Concentration In the Plasma An...mentioning

confidence: 99%

Decreases in the number of microglia and neural circuit dysfunction elicited by developmental exposure to neonicotinoid pesticides in mice

Namba,

Tominaga,

Ishihara

2024

Environmental Toxicology

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“…The BCF value of IMI was greater than that of THM, indicating that IMI had stronger enrichment ability in zebrafish gonads and muscles compared to THM. A recent study shows that IMI crossed the placental barrier and was detected in the fetal tissues following oral exposure in pregnant mice, 60 causing lasting changes in fetal behavior and brain function in mice. Though there is no similar report about THM, relatively high residual concentrations of THM in the ovary were observed.…”

Section: Transcriptional Alterations In F1mentioning

confidence: 99%

Chronic Paternal/Maternal Exposure to Environmental Concentrations of Imidacloprid and Thiamethoxam Causes Intergenerational Toxicity in Zebrafish Offspring

Zhang,

Shi,

et al. 2023

Environ. Sci. Technol.

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Imidacloprid (IMI) and thiamethoxam (THM) are ubiquitous in aquatic ecosystems. Their negative effects on parental fish are investigated while intergenerational effects at environmentally relevant concentrations remain unclear. In this study, F0 zebrafish exposed to IMI and THM (0, 50, and 500 ng L −1 ) for 144 days post-fertilization (dpf) was allowed to spawn with two modes (internal mating and cross-mating), resulting in four types of F1 generations to investigate the intergenerational effects. IMI and THM affected F0 zebrafish fecundity, gonadal development, sex hormone and VTG levels, with accumulations found in F0 muscles and ovaries. In F1 generation, paternal or maternal exposure to IMI and THM also influenced sex hormones levels and elevated the heart rate and spontaneous movement rate. LncRNA−mRNA network analysis revealed that cell cycle and oocyte meiosis-related pathways in IMI groups and steroid biosynthesis related pathways in THM groups were significantly enriched in F1 offspring. Similar transcriptional alterations of dmrt1, insl3, cdc20, ccnb1, dnd1, ddx4, cox4i1l, and cox5b2 were observed in gonads of F0 and F1 generations. The findings indicated that prolonged paternal or maternal exposure to IMI and THM could severely cause intergenerational toxicity, resulting in developmental toxicity and endocrine-disrupting effects in zebrafish offspring.

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“…Microbial degradation decides the fate of neonicotinoid insecticides in the soil (355,356). Further, studies suggested that several neonicotinoids, including imidacloprid, acetamiprid, and thiacloprid can readily cross the intestinal barrier (357,358) and the blood-brain barrier (358)(359)(360)(361)(362), and these pesticides and their metabolites were found in human biological samples, confirming human exposure (363)(364)(365)(366)(367)(368)(369). The European Union (EU) restricted the use of the neonicotinoids Clothianidin, Imidacloprid, and Thiamethoxam in plant protection and seed treatment products, due to their deleterious effects on pollinators, honeybees, and other non-target insects.…”

Section: Neonicotinoid Thiaclopridmentioning

confidence: 99%

Short-term impact of anthropogenic environment on neuroplasticity

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An integrated approach, based on mass spectrometry, for the assessment of imidacloprid metabolism and penetration into mouse brain and fetus after oral treatment

Cited by 13 publications

References 28 publications

Decreases in the number of microglia and neural circuit dysfunction elicited by developmental exposure to neonicotinoid pesticides in mice

Decreases in the number of microglia and neural circuit dysfunction elicited by developmental exposure to neonicotinoid pesticides in mice

Chronic Paternal/Maternal Exposure to Environmental Concentrations of Imidacloprid and Thiamethoxam Causes Intergenerational Toxicity in Zebrafish Offspring

Short-term impact of anthropogenic environment on neuroplasticity

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