Abstract
Pesticides are viewed as a major wellspring of ecological contamination and causing serious risky consequences for people and animals. Imidacloprid (IM) and hexaflumuron (HFM) are extensively utilized insect poisons for crop assurance on the planet. A few investigations examined IM harmfulness in rodents, but its exact mechanism hasn’t been mentioned previously as well as the toxicity of HFM doesn’t elucidate yet. For this reason, the present study was designed to explore the mechanism of each IM and HFM–evoked rat liver and kidney toxicity and to understand its molecular mechanism. 21 male Wistar albino rats were divided into 3 groups, as follows: group (1), normal saline; group (2), IM; and group (3), HFM. Both insecticides were orally administered every day for 28 days at a dose equal to 1/10 LD50 from the active ingredient. After 28 days postdosing, rats were anesthetized to collect blood samples then euthanized to collect liver and kidney tissue specimens. The results showed marked changes in walking, body tension, alertness, and head movement with a significant reduction in rats’ body weight in both IM and HFM receiving groups. Significant increases in MDA levels and decrease of GHS levels were recorded in liver and kidney homogenates of either IM or HFM groups. Liver and kidney tissues obtained from both pesticide receiving groups showed extensive histopathological alterations with a significant increase in the serum levels of ALT, AST, urea, and creatinine and a decrease in total proteins, albumin, and globulin levels. In addition, there was upregulation of the transcript levels of casp-3, JNK, and HO-1 genes with strong immunopositivity of casp-3, TNF-ὰ, and NF-KB protein expressions in the liver and kidneys of rats receiving either IM or HFM compared with the control group. In all studied parameters, HFM caused hepatorenal toxicity more than those induced by IM. We can conclude that each IM and HFM provoked liver and kidneys damage through overproduction of ROS, activation of NF-KB signaling pathways and mitochondrial/JNK-dependent apoptosis pathway.
Highlights
Exposure to ecological contamination stays a significant wellspring of safety hazards around the world, in agricultural nations, where destitution, absence of interest in current innovation, and feeble natural enactment join to cause high contamination levels
Administration of either imidacloprid or hexaflumuron caused a significant decrease in the average body weight of rats compared to the control group
The results of the present study revealed that IM and HFM induced hepatorenal oxidative stress damage manifested by increased MDA levels and decreased Reduced glutathione (GSH) levels triggered by upregulation of HO-1 gene and down-regulation of Keap1 gene
Summary
Exposure to ecological contamination stays a significant wellspring of safety hazards around the world, in agricultural nations, where destitution, absence of interest in current innovation, and feeble natural enactment join to cause high contamination levels. Pesticides have discovered broad applications in horticultural and veterinary practices and have the potential for accidental effects on natural life, human and domesticated animals (De et al 2014). Imidacloprid, 1[(6-chloro-3-pyridinyl) methyl]-N-nitro2-imidazolidinimine, is a neonicotinoid insecticide widely used to fight pests of cereals, fruits, and vegetables due to its low soil persistence and high insecticidal activity at a low application rate (Casida and Durkin 2013). Several studies reported that IM is causing severe hepatotoxicity, nephrotoxicity, male infertility, and neurological disorders in mice (Bhardwaj et al 2010; Li et al 2021). Another example of broadly used insecticides is hexaflumuron (HFM), Benzoylphenyl urea (BPU) insecticide; it is an insect growth regulator that works by inhibiting a chitin synthesis (Khajepour et al 2012). Its active ingredient is categorized as unlikely toxic to humans while one recent study about its local formulation showed hepatotoxicity and immunotoxicity in rats but with unclear mechanism of action (Noaishi et al 2019)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
