Title:Green Tea (Camellia sinensis) Protects Against Arsenic Neurotoxicity via Antioxidative Mechanism and Activation of Superoxide Dismutase Activity
Volume: 17
Issue: 3
Author(s): Smarajit Maiti*, Nirmallya Acharyya, Tamal K. Ghosh, Sk. Sajed Ali, Emili Manna, Aarifa Nazmeen and Nirmalya K. Sinha
Affiliation:
- Post Graduate Department of Biochemistry and Biotechnology, Cell & Molecular Therapeutics Laboratory, OIST, Midnapore-721102, West Bengal,India
Keywords:
Antioxidant system, arsenic toxicity, cytosolic, DNA fragmentation, neuroprotection by Camellia sinensi, SOD1.
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.
