Effects of low-level imidacloprid oral exposure on cholinesterase activity, oxidative stress responses, and primary DNA damage in the blood and brain of male Wistar rats

Katić, Anja; Kašuba, Vilena; Kopjar, Nevenka; Lovaković, Blanka Tariba; Čermak, Ana Marija Marjanović; Mendaš, Gordana; Micek, Vedran; Milić, Mirta; Pavičić, Ivan; Pizent, Alica; Žunec, Suzana; Želježić, Davor

doi:10.1016/j.cbi.2020.109287

Cited by 48 publications

(47 citation statements)

References 103 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similarly, in the research by Katić et al [15] after treatment with IMI for 28 days with doses of 0.8 mg/kg and 2.25 mg/kg, approximate levels of 0.3 and 0.5 µg/g, respectively, were detected in the brain. Burke et al [57] observed that the treatment of rats with 0.5 mg/kg of IMI during pregnancy and the early postnatal stage was associated with brain concentrations of pesticide of 1.18 pmol/g in mothers and 0.044 pmol/g in offspring.…”

Section: Effects Of Nns On Rodentssupporting

confidence: 53%

“…In line with the above, Kapoor et al [59] and Vohra et al [117] reported that both acute and chronic administration of IMI caused a significant inhibition in acetylcholinesterase (AChE) activity in the rodent brain, although no significant effects have been observed in other studies [15]. Because of this inhibition, acetylcholine is not degraded and accumulates in the synaptic cleft, where it remains for a longer period.…”

Section: Changes In Neurotransmissionmentioning

confidence: 75%

“…The toxic effects that NNs can produce in the brain depend on their ability to cross the BBB, which is the protection system that controls the exchange of endogenous and exogenous substances between the blood and the extracellular environment of the brain [56]. The studies analyzed confirmed that NNs do cross the BBB, based on the detection of pesticides and their metabolites in the brains of exposed animals [15,[57][58][59][60].…”

Section: Effects Of Nns On Rodentsmentioning

confidence: 84%

“…It has been shown that exposure to NNs for approximately one month caused an increase in the activity of the enzymes catalase (CAT) and glutathione peroxidase (GSH-Px) in the brain [15,128]. However, a longer treatment with NNs decreased the antioxidant capacity, decreasing the activity of these two antioxidant enzymes [70,156].…”

Section: Induction Of Oxidative Stressmentioning

confidence: 99%

“…However, although NNs were previously thought to have a short biological half-life, recent studies have shown that these insecticides can remain in the environment for periods ranging from 1 day to almost 19 years [15]. Thus, humans are continuously exposed to these pesticides, which can be absorbed through food or drinking water, by inhalation or dermal contact with occupational spray by-products, as well as by indoor air contamination following termite or pet pest control treatments [4,16].…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Neurotoxic Effects of Neonicotinoids on Mammals: What Is There beyond the Activation of Nicotinic Acetylcholine Receptors?—A Systematic Review

Costas-Ferreira

Faro

2021

IJMS

View full text Add to dashboard Cite

Neonicotinoids are a class of insecticides that exert their effect through a specific action on neuronal nicotinic acetylcholine receptors (nAChRs). The success of these insecticides is due to this mechanism of action, since they act as potent agonists of insect nAChRs, presenting low affinity for vertebrate nAChRs, which reduces potential toxic risk and increases safety for non-target species. However, although neonicotinoids are considered safe, their presence in the environment could increase the risk of exposure and toxicity. On the other hand, although neonicotinoids have low affinity for mammalian nAChRs, the large quantity, variety, and ubiquity of these receptors, combined with its diversity of functions, raises the question of what effects these insecticides can produce in non-target species. In the present systematic review, we investigate the available evidence on the biochemical and behavioral effects of neonicotinoids on the mammalian nervous system. In general, exposure to neonicotinoids at an early age alters the correct neuronal development, with decreases in neurogenesis and alterations in migration, and induces neuroinflammation. In adulthood, neonicotinoids induce neurobehavioral toxicity, these effects being associated with their modulating action on nAChRs, with consequent neurochemical alterations. These alterations include decreased expression of nAChRs, modifications in acetylcholinesterase activity, and significant changes in the function of the nigrostriatal dopaminergic system. All these effects can lead to the activation of a series of intracellular signaling pathways that generate oxidative stress, neuroinflammation and, finally, neuronal death. Neonicotinoid-induced changes in nAChR function could be responsible for most of the effects observed in the different studies.

show abstract

Section: Effects Of Nns On Rodentssupporting

confidence: 53%

Section: Changes In Neurotransmissionmentioning

confidence: 75%

Section: Effects Of Nns On Rodentsmentioning

confidence: 84%

Section: Induction Of Oxidative Stressmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Neurotoxic Effects of Neonicotinoids on Mammals: What Is There beyond the Activation of Nicotinic Acetylcholine Receptors?—A Systematic Review

Costas-Ferreira

Faro

2021

IJMS

View full text Add to dashboard Cite

show abstract

Berberine chloride loaded nano‐PEGylated liposomes attenuates imidacloprid‐induced neurotoxicity by inhibiting NLRP3/Caspase‐1/GSDMD‐mediated pyroptosis

El Gazzar,

Farag,

Samir

et al. 2024

BioFactors

View full text Add to dashboard Cite

Concerns have been expressed about imidacloprid (IMI), one of the most often used pesticides, and its potential neurotoxicity to non‐target organisms. Chronic neuroinflammation is central to the pathology of several neurodegenerative disorders. Hence, exploring the molecular mechanism by which IMI would trigger neuroinflammation is particularly important. This study examined the neurotoxic effects of oral administration of IMI (45 mg/kg/day for 30 days) and the potential neuroprotective effect of berberine (Ber) chloride loaded nano‐PEGylated liposomes (Ber‐Lip) (10 mg/kg, intravenously every other day for 30 days) using laboratory rat. The histopathological changes, anti‐oxidant and oxidative stress markers (GSH, SOD, and MDA), proinflammatory cytokines (IL1β and TNF‐α), microglia phenotype markers (CD86 and iNOS for M1; CD163 for M2), the canonical pyroptotic pathway markers (NLRP3, caspase‐1, GSDMD, and IL‐18) and Alzheimer's disease markers (Neprilysin and beta amyloid [Aβ] deposits) were assessed. Oral administration of IMI resulted in apparent cerebellar histopathological alterations, oxidative stress, predominance of M1 microglia phenotype, significantly upregulated NLRP3, caspase‐1, GSDMD, IL‐18 and Aβ deposits and significantly decreased Neprilysin expression. Berberine reduced the IMI‐induced aberrations in the measured parameters and improved the IMI‐induced histopathological and ultrastructure alterations brought on by IMI. This study highlights the IMI neurotoxic effect and its potential contribution to the development of Alzheimer's disease and displayed the neuroprotective effect of Ber‐Lip.

show abstract

Design and Synthesis of Pyrazole Carboxamide Derivatives as Selective Cholinesterase and Carbonic Anhydrase Inhibitors: Molecular Docking and Biological Evaluation

Durgun,

Akocak,

Lolak

et al. 2024

Chemistry & Biodiversity

View full text Add to dashboard Cite

The present study focused on the synthesis and characterization of novel pyrazole carboxamide derivatives (SA1‐12). The inhibitory effect of the compounds on cholinesterases (ChEs; AChE and BChE) and carbonic anhydrases (hCAs; hCA I and hCA II) isoenzymes were screened as in vitro. These series compounds have been identified as potential inhibitors with a KI values in the range of 10.69 ± 1.27‐70.87 ± 8.11 nM for hCA I, 20.01 ± 3.48‐ 56.63 ± 6.41 nM for hCA II, 6.60 ± 0.62‐14.15 ± 1.09 nM for acetylcholinesterase (AChE) and 54.87 ± 7.76‐137.20 ±9.61 nM for butyrylcholinesterase (BChE). These compounds have a more effective inhibition effect when compared to the reference compounds. In addition, the potential binding positions of the compounds with high affinity for ChE and hCAs were demonstrated by in silico methods. The results of in silico and in vitro studies support each other. As a result of the present study, the compounds with high inhibitory activity for metabolic enzymes, such as ChE and hCA were designed. The compounds may be potential alternative agents used as selective ChE and hCA inhibitors in the treatment of Alzheimer's disease and glaucoma.

show abstract

Effects of low-level imidacloprid oral exposure on cholinesterase activity, oxidative stress responses, and primary DNA damage in the blood and brain of male Wistar rats

Cited by 48 publications

References 103 publications

Neurotoxic Effects of Neonicotinoids on Mammals: What Is There beyond the Activation of Nicotinic Acetylcholine Receptors?—A Systematic Review

Neurotoxic Effects of Neonicotinoids on Mammals: What Is There beyond the Activation of Nicotinic Acetylcholine Receptors?—A Systematic Review

Berberine chloride loaded nano‐PEGylated liposomes attenuates imidacloprid‐induced neurotoxicity by inhibiting NLRP3/Caspase‐1/GSDMD‐mediated pyroptosis

Design and Synthesis of Pyrazole Carboxamide Derivatives as Selective Cholinesterase and Carbonic Anhydrase Inhibitors: Molecular Docking and Biological Evaluation

Contact Info

Product

Resources

About