Neuroprotective efficacy of curcumin in arsenic induced cholinergic dysfunctions in rats

Yadav, Rajesh Singh; Chandravanshi, Lalit P.; Shukla, Rohit; Sankhwar, Madhu Lata; Ansari, Reyaz W.; Shukla, Pradeep Kumar; Pant, Aditya B.; Khanna, Vinay K.

doi:10.1016/j.neuro.2011.07.004

Cited by 107 publications

(51 citation statements)

References 98 publications

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“…CMN and QR are widely considered to be responsible for its protective effects in different tissues (Haleagrahara et al 2013;Ciftci et al 2012;Yadav et al 2011). CMN and QR cotreatment for in vitro study has been evidenced to be beneficial for the mitochondria and mitigates the induced toxic response (Sandoval-Acuña et al 2012;Yadav et al 2011). In our results, CMN and QR pretreatment prevented the increase of brain PC content caused by Oxa.…”

Section: Discussionsupporting

confidence: 62%

“…CMN and QR both have been reported to act as a electrophilic scavenger (Kahraman et al 2012;Barzegar and Moosavi-Movahedi 2011;Kluth et al 2007), as well as an antioxidant (Waseem and Parvez 2013;Tang et al 2012). CMN and QR are widely considered to be responsible for its protective effects in different tissues (Haleagrahara et al 2013;Ciftci et al 2012;Yadav et al 2011). CMN and QR cotreatment for in vitro study has been evidenced to be beneficial for the mitochondria and mitigates the induced toxic response (Sandoval-Acuña et al 2012;Yadav et al 2011).…”

Section: Discussionmentioning

confidence: 99%

“…It is largely present in fruits, vegetables, aromatic plants, tea, and red wine (Pandey and Rizvi 2009). The use of both CMN and QR has been reported as a therapeutic agent to mitigate various kinds of toxicity including cardiotoxicity (Matouk et al 2013;Swamy et al 2012), nephrotoxicity (Ciftci et al 2012;Nabavi et al 2012), hepatotoxicity (Waseem and Parvez 2013;Sekaran et al 2012), and neurotoxicity (Haleagrahara et al 2013;Yadav et al 2011). Pretreatment with CMN and QR was found to modulate mitochondrial dysfunction in rodents, and its property as an antioxidant is widely held to be responsible for its protective effects in the mitochondria (Carrasco-Pozo et al 2012;Sood et al 2011).…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Waseem

Parvez

2015

Protoplasma

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Peripheral neurotoxicity is one of the serious dose-limiting side effects of oxaliplatin (Oxa) when used in the treatment of malignant conditions. It is documented that it elicits major side effects specifically neurotoxicity due to oxidative stress forcing the patients to limit its clinical use in long-term treatment. Oxidative stress has been proven to be involved in Oxa-induced toxicity including neurotoxicity. The mitochondria have recently emerged as targets for anticancer drugs in various kinds of toxicity including neurotoxicity that can lead to neoplastic disease. However, there is paucity of literature involving the role of the mitochondria in mediating Oxa-induced neurotoxicity and its underlying mechanism is still debatable. The purpose of this study was to investigate the dose-dependent damage caused by Oxa on isolated brain mitochondria under in vitro conditions. The study was also designed to investigate the neuroprotective effects of nutraceuticals, curcumin (CMN), and quercetin (QR) on Oxa-induced mitochondrial oxidative stress and respiratory chain complexes in the brain of rats. Oxidative stress biomarkers, levels of nonenzymatic antioxidants, activities of enzymatic antioxidants, and mitochondrial complexes were evaluated against the neurotoxicity induced by Oxa. Pretreatment with CMN and QR significantly replenished the mitochondrial lipid peroxidation levels and protein carbonyl content induced by Oxa. CMN and QR ameliorated altered nonenzymatic and enzymatic antioxidants and complex enzymes of mitochondria. We conclude that CMN and QR, by attenuating oxidative stress as evident by mitochondrial dysfunction, hold promise as agents that can potentially reduce Oxa-induced adverse effects in the brain.

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Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Waseem

Parvez

2015

Protoplasma

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“…Curcumin protected cultured neurons against direct oxidative insults including exposure to copper , hydrogen peroxide (Ray et al, 2011), and tert-butyl hydroperoxide . In vivo studies in rats and mice demonstrated that curcumin treatment ameliorates learning and memory deficits caused by exposure to arsenic (Yadav et al, 2011), Ab (Ahmed et al, 2010, and severe epileptic seizures (Choudhary et al, 2013). In cell culture and mouse models of PD, curcumin protected dopaminergic neurons against glutathione depletion and protein oxidation (Jagatha et al, 2008).…”

Section: A Oxidative Stressmentioning

confidence: 99%

Adaptive Cellular Stress Pathways as Therapeutic Targets of Dietary Phytochemicals: Focus on the Nervous System

et al. 2014

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“…A number of studies have been carried out to assess the protective profile of herbal or synthetic agents against arsenic induced oxidative stress in animal models [2,[13][14][15]. Amla, an important fruit of E. officinalis, a well-known medicinal herb, has been widely used as an indigenous medicine in the traditional Indian system of medicine.…”

Section: Introductionmentioning

confidence: 99%

Arsenic-Induced Hepatic Toxicity and Its Attenuation by Fruit Extract of Emblica officinalis (Amla) in Mice

et al. 2013

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Arsenic a metalloid and environmental contaminated has been found to be associated with public health problems in the affected areas. It is naturally occurred in groundwater and its accumulation in plant and animals leads to toxicity in several tissues most notably hepatic organ. Arsenic exposures (3 mg/kg body weight/ day for 30 days) in mice exhibited increased arsenic and Zn levels in hepatocytes associated with enhanced oxidative stress in hepatocytes while there were no significantly changes were observed in Cu level. An increase in the lipid peroxidation and decrease in the levels of reduced glutathione and activity of superoxide dismutase, catalase, and glutathione peroxidase were observed in arsenic treated mice as compared to controls. Arsenic exposure in mice also caused a significant change in serum biomarkers in the SGOT, SGPT and creatinine as compared to the controls. There were no significant changes in the serum levels of total protein in these mice. Co-administration of arsenic and fruit extract of amla (500 mg/kg body weight/day for 30 days) caused a significant reduction of arsenic transference associated with significantly decreases hepatic arsenic levels and balanced the antioxidant enzyme and levels of serum hepatic enzymes like SGOT and SGPT. The results of the present study clearly demonstrate the antioxidant property of amla that could be responsible for its protective efficacy in arsenic induced hepatic toxicity.

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Neuroprotective efficacy of curcumin in arsenic induced cholinergic dysfunctions in rats

Cited by 107 publications

References 98 publications

Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Adaptive Cellular Stress Pathways as Therapeutic Targets of Dietary Phytochemicals: Focus on the Nervous System

Arsenic-Induced Hepatic Toxicity and Its Attenuation by Fruit Extract of Emblica officinalis (Amla) in Mice

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