Trophoblast toxicity of the neonicotinoid insecticide acetamiprid and an acetamiprid-based formulation

Gomez, Sebastian Diego; Bustos, Pamela Soledad; Sánchez, Victoria Guadalupe; Ortega, Marı́a Gabriela; Guiñazú, Natalia

doi:10.1016/j.tox.2020.152363

Cited by 26 publications

(11 citation statements)

References 72 publications

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“…It has been shown that ACE could lead to oxidative damage by producing ROS in various bacteria [46][47][48] and resulting in disturbance of oxidative status, and loss of mitochondrial membranes integrity in the rat reproductive tract and brain. It has also been reported that the insecticide ACE increased ROS levels, induced lipid peroxidation and decreased levels of antioxidant defense system components including GST, CAT and SOD activity [13,45,49]. In the present study, ACE induced oxidative stress in SH-SY5Y cells by increasing ROS, TOS and TAS levels, but in contrast, GSH levels and OSI did not change after ACE exposure for 24 h. Parallel to our results, Gomez et al (2020) [45] observed that GSH content showed no changes while ROS production induced drastically in the studied concentrations (0.1-100 µM).…”

Section: Discussionmentioning

confidence: 99%

“…The results have been supported by other in vitro studies in which the IC 50 value of ACE was determined as 2.16 and 6.68 mM in SH-SY5Y [ 42 ] and SK-N-SH human neuroblastoma cells [ 43 ], respectively. On the other hand, the IC 50 values of ACE have also been observed less than 1 mM in different cell lines such as human lung fibroblast IMR-90 [ 44 ], human placenta trophoblast HTR-8/SVneo [ 45 ] and rat adrenal gland pheochromocytoma PC-12 [ 13 ] cells. In view of these data, it can be suggested that human neural cells are more resistant to the cytotoxic effects of ACE.…”

Section: Discussionmentioning

confidence: 99%

“…The alterations in redox status could also cause the onset of apoptosis, and it has been reported that the induction of apoptosis in ACE-mediated toxicity was shown in many studies [ 13 , 45 , 46 ]. Among the studied genes, Bcl-2 has an anti-apoptotic function; however, Bcl-2 overexpression was also observed after exposure of ACE in SH-SY5Y cells.…”

Section: Discussionmentioning

confidence: 99%

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Cellular Stress Pathways Are Linked to Acetamiprid-Induced Apoptosis in SH-SY5Y Neural Cells

Öztaş

Kara

Boran

et al. 2021

Biology

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Acetamiprid (ACE), a commonly used neonicotinoid insecticide, is correlated with neurological symptoms, immunotoxicity and hepatotoxicity. Cellular stress and damage could play an important role in ACE-induced neurotoxicity; however, its mechanism has not been fully understood. We evaluated the effects of ACE on oxidative stress, endoplasmic reticulum (ER) stress, cellular death, mRNA expression levels of related genes and protein expressions of related molecular mechanisms in SH-SY5Y human neuroblastoma cells. The half maximal inhibition of enzyme activity (IC50) value of ACE was determined as 4.26 mM after 24 h of treatment by MTT assay. We revealed an increase in reactive oxygen species (ROS) production and calcium release. Significant increases were measured in inositol-requiring enzyme 1-alpha (IRE1-α) and binding immunoglobulin protein 90 (GRP90) levels as well as mRNA expression levels of caspase 3, 4 and 9 genes indicating enhanced ER stress. Apoptosis and ER stress-related genes were significantly upregulated at ≥2 mM. Indeed, ACE caused apoptosis and necroptosis while necrosis was not observed. There was a significant increase in the protein level of mitogen-activated protein kinase-8 (MAPK8) at 4 mM of ACE while no change was seen for nuclear factor kappa-B (NF-κB) and tumor necrosis factor-alpha (TNF-α). In conclusion, increased cellular stress markers could be proposed as an underlying mechanism of ACE-induced cell death in neural cells.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Cellular Stress Pathways Are Linked to Acetamiprid-Induced Apoptosis in SH-SY5Y Neural Cells

Öztaş

Kara

Boran

et al. 2021

Biology

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“…For acetamiprid, three studies for the in vitro line of evidence were available; these studies focused on the following toxicology assessment endpoints categories: genotoxicity (RefID 7 – Senyildiz et al, 2018 ), developmental toxicity (RefID 9 – Gomez et al, 2020 ) and neurotoxicity (2018; RefID 30, Çamlica et al, 2019 ). The study from Çamlica et al ( 2019 ) was considered in the context of the human health evaluation even though the study was conducted on the sciatic nerve of Rana ridibunda .…”

Section: Human Healthmentioning

confidence: 99%

Statement on the active substance acetamiprid

Hernandez-Jerez¹,

Adriaanse²,

Berny³

et al. 2022

EFS2

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Acetamiprid is a pesticide active substance with insecticidal action currently under the third renewal (AIR3) of the Commission implementing regulation (EU) No 844/2012. Following concerns that this substance may pose high risks to humans and the environment, the French authorities asked the Commission to restrict its uses under Article 69 of Regulation (EC) No 1107/2009. To support this request, competent Authorities from France cited a series of literature papers investigating its hazards and/or exposure to humans and the environment. Consequently, the EFSA PPR Panel was mandated to advise on the likelihood that body of evidence would constitute proof of serious risks to humans or the environment. Therefore, the EFSA PPR Panel evaluated the likelihood of these studies indicating new or higher hazards and exposure to humans and the environment compared to previous EU assessments.A stepwise methodology was designed, including: (i) the initial screening; (ii) the data extraction and critical appraisal based on the principles of OHAT/NTP; (iii) the weight of evidence, including consideration of the previous EU assessments; (iv) the uncertainty analysis, followed, whenever relevant, by an expert knowledge elicitation process. For human health, no conclusive evidence of higher hazards compared to previous assessment was found for genotoxicity, developmental toxicity, neurotoxicity including developmental neurotoxicity and immunotoxicity. However, due to the lack of adequate assessment of the current data set, the PPR Panel recommends conducting an assessment of endocrine disrupting properties for acetamiprid in line with EFSA/ECHA guidance document for the identification of endocrine disruptors. For environment, no conclusive, robust evidence of higher hazards compared to the previous assessment was found for birds, aquatic organisms, bees and soil organisms. However, the potential of high inter-species sensitivity of birds and bees towards acetamiprid requires further consideration.

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“…Os agrotóxicos, também denominados pesticidas, defensivos agrícolas, praguicidas ou biocidas, são compostos químicos utilizados pela agricultura para eliminar, repelir ou controlar organismos que possam trazer prejuízos para a produção de alimentos (Gomez et al 2020). Do ponto de vista econômico, o uso de pesticidas baseia-se no aumento da produção do cultivo, melhoria na qualidade da produção e a redução do custo em mão-de-obra e energia.…”

Section: O Uso De Agrotóxicos No Brasilunclassified

Inseticidas Neonicotinóides: uma ameaça aos corpos hídricos brasileiros

Queiroz¹,

Silva²

2021

RECURSO ÁGUA - Tecnologias E Pesquisas Para O Uso E a Conservação De Ecossistemas Aquáticos

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Trophoblast toxicity of the neonicotinoid insecticide acetamiprid and an acetamiprid-based formulation

Cited by 26 publications

References 72 publications

Cellular Stress Pathways Are Linked to Acetamiprid-Induced Apoptosis in SH-SY5Y Neural Cells

Cellular Stress Pathways Are Linked to Acetamiprid-Induced Apoptosis in SH-SY5Y Neural Cells

Statement on the active substance acetamiprid

Inseticidas Neonicotinóides: uma ameaça aos corpos hídricos brasileiros

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