Imidacloprid Induced Neurotoxic and Histological Changes in Female Albino Rats

Vohra, Prerna; Khera, Kuldeep Singh

doi:10.15373/22778179/jan2014/170

Cited by 2 publications

(1 citation statement)

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“…These results are in accordance with that of Nellore et al [55] who reported that oral administration of the IMI leads to histopathological changes in the brain regions and [56] who revealed vacuolation around neuronal cell body, chromatolysis and marked congestion after 28 days of administration of 80 mg/kg BW of IMI. Exposure of high dose of IMI for 60 days produced dead purkinji cells with loss of dendrites in brain of female rats [57]. Japanese quail exposed to IMI for 6 weeks showed similar histopathological lesions in brain [58] and layer chickens exposed to 139 mg/kg IMI [59].…”

Section: Discussionmentioning

confidence: 99%

Modulatory Effect of Ginger Aqueous Extract against Imidacloprid-Induced Neurotoxicity in Rats

Farag

Fotoh

EL-Sayed

et al. 2019

Zagazig Veterinary Journal

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The current study was aimed to investigate neurotoxic impact of imidacloprid in rats and the potential modulatory role of Zingiber officinale Roscoe aqueous extract against such effects. Sixty male albino rats were randomly assigned into six groups (n = 10) as following: G1 is (-ve) control group (0.1 ml of distilled water for 90 days). G2 is (+ve) control group (1ml of aqueous extract of ginger (GAE) for 90 days). G3 group was administered with 0.1 ml of Imidacloprid (IMI) for 90 days. G4 group was administered with 1 ml of GAE for 2 weeks followed by administration of 0.1 ml of IMI/rat for 90 days. G5 group was administered with 0.1 ml of IMI for 90 days then 1ml of GAE for 2 weeks and the last group administered 0.1 ml of IMI and 1ml of GAE simultaneously for 90 days (G6) oral dosing of IMI and ginger aqueous extract was triple weekly. IMI exposure caused significant decrease in gamma amino butyric acid (GABA) level, significant increase in sorbitol dehydrogenase (SDH), significant depletion in glutathione (GSH), superoxide dismutase (SOD) was not affected by IMI exposure. IMI exposure upregulates toll like receptor 2 (TLR2) gene in the brain, intense immuno positive reactivity of TLR2 in the brain of IMI-treated group. Histopathologically, significant alterations in the brain were observed, such as neuronal degeneration, hemorrhages, necrosis, demyelination and gliosis. In conclusion, IMI neurotoxic effect could be modulated by the use of ginger aqueous extract.

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Section: Discussionmentioning

confidence: 99%