Curcumin loaded nanoparticles reversed monocrotophos induced motor impairment and memory deficit: Role of oxidative stress and intracellular calcium level

Mandal, M. N. A.; Jaiswal, Pawan; Mishra, Awanish

doi:10.1016/j.jddst.2020.101559

Cited by 14 publications

(6 citation statements)

References 77 publications

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“…Monocrotophos exposure is known to induce oxidative stress, reduction of antioxidant levels and causes apoptosis that could lead to multi-organ failure and severe genetic alterations [ 10 , 59 , 60 ]. Accumulating evidence from recent studies has suggested the liver as the main targeted organ for pesticide-induced toxicity [ 61 , 62 , 63 ].…”

Section: Discussionmentioning

confidence: 99%

N-Acetylcysteine Reverses Monocrotophos Exposure-Induced Hepatic Oxidative Damage via Mitigating Apoptosis, Inflammation and Structural Changes in Rats

et al. 2021

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Oxidative stress-mediated tissue damage is primarily involved in hepatic injuries and dysfunctioning. Natural antioxidants have been shown to exert hepatoprotective, anti-inflammatory and antiapoptotic properties. The present study evaluated the effect of N-acetylcysteine (NAC) against monocrotophos (MCP) exposure-induced toxicity in the rat liver. Albino Wistar rats were divided into four groups: (1) control, (2) NAC-treated, (3) MCP-exposure, (4) NAC and MCP-coexposure group. The dose of MCP (0.9 mg/kg b.wt) and NAC (200 mg/kg b.wt) were administered orally for 28 days. Exposure to MCP caused a significant increase in lipid peroxidation, protein oxidation and decreased glutathione content along with the depletion of antioxidant enzyme activities. Further MCP exposure increased pro-inflammatory cytokines levels and upregulated Bax and Caspase-3 expressions. MCP exposure also caused an array of structural alternations in liver tissue, as depicted by the histological and electron microscopic analysis. Thepretreatment of NAC improved glutathione content, restored antioxidant enzyme activities, prevented oxidation of lipids and proteins, decreased pro-inflammatory cytokines levels and normalized apoptotic protein expression. Treatment of NAC also prevented histological and ultrastructural alternations. Thus, the study represents the therapeutic efficacy and antioxidant potential of NAC against MCP exposure in the rat liver.

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Section: Discussionmentioning

confidence: 99%

N-Acetylcysteine Reverses Monocrotophos Exposure-Induced Hepatic Oxidative Damage via Mitigating Apoptosis, Inflammation and Structural Changes in Rats

et al. 2021

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“…For the estimation of brain acetylcholinesterase (AChE) activity, the method previously described by Ellman et al [ 26 ] was used with slight modification. [ 22,27,28 ] Briefly, brain homogenate (20%, w/v) was prepared in 50 mM phosphate buffer (pH 7.4), and centrifuged at 10 000 rpm for 10 minutes at 4°C. For the estimation of cholinesterase activity, 10 µL of brain/plasma sample was mixed with 100 µL phosphate buffer (pH 7.4) and 142 µL of reaction mixture (containing 8.5 µL of 10 mM 5,5′‐dithio‐bis‐[2‐nitrobenzoic acid], 3.5 µL of 75 mM acetylthiocholine iodide, and 100 µL of 50 mM phosphate buffer) in a microplate.…”

Section: Methodsmentioning

confidence: 99%

“…Motor coordination in animals was assessed in rotarod test apparatus (Rotamex‐5; Columbus Instruments) following the protocol previously standardized in our laboratory. [ 21,22 ] Briefly, each animal was placed on the rotating cylindrical rod (at a constant speed of 25 rpm), and the fall‐off time was recorded.…”

Section: Methodsmentioning

confidence: 99%

“…Thiobarbituric acid reactive substance (TBARS) was an end product of lipid per oxidation; it was measured in plasma/brain sample by using thiobarbituric acid (TBA) reactive substance method, according to the method described earlier by Ohkawa et al [ 30 ] and standardized in our laboratory. [ 22,27,28 ] One hundred microliters of supernatant of brain tissue homogenate (20%)/plasma was mixed with 200 µL of 8.1% sodium dodecyl sulfate, 1500 µL of 20% acetic acid, and 1500 µL of 0.8% TBA (w/v). The mixture was heated at 95°C for 60 minutes.…”

Section: Methodsmentioning

confidence: 99%

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Effect of hesperidin on fluoride‐induced neurobehavioral and biochemical changes in rats

Jaiswal

Mandal

Mishra

2020

J Biochem & Molecular Tox

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Fluoride is the second largest contaminant of drinking water. Fluoride toxicity is a major concern in the endemic areas where a high amount of fluoride is present in ground water. Oxidative stress has been proposed to be one of the mechanisms of fluoride‐induced toxicity. Antioxidant‐rich food has been found to alleviate fluoride‐induced toxicity. Therefore, in this study, we have examined the effect of hesperidin on fluoride‐induced neurobehavioral changes in rats. In the current study, male Sprague‐Dawley rats were exposed to sodium fluoride through drinking water (120 ppm). Hesperidin (200 mg kg−1 d−1; per os) was administered either alone or in combination with fluoride‐containing drinking water. Bisphinol A diglycidyl ether (BADGE) was used as peroxisome proliferator‐activated receptor‐γ (PPAR‐γ) antagonist and was administered (10 mg kg−1 d−1; intraperitoneal injection) with/without hesperidin along with fluoride‐containing drinking water. The behavioral changes in the animals were assessed by analyzing rotarod test, novel object recognition test, and forced swim test (FST). After 8 weeks, animals were killed to isolate blood and brain for monitoring biochemical changes. The 8‐week exposure of fluoride resulted in motor impairment as observed with reduced fall time in rotarod test, memory impairment as observed with reduced preference index in novel object recognition test, and depression‐like behavior as observed with reduced mobility index in the FST. Treatment with hesperidin improved neurobehavioral impairment along with restoration in brain biochemical changes (ie, acetylcholinesterase activity and antioxidant and oxidative stress parameters). The protective effect of hesperidin was reversed by coadministration of BADGE. The neuroprotective effect of hesperidin appears to be contributed through PPAR‐γ receptor.

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“…The residue of MCP have been reported in fruits, vegetables, dairy products, soil and water (Leuthold 2013;Mishra 2013;Kumar et al 2014;Singh et al 2021). Monocrotophos exposure is known to induce oxidative stress, reduction of antioxidant levels and causes apoptosis that could lead to multi-organ failure and genetic alterations (Velmurugan et al 2013;Sankhwar et al 2016;Mandal et al 2020). Recent studies have suggested liver as the prime targeted organ for pesticide related toxicity (Yilmaz et al 2017;Milošević et al 2018;Refaie et al 2020).…”

Section: Discussionmentioning

confidence: 99%

N-Acetylcysteine Attenuates Monocrotophos-induced Toxicity by Mitigating Oxidative Stress and Structural Changes in Rat Liver

Singh

Phogat

Prakash

et al. 2021

Preprint

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The present study evaluated the effect of N-acetylcysteine (NAC) against sub chronic monocrotophos (MCP) exposure induced oxidative stress in rat liver. Albino wistar rats were divided into control, NAC treated, MCP and MCP treated groups. An oral dose of MCP (0.9 mg/kg b.wt) and NAC (200 mg/kg b.wt) was administered for 28 days. We observed high oxidative stress generation on MCP exposure in liver tissue as evident by significant increase in lipid peroxidation, protein oxidation and decreased glutathione content followed by altered activities of superoxide dismutase, catalase and acetylcholinesterase. Sub chronic MCP exposure caused an array of cellular and structural alternations in lipids and proteins of liver tissue as depicted by the FTIR, histopathological and electron microscopic analysis. N-acetylcysteine attenuated the loss of glutathione and prevented lipid peroxidation and protein oxidation. Pre-treatment of NAC also restored histological and ultra space structural alternations. So NAC protects oxidative stress and tissue damage induced by sub chronic MCP exposure in rat liver; suggesting the therapeutic and antioxidant potential of NAC.

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Curcumin loaded nanoparticles reversed monocrotophos induced motor impairment and memory deficit: Role of oxidative stress and intracellular calcium level

Cited by 14 publications

References 77 publications

N-Acetylcysteine Reverses Monocrotophos Exposure-Induced Hepatic Oxidative Damage via Mitigating Apoptosis, Inflammation and Structural Changes in Rats

N-Acetylcysteine Reverses Monocrotophos Exposure-Induced Hepatic Oxidative Damage via Mitigating Apoptosis, Inflammation and Structural Changes in Rats

Effect of hesperidin on fluoride‐induced neurobehavioral and biochemical changes in rats

N-Acetylcysteine Attenuates Monocrotophos-induced Toxicity by Mitigating Oxidative Stress and Structural Changes in Rat Liver

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