Imidacloprid insecticide exposure induces stress and disrupts glucose homeostasis in male rats

Khalil, Samah R.; Awad, Ashraf; Mohammed, Hesham H.; Nassan, Mohamed A.

doi:10.1016/j.etap.2017.08.017

Cited by 56 publications

(42 citation statements)

References 74 publications

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“…This effect was more pronounced in the TMX mild and high dose-groups. TMX provoke an increase in glucose levels those results are in agreement with the study of Khalil et al (2017) 24 who show that imidacloprid perturbed the glucose regulation through hyperglycemic activity in both developing and adult rats.…”

Section: Discussionsupporting

confidence: 92%

Thiamethoxam Actara® induced alterations in kidney liver cerebellum and hippocampus of male rats

Khaldoun-Oularbi

Bouzid²,

Boukreta

et al. 2017

J Xenobiotics

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Thiamethoxam (TMX), a second-generation neonicotinoid insecticide, is one of the most widely used insecticides in Algeria. The present study assessed the effects of repeated subchronic exposure to the commercial formulation of thiamethoxam (Actara®, 25% WG) in albino male rats. The toxic effects of thiamethoxam (TMX) were studied biochemically and histopathologically. Twenty-eight male albino rats weighing between 226 and 243 g were randomly assigned to four groups. One group served as control, and the other three were served as experimental groups administered a neonicotinoid thiamethoxam (TMX; 26, 39 and 78 mg/kg/day) for 6 weeks. The effects of the insecticide on various biochemical parameters were evaluated at 2, 4 and 6 weeks. Histopathological studies were carried out in the liver, kidney, cerebellum and hippocampus at the end of the experiment. Changes in biochemical parameters glucose, ALT (alanine aminotransferase), AST (aspartate aminotransferase), γGT (gamma-glutamyltransferase) ALP (alkaline phosphatase) urea and creatinine were observed in treated-groups in a dose dependent manner when compared to the control. Histopathological alterations were more intense in male rats from the TMX high dose group than those from group 2 and 3. Based on these results, subchronic oral administration of thiamethoxam altered the biochemical parameters, which correlated with histopathological changes in the liver kidney and brain.

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Section: Discussionsupporting

confidence: 92%

Thiamethoxam Actara® induced alterations in kidney liver cerebellum and hippocampus of male rats

Khaldoun-Oularbi

Bouzid²,

Boukreta

et al. 2017

J Xenobiotics

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“…Total RNA was extracted from the frozen kidney specimens using the RNeasy Mini Kit (Qiagen, Germany) followed by the creation of the first-strand cDNA, which was reverse-transcribed from the extracted total RNA using a QuantiTect Reverse Transcription kit (Qiagen, Heidelberg, Germany). The primer sequences needed for the RT-PCR analysis are nuclear factor-kappa B (NF-kB) primers, 5-GCTTTGCAAACCTGG GAATA-3 and R: 5-CAAGGTCAGAAT GCACCAGA-3 [34]; interleukin (IL-6) primers, F: 5 -AAAGCCAGAGTC ATTCAGAGC-3 , R: 5 -GAGCATTGGAAGTTGGGGTA-3 (NM_012589.2); and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) primers, F: 5 -TGACGT GGACATCCGCAAAG-3 , R: 5 -CTGGAAGGTGGACAGCGGAGG-3 [35].…”

Section: Real-time Quantitative Pcr (Rt-qpcr) Analysis Of Genes Encodmentioning

confidence: 99%

Ethanolic Extract of Moringa oleifera Leaves Influences NF-κB Signaling Pathway to Restore Kidney Tissue from Cobalt-Mediated Oxidative Injury and Inflammation in Rats

et al. 2020

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This study aimed to describe the protective efficacy of Moringa oleifera ethanolic extract (MOEE) against the impact of cobalt chloride (CoCl2) exposure on the rat’s kidney. Fifty male rats were assigned to five equal groups: a control group, a MOEE-administered group (400 mg/kg body weight (bw), daily via gastric tube), a CoCl2-intoxicated group (300 mg/L, daily in drinking water), a protective group, and a therapeutic co-administered group that received MOEE prior to or following and concurrently with CoCl2, respectively. The antioxidant status indices (superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH)), oxidative stress markers (hydrogen peroxide (H2O2), 8-hydroxy-2-deoxyguanosine (8-OHdG), and malondialdehyde (MDA)), and inflammatory response markers (nitric oxide (NO), tumor necrosis factor (TNF-α), myeloperoxidase (MPO), and C-reactive protein (CRP)) were evaluated. The expression profiles of pro-inflammatory cytokines (nuclear factor-kappa B (NF-kB) and interleukin-6 (IL-6)) were also measured by real-time quantitative polymerase chain reaction (qRT-PCR). The results showed that CoCl2 exposure was associated with significant elevations of oxidative stress and inflammatory indices with reductions in the endogenous tissue antioxidants’ concentrations. Moreover, CoCl2 enhanced the activity of the NF-κB inflammatory-signaling pathway that plays a role in the associated inflammation of the kidney. MOEE ameliorated CoCl2-induced renal oxidative damage and inflammatory injury with the suppression of the mRNA expression pattern of pro-inflammatory cytokine-encoding genes. MOEE is more effective when it is administered with CoCl2 exposure as a prophylactic regimen. In conclusion, MOEE administration exhibited protective effects in counteracting CoCl2-induced renal injury in rats.

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“…There is a lot of evidence that imidacloprid has the potential to adversely impact ecosystems and human health. For instance, it was gradually discovered that imidacloprid is toxic to humans, and that imidacloprid is lethal to non-target organisms such as bats, earthworms, bees, fish, and shrimp (Table 1) [17][18][19][20][21]. Inhibits thyroid hormone secretion, causes abnormal alignment of the spermatogenic epithelium, epididymal hyperplasia, and oligospermia in male lizards [28][29][30] 7.…”

Section: Toxicity Of Imidaclopridmentioning

confidence: 99%

“…After two weeks of exposure to 1.0 mg•kg −1 of imidacloprid in rats, their cortisone and catecholamine levels changed and led to behavioral defects, especially in developing ones, whose mRNA levels of glucose transporters changed; the histopathological and immunohistochemical data showed that the pancreatic tissue structure was disordered, and the expression of insulin was decreased. Imidacloprid has also been shown to disrupt blood glucose regulation in developing and adult rats through hyperglycemic activity [18]. Imidacloprid has further been shown to interfere with the echolocation system of insect-eating bats; after imidacloprid poisoning, insect-eating bats may reduce the expression of auditory related proteins in the cochlea, the expression of sound-related FOXP2 in the superior colliculus, and the expression of auditory related otoferlin in the cochlea and lower colliculus, thus causing inflammation and cell apoptosis associated with mitochondrial dysfunction in the hippocampus and medial entorhinal cortex [19].…”

Section: Toxicity To Humans and Terrestrial Animalsmentioning

confidence: 99%

Section: Toxicity Of Imidaclopridmentioning

confidence: 99%

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Insights into the Toxicity and Degradation Mechanisms of Imidacloprid Via Physicochemical and Microbial Approaches

Pang

Lin

Zhang

et al. 2020

Toxics

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Imidacloprid is a neonicotinoid insecticide that has been widely used to control insect pests in agricultural fields for decades. It shows insecticidal activity mainly by blocking the normal conduction of the central nervous system in insects. However, in recent years, imidacloprid has been reported to be an emerging contaminant in all parts of the world, and has different toxic effects on a variety of non-target organisms, including human beings, due to its large-scale use. Hence, the removal of imidacloprid from the ecosystem has received widespread attention. Different remediation approaches have been studied to eliminate imidacloprid residues from the environment, such as oxidation, hydrolysis, adsorption, ultrasound, illumination, and biodegradation. In nature, microbial degradation is one of the most important processes controlling the fate of and transformation from imidacloprid use, and from an environmental point of view, it is the most promising means, as it is the most effective, least hazardous, and most environmentally friendly. To date, several imidacloprid-degrading microbes, including Bacillus, Pseudoxanthomonas, Mycobacterium, Rhizobium, Rhodococcus, and Stenotrophomonas, have been characterized for biodegradation. In addition, previous studies have found that many insects and microorganisms have developed resistance genes to and degradation enzymes of imidacloprid. Furthermore, the metabolites and degradation pathways of imidacloprid have been reported. However, reviews of the toxicity and degradation mechanisms of imidacloprid are rare. In this review, the toxicity and degradation mechanisms of imidacloprid are summarized in order to provide a theoretical and practical basis for the remediation of imidacloprid-contaminated environments.

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Imidacloprid insecticide exposure induces stress and disrupts glucose homeostasis in male rats

Cited by 56 publications

References 74 publications

Thiamethoxam Actara® induced alterations in kidney liver cerebellum and hippocampus of male rats

Thiamethoxam Actara® induced alterations in kidney liver cerebellum and hippocampus of male rats

Ethanolic Extract of Moringa oleifera Leaves Influences NF-κB Signaling Pathway to Restore Kidney Tissue from Cobalt-Mediated Oxidative Injury and Inflammation in Rats

Insights into the Toxicity and Degradation Mechanisms of Imidacloprid Via Physicochemical and Microbial Approaches

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