Please use this identifier to cite or link to this item: http://localhost:80/xmlui/handle/123456789/543
Full metadata record
DC FieldValueLanguage
dc.contributor.authorMaiti, Smarajit-
dc.contributor.authorAcharyya, Nirmallya-
dc.contributor.authorGhosh, Tamal K.-
dc.contributor.authorAli, Sk. Sajed-
dc.contributor.authorManna, Emili-
dc.contributor.authorNazmeen, Aarifa-
dc.contributor.authorSinha, Nirmalya K-
dc.date.accessioned2022-04-18T09:14:05Z-
dc.date.available2022-04-18T09:14:05Z-
dc.date.issued2017-02-
dc.identifier.issn1871-5249-
dc.identifier.urihttp://111.93.204.14:8080/xmlui/handle/123456789/543-
dc.description.abstractAbstract: 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.isoenen_US
dc.publisherCentral Nervous System Agents in Medicinal Chemistry (Bentham Science Publishers)en_US
dc.subjectAntioxidant systemen_US
dc.subjectArsenic toxicityen_US
dc.subjectDNA fragmentationen_US
dc.subjectNeuroprotection by Camellia sinensien_US
dc.subjectSOD1en_US
dc.titleGreen Tea (Camellia sinensis) Protects Against Arsenic Neurotoxicity via Antioxidative Mechanism And Activation of Superoxide Dismutase Activityen_US
dc.typeArticleen_US
Appears in Collections:Articles

Files in This Item:
File Description SizeFormat 
2017 Green Tea protects against arsenic neurotoxicity-CNSAMC.pdf749.07 kBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.