Protective effects of quercetin against sodium fluoride-induced oxidative stress in rat erythrocytes

2011 ◽  
Vol 93 (8) ◽  
pp. 1666-1675
Author(s):  
Seyed Fazel Nabavi ◽  
Shahram Eslami ◽  
Akbar Hajizadeh Moghaddam ◽  
Naser Jafari ◽  
Seyed Mohammad Nabavi ◽  
...  
2013 ◽  
Vol 64 (4) ◽  
pp. 553-559 ◽  
Author(s):  
Seyed Fazel Nabavi ◽  
Solomon Habtemariam ◽  
Antoni Sureda ◽  
Akbar Hajizadeh Moghaddam ◽  
Maria Daglia ◽  
...  

Abstract Gallic acid has been identified as an antioxidant component of the edible and medicinal plant Peltiphyllum peltatum. The present study examined its potential protective role against sodium fluoride (NaF)-induced oxidative stress in rat erythrocytes. Oxidative stress was induced by NaF administration through drinking water (1030.675 mg m-3 for one week). Gallic acid at 10 mg kg-1 and 20 mg kg-1 and vitamin C for positive controls (10 mg kg-1) were administered daily intraperitoneally for one week prior to NaF administration. Thiobarbituric acid reactive substances, antioxidant enzyme activities (superoxide dismutase and catalase), and the level of reduced glutathione were evaluated in rat erythrocytes. Lipid peroxidation in NaF-exposed rats significantly increased (by 88.8 %) when compared to the control group (p<0.05). Pre-treatment with gallic acid suppressed lipid peroxidation in erythrocytes in a dose-dependent manner. Catalase and superoxide dismutase enzyme activities and glutathione levels were reduced by NaF intoxication by 54.4 %, 63.69 %, and 42 % (p<0.001; vs. untreated control group), respectively. Pre-treatment with gallic acid or vitamin C significantly attenuated the deleterious effects. Gallic acid isolated from Peltiphyllum peltatum and vitamin C mitigated the NaF-induced oxidative stress in rat erythrocytes.


2007 ◽  
Vol 25 (2) ◽  
pp. 221-231 ◽  
Author(s):  
S. Asha Devi ◽  
R. Vani ◽  
M. V. V. Subramanyam ◽  
Shiva Shankar Reddy ◽  
K. Jeevaratnam

2012 ◽  
Vol 132 (2) ◽  
pp. 931-935 ◽  
Author(s):  
Seyed Mohammad Nabavi ◽  
Seyed Fazel Nabavi ◽  
Shahram Eslami ◽  
Akbar Hajizadeh Moghaddam

2016 ◽  
Vol 9 (2) ◽  
pp. 78-82 ◽  
Author(s):  
Chandra Shakar Reddy Nalagoni ◽  
Pratap Reddy Karnati

Abstract Aluminum has no defined biological function and it is potentially involved in the pathogenesis of neurodegenerative disorders. Furthermore, the presence of fluoride causes more aluminum to accumulate in the brain, resulting in increased neuronal damage. In recent years, resveratrol through its ameliorative effects was found to be a neuroprotectant. This study reports the protective effects of resveratrol on combined aluminum and fluoride induced neuronal damage through oxidative stress in rats. Protective effects of resveratrol (30 mg/kg b.w) on markers of oxidative stress were determined in rats exposed to aluminum chloride (100 mg/kg b.w) along with sodium fluoride (10 mg/kg b.w) for 8 weeks. The results showed a statistically significant (p<0.05) increase in lipid peroxidation (LPx) as well as a significant (p<0.05) decrease in superoxide dismutase and catalase activity. Enlarged cells, neurofibrillary tangles, and vacuolar spaces showing oxidative stress in the cerebral cortex were also observed in hematoxylin and eosin stained sections in aluminum and fluoride treated rats. Administration of resveratrol along with aluminum + fluoride showed significant reversal of oxidative stress and neuronal damage in rats. Thus resveratrol potentially acts as a neuroprotectant against aluminum chloride + sodium fluoride induced neuronal damage through its anti-oxidant efficacy.


2020 ◽  
Vol 15 (3) ◽  
pp. 1934578X2091147
Author(s):  
Na Li ◽  
Dongdong Xin ◽  
Hongbo Li ◽  
Yanyan Zhao ◽  
Wei Zhou ◽  
...  

Fluoride is an essential trace element, but its beneficial range is narrow, and excess fluoride may have negative health effects. The objective of this study was to investigate the potential cytoprotective effects of epigallocatechin-3-gallate (EGCG) in cultured neuro-2a neuroblastoma cells exposed to sodium fluoride (NaF)-induced oxidative stress. Isolated Neuro-2a cells were exposed to increasing concentrations of NaF (0, 1, 2, 4, 6, and 8 mM) for 24 hours to induce oxidative stress. Moreover, to determine the concentration of EGCG necessary for protective effects, we exposed isolated Neuro-2a cells to increasing concentrations of EGCG (0, 0.5, 1, 5, 10, 20, 40, 60, 80, and 100 μg/mL) for 24 and 48 hours. Pretreatment with EGCG at various doses (0, 0.5, 1, 5, 10, 20, and 40 μg/mL) was evaluated in Neuro-2a cells for 24 hours, followed by an NaF (4 mM per culture well) challenge for 24 hours. As shown in this study, EGCG can protect Neuro-2a cells from NaF-induced apoptosis. This effect may be due to the reactive oxygen species scavenging activity of EGCC.


2008 ◽  
Vol 13 (2) ◽  
pp. 84-89 ◽  
Author(s):  
Na-Ri Yi ◽  
Kyoung-Chun Seo ◽  
Ji-Myung Choi ◽  
Eun-Ju Cho ◽  
Young-Ok Song ◽  
...  

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