Please use this identifier to cite or link to this item: http://hdl.handle.net/10603/304486
Title: Targeting arsenic induced metabolic disturbances and genotoxicity its mitigation by epigallocatechin gallate EGCG to prevent malignant transformation
Researcher: Kaushal, Surbhi
Guide(s): Sharma, V. L. and Chopra, Mani
Keywords: EGCG
Genotoxicity
Metabolic perturbations
Oxidative stress
ROS
University: Panjab University
Completed Date: 2019
Abstract: The present research work has explored the mitigating potential of EGCG against arsenic induced oxidative stress mediated cellular and sub-cellular changes, genotoxicity, apoptosis and metabolic disturbances that formed the basis of malignant transformation in hepato-renal tissues of mice. Out of pre and post treatments of EGCG, pre treatments of EGCG (25 mg and 50 mg/kg b.wt.) effectively reduced arsenic bioaccumulation, ROS production, serum and metabolic marker levels, recuperated the disturbed biochemical and morphological alterations. EGCG pre treatments reduced the genotoxin burden, cellular apoptosis, prevented metabolic disturbances by regulating the disturbed glucose metabolism and inhibited the malignant transformation. Thus, this data confers EGCG to possess geno-protective, anti-apoptotic and glucoregulatory efficacy against arsenic induced genotoxic and metabolic disturbances. Hence, EGCG could be explored as a potential pharmacological candidate for drug designing against metal induced genotoxicity, metabolic perturbations and malignant transformation. newline
Pagination: 269p.
URI: http://hdl.handle.net/10603/304486
Appears in Departments:Department of Zoology

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03_acknowledgement.pdf95.33 kBAdobe PDFView/Open
04_content.pdf208.74 kBAdobe PDFView/Open
05_list of tables.pdf36.05 kBAdobe PDFView/Open
06_list of figures.pdf294.95 kBAdobe PDFView/Open
07_abbreviations.pdf138.88 kBAdobe PDFView/Open
08_abstract.pdf54.63 kBAdobe PDFView/Open
09_chapter 1.pdf285.13 kBAdobe PDFView/Open
10_chapter 2.pdf1.12 MBAdobe PDFView/Open
11_chapter 3.pdf876.71 kBAdobe PDFView/Open
12_chapter 4.pdf9.64 MBAdobe PDFView/Open
13_chapter 5.pdf1.52 MBAdobe PDFView/Open
14_chapter 6.pdf327.14 kBAdobe PDFView/Open
15_bibliography.pdf762.45 kBAdobe PDFView/Open
80_recommendation.pdf327.14 kBAdobe PDFView/Open
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