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Green Tea (Camellia sinensis) Protects Against Arsenic Neurotoxicity via Antioxidative Mechanism and Activation of Superoxide Dismutase Activity

[ Vol. 17 , Issue. 3 ]

Author(s):

Smarajit Maiti*, Nirmallya Acharyya, Tamal K. Ghosh, Sk. Sajed Ali, Emili Manna, Aarifa Nazmeen and Nirmalya K. Sinha   Pages 187 - 195 ( 9 )

Abstract:


Background: Chronic arsenic-exposure even at a low-dose results in the neural impairment and motor/cognitive dysfunction. However, several preventive approaches are made mainly against hepatic/ gastrointestinal damages. Only a few investigations postulate therapeutic strategies for neural anomalies. Here, the protective role of Green tea (Camellia sinensis or CS; 10mg/ml aqueous) has been evaluated against arsenic-induced (0.6ppm/100g bw/28 days) cerebral/cerebellar tissue degeneration, oxidative-threats and neurotransmitter deregulation in female rats.

Methods and Results: The Dunnett's t test and multiple-comparison ANOVA-test suggest that arsenic significantly decreased free thiol level with an increase in lipid-peroxidised product and damages to the tissue-structure. A significant decrease in serum urate accompanied by increases in C-reactive protein and TNF-α, an acute-phase inflammatory cytokine, strongly suggests a possible mechanism of oxidative- inflammatory tissue injury being supported by the increase in lactate-dehydrogenase activity. In addition, suppression in cytosolic superoxide-dismutase (Cu-Zn isoform/SOD1; NBT reduction-test) and an insufficient protection through catalase activity culminate free radical-related damages. In-vitro, H2O2 inactivated partially-purified (dialyzed/concentrated, 6-8kd cutoff-Millipore) rat liver SOD1 and that was markedly protected by 2-mercaptoethanol. Though significant signs of toxicities were noticed at biochemical/cellular level, the present treatment did not affect DNA (DNA-fragmentation assay) in the brain tissues. The CS supplementation significantly protected serum/tissue antioxidant-components, prevented inflammatory-responses and decreased lipid-peroxidation in brain resulting in increased tissue integrity. Moreover, arsenic-induced impairment of neurotransmitters i.e. glycine, glutamate and aspartate levels in cerebral tissue were significantly restored in CS-supplemented group.

Conclusion: Taken together, this investigation indicates the potent neuroprotective and antioxidative efficiencies of Camellia sinensis against arsenic-induced oxidative threat.

Keywords:

Antioxidant system, arsenic toxicity, cytosolic, DNA fragmentation, neuroprotection by Camellia sinensi, SOD1.

Affiliation:

Post Graduate Department of Biochemistry and Biotechnology, Cell & Molecular Therapeutics Laboratory, OIST, Midnapore-721102, West Bengal, Post Graduate Department of Biochemistry and Biotechnology, Cell and Molecular Therapeutics Laboratory, Oriental Institute of Science and Technology, Midnapore-721102, West Bengal, Medical Education, Government of West Bengal, Swasthya Bhawan, Calcutta-91, Post Graduate Department of Biochemistry and Biotechnology, Cell and Molecular Therapeutics Laboratory, Oriental Institute of Science and Technology, Midnapore-721102, West Bengal, Post Graduate Department of Biochemistry and Biotechnology, Cell and Molecular Therapeutics Laboratory, Oriental Institute of Science and Technology, Midnapore-721102, West Bengal, Post Graduate Department of Biochemistry and Biotechnology, Cell and Molecular Therapeutics Laboratory, Oriental Institute of Science and Technology, Midnapore-721102, West Bengal, Department of Nutrition, Raja N.L Khan Women's College, Midnapore, West Bengal

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