Sections passing through the deep cerebellar nuclei of the mouse brain showing AChE activity. D: nucleus dentatus; F: nucleus fastigii; I: nucleus interpositus; a: control group; b: lindane treated group; c: antioxidants treated group; d: antioxidants + lindane treated group. Magnification; x25.  

Sections passing through the deep cerebellar nuclei of the mouse brain showing AChE activity. D: nucleus dentatus; F: nucleus fastigii; I: nucleus interpositus; a: control group; b: lindane treated group; c: antioxidants treated group; d: antioxidants + lindane treated group. Magnification; x25.  

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Objective: The present investigation ascertains a protective potential of a combination of antioxidants against lindane-induced toxicity in cerebellum of mice. Methods: For the study, animals are divided into four groups. First group is control and it is given only vehicle. Second group is treated with lindane and analysed if there are any lesions...

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... After being accumulated in the brain, lindane alters the phospholipids and fatty acid composition as well as fluidity of the membrane, consequently leading to dysfunction of membrane-bound adenosine triphosphatase (ATPase) and acetylcholinesterase (AChE) activity [3][4][5]. In addition to membrane perturbation, lindane enhances oxidative stress by interacting with the cell membrane, triggering the generation of reactive oxygen species (ROS) and altering the level of antioxidant molecules and enzymes. ...
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Background: Current study evaluated the protective potential of quercetin against lindane induced toxicity in mice brain. For investigation, mice were allocated into four groups; First group was control. Second group was administered with oral dose of lindane (25 mg/kg bw) for 4 consecutive days. Third group was exposed to quercetin (40 mg/kg bw) and in fourth group, quercetin was administered 1 hour prior to the exposure of lindane. Objective: Two major objectives were decided for study. First was to create lesions in the brain by lindane and; second was to evaluate the neuroprotective potential of quercetin. Methods: To study oxidative responses, level of thiobarbituric acid reactive substances (TBARS), protein carbonyl content (PCC), reduced glutathione (GSH), superoxide dismutase (SOD), Catalase (CAT), and glutathione peroxidase (GPx) were measured in brain homogenates. Three key step regulating enzymes of tricarboxylic acid (TCA) cycle viz citrate synthase (CS), pyruvate dehydrogenase (PDH) and fumarase were also assayed. Results: Lindane treatment significantly enhanced the levels of TBARS (P<0.001),PCC (P<0.001), GPx (P<0.001), SOD (P<0.05), PDH (P<0.05) and fumarase (P<0.001) in brains of mice compared to control. Meanwhile, it alleviated GSH, CAT and CS (P<0.05) activity. Conclusion: Pretreatment with quercetin in lindane treated group not only restored, previously altered biochemical parameters after lindane treatment and also significantly improved them too which suggests that quercetin is not only invulnerable rather neuroprotective against lindane intoxication.
... Similar results were obtained by Kumar et al. (2009) and Sharma et al. (2014). AChE has two sites which bind to the cationic and esteric domains of acetylcholine, cleaving the molecule between these sites (Bist et al., 2013). α-CYP may show AChE inhibitory activity by interacting with anionic substrate binding site (Sharma et al., 2014). ...
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... There is shown an increase in serum MDA levels of dichlorvos exposed mice when compared with control group (Fig. 1). MDA, a reactive species which is one of the LPO end products and used as redox marker, is measured for elevated oxidative stress [44]. Earlier studies also had shown that the high amount of dichlorvos stimulate LPO through increasing plasma MDA levels [45]. ...
... GSH is a non-enzymatic antioxidant which plays a key role in the detoxification of xenobiotic compounds, ROS and free radicals. Increasing oxidative stress is usually accompanied by a decline in GSH level [44]. Intoxication with dichlorvos is reported to induce an oxidative stress leading to generation of ROS and free radicals that convert GSH to oxidized form GSSG [40,56]. ...
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