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DC Field | Value | Language |
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dc.contributor.author | Maiti, Smarajit | - |
dc.contributor.author | Acharyya, Nirmallya | - |
dc.contributor.author | Ghosh, Tamal K. | - |
dc.contributor.author | Ali, Sk. Sajed | - |
dc.contributor.author | Manna, Emili | - |
dc.contributor.author | Nazmeen, Aarifa | - |
dc.contributor.author | Sinha, Nirmalya K | - |
dc.date.accessioned | 2022-04-18T09:14:05Z | - |
dc.date.available | 2022-04-18T09:14:05Z | - |
dc.date.issued | 2017-02 | - |
dc.identifier.issn | 1871-5249 | - |
dc.identifier.uri | http://111.93.204.14:8080/xmlui/handle/123456789/543 | - |
dc.description.abstract | 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- , 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. | en_US |
dc.language.iso | en | en_US |
dc.publisher | Central Nervous System Agents in Medicinal Chemistry (Bentham Science Publishers) | en_US |
dc.subject | Antioxidant system | en_US |
dc.subject | Arsenic toxicity | en_US |
dc.subject | DNA fragmentation | en_US |
dc.subject | Neuroprotection by Camellia sinensi | en_US |
dc.subject | SOD1 | en_US |
dc.title | Green Tea (Camellia sinensis) Protects Against Arsenic Neurotoxicity via Antioxidative Mechanism And Activation of Superoxide Dismutase Activity | en_US |
dc.type | Article | en_US |
Appears in Collections: | Articles |
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File | Description | Size | Format | |
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2017 Green Tea protects against arsenic neurotoxicity-CNSAMC.pdf | 749.07 kB | Adobe PDF | View/Open |
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