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Protective Role of Gallic Acid on Sodium Fluoride Induced Oxidative Stress in Rat Brain

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Abstract

Gallic acid is known as a potent antioxidant active compound of the edible and medicinal plant Peltiphyllum peltatum. The main objective of this study was to evaluate the neuroprotective effects of gallic acid against sodium fluoride induced oxidative stress in rat brain. Gallic acid (10 and 20 mg/kg) and vitamin C (10 mg/kg) were intraperitoneally administrated for 1 week prior to sodium fluoride intoxication. After the treatment period, brain tissues were collected and homogenized, and antioxidant parameters were measured in the homogenates. The level of thiobarbituric acid reactive substances in sodium fluoride intoxicated rats (42.04 ± 2.14 nmol MDA eq/g tissue, p < 0.01 vs. normal) increased compared to the normal rats (35.99 ± 1.08 nmol MDA eq/g tissue). Pretreatment with gallic acid at 20 mg/kg was exhibited significant reduction in the thiobarbituric acid reactive substances level (37.06 ± 1.4 nmol MDA eq/g tissue, p > 0.05 vs. normal). This increasing in thiobarbituric acid reactive substances level was accompanied with a decrease in the level of reduced glutathione (6.74 ± 0.28 μg/mg of protein, p < 0.001 vs. normal), superoxide dismutase (53.24 ± 1.62 U/mg of protein, p < 0.001 vs. normal) and catalase (70.73 ± 2.94 μmol/min/mg of protein p < 0.001 vs. normal) activities in sodium fluoride intoxicated rat. Gallic acid at 20 mg/kg was significantly modified the level of reduced glutathione (11.02 ± 0.53 μg/mg of protein, p < 0.05 vs normal) and catalase activity (89.22 ± 3.67 μmol/min/mg of protein, p > 0.05 vs. normal) in rat brain. However, gallic acid at 20 mg/kg was significantly more effective in retrieving superoxide dismutase (124.78 ± 5.7 U/mg of protein) activity than vitamin C (115.5 ± 4.97 U/mg of protein).

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Acknowledgments

The authors acknowledge the financial support of National elite’s foundation of Iran (Tehran, Iran) for this study. This paper is dedicated to Seyed Maryam Nabavi, Seyed Morteza Nabavi and with memory of Seyed Ali Asghar Nabavi.

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Authors and Affiliations

  1. Applied Biotechnology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran

    Seyed Fazel Nabavi & Seyed Mohammad Nabavi

  2. National Elites Foundation of Iran, Tehran, Iran

    Seyed Fazel Nabavi & Seyed Mohammad Nabavi

  3. Pharmacognosy Research Laboratories, Medway School of Science, University of Greenwich, Central Avenue, Chatham-Maritime, Kent, ME4 4TB, UK

    Solomon Habtemariam

  4. Department of Pharmaceutical Sciences, University of California, Irvine, Irvine, CA, USA

    Mahtab Jafari

  5. Laboratori de Ciències de l’Activitat Física, Departament de Biologia Fonamental i Ciències de la Salut, Universitat de les Illes Balears, Illes Balears, Spain

    Antoni Sureda

Authors
  1. Seyed Fazel Nabavi
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  2. Solomon Habtemariam
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  3. Mahtab Jafari
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  4. Antoni Sureda
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  5. Seyed Mohammad Nabavi
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Correspondence to Seyed Mohammad Nabavi.

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Nabavi, S.F., Habtemariam, S., Jafari, M. et al. Protective Role of Gallic Acid on Sodium Fluoride Induced Oxidative Stress in Rat Brain. Bull Environ Contam Toxicol 89, 73–77 (2012). https://doi.org/10.1007/s00128-012-0645-4

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  • DOI: https://doi.org/10.1007/s00128-012-0645-4

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