Format

Send to

Choose Destination
Cent Nerv Syst Agents Med Chem. 2017;17(3):187-195. doi: 10.2174/1871524917666170201145102.

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

Author information

1
Post Graduate Department of Biochemistry and Biotechnology, Cell & Molecular Therapeutics Laboratory, OIST, Midnapore-721102, West Bengal. India.
2
Post Graduate Department of Biochemistry and Biotechnology, Cell and Molecular Therapeutics Laboratory, Oriental Institute of Science and Technology, Midnapore-721102, West Bengal. India.
3
Medical Education, Government of West Bengal, Swasthya Bhawan, Calcutta-91. India.
4
Department of Nutrition, Raja N.L Khan Women's College, Midnapore, West Bengal. India.

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; DNA fragmentation; SOD1; arsenic toxicity; cytosolic; neuroprotection by Camellia sinensi

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Bentham Science Publishers Ltd.
Loading ...
Support Center