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Title
DECLARATION
CERTIFICATE
DEDICATION
CONTENTS
ACKNOWLEDGEMENT
ABBREVIATIONS
1. Introduction and Review of Literature
Introduction
Review Of Literature
1.1 Reactive oxygen species in biological systems
1.1.1 Oxidative stress in lipids
1.1.2 Oxidative damage in DNA
1.1.3 Oxidative stress in proteins
1.1 .4 Oxidative stress in other diseases
1.1 .5 Oxidative stress in chemical carcinogenesis
Oxidative Stress In Nongenotoxic Hepatocarcinogenesis
1.1.6 Role of ROS in radiotherapy and chemotherapy
1.1.6.1 Radioprotectors and chemoprotecters
1.2 Molecular mechanism of reactive oxygen species
1.2.1 Reactive oxygen species regulate gene expression
1.2.2 Extracellular Reactive oxygen species can initiate cellular signaling
1.2.3 lntracellular reactive oxygen species are generated as second messengers
1.2.4 Mitogenic activated protein (MAP) kinase signaling pathways
1.2.5 Reactive oxygen species and oncogenes
1.3. Antioxidants
1.3.1 Endogenous antioxidants
1.3.1.1 Superoxide dismutase (SOD)
1.3.1.2 Catalase
1.3.1.3 Glutathione system
1.3.1.4 Glutathione peroxidase (GPX)
1.3.1.5 Glutathione reductase (GR)
1.3.1.6 Gulatathone-S-transferase (GST)
1.3.2 Exogenous antioxidants
1.3.2.1 Natural antioxidants
1.3.2.2 Antioxidants of plant origin
1.3.2.3 Synthetic antioxidants
1.4 Cancer chemoprevention
1.4.1 Detoxification Enzymes and Chemoprevention
1.4.1.1 Molecular mechanism of induction
1.4.1.2 Mechanism by which food phytochemicals affect xenobiotic metabolism
1.4.2 Chemoprevention of initiation step
1.4.3 Chemoprevention of promotion and / or progression step
1.5 Emblica officinalis
1.6 Scope of the present study
2. Materials and Methods
2.1. Drugs
2.1.1 Emblica officinalis
2.1.2 Chyavanaprash
2.2 Chemicals
2.3. Cell lines
2.4. Animals
2.5. Instruments
2.6. Antioxidant studies
2.6.1 Determination of superoxide scavenging activity
2.6.1.1 Riboflavin photoreduction method
2.6.1.2 Xanthine - xanthine oxidase method
2.6.2 Measurement of lipid peroxidation and its inhibition
2.6.2.1 Induction of lipid peroxide by Fe2+/ ascorbate system
2.6.2.2 Induction of lipid peroxidation by Fe3+ / ADP-ascorbate system
2.6.3 Measurement of hydroxyl radical scavenging activity
2.7 Inhibition of phase - 1 enzymes
2.7.1 Measurement of aniline hydroxylase (AH) activity
2.7.2 Measurement of aminopyrene - N-demethylase (AD) activity
2.8 Estimation of superoxide generation in peritoneal macrophages
2.9 Detrmination of antiinflammatory activity
2.10 In vitrocytotoxicity studies
2.10.1 Determination of short term in vitro cytotoxicity
2.10.2 Determination of cytotoxicity by tissue culture method
2.11 Determination of tumour reducing activity
2.11.1 Ascites tumour model
2.11.2 Solid turnour model
2.12 Determination of antimutagenic activity
2.12.1 Spizizens salt solution (10X)
2.12.2 Histidine / biotin solution (0.5 mM)
2.12.3 Top agar
2.12.4 Minimal agar plates
2.12.5 Preparation of S9 mixture
2.12.6 Preparation of S9 fraction
2.12.7 Arnes assay procedure
2.13 Determination of DNA-Adduct formation
2.14 Determination of ant carcinogenic activity
2.14.1 Induction of Methylcholanthrene induced sarcoma in mice
2.14.2 N-Nitroso diethylamine (NDEA) induced hepatic cancers in rats
2.15 Determination of hepatoprotective activity
2.15.1 Hepatotoxicity induced by acute CCI, administration
2.16 Induction of liver fibrosis in rats
2.16.1 Carbon tetrachloride (CCI4)
2.16. 2 Thioacetamide (TAA)
2.17 Histological examinations
2.18 Biochemical parameters
2.18.1 Estimation of tissue lipid peroxide
2.18.2 Estimation of protein
2.18.3 Estimation of serum lipid peroxide
2.18.4 Estimation of tissue superoxide dismutase (SOD) activity
2.18.5 Estimation of tissue glutathione peroxidase (GPX) activity
2.18.6 Estimation of tissue glutathione (GSH)
2.18.7 Estimation of cytosolic glutathione - S - transferase (GST) activity
2.18.8 Estimation of cytosolic glutathione reductase (GR) activity
2.18.9 Estimation of Aniline hydroxylase
2.18.10 Estimation of glutamate - pyruvate transaminase (GPT) activity
2.18.11 Estimation of alkaline phosphatase (ALP) activity
2.18.12 Estimation of Y-glutamyl transpeptidase (GGT) activity in tissue
2.18.13 Estimation of serum Y-glutamyl transpeptidase (GGT) activity
2.18.14 Estimation of tissue hydroxyproline
2.18.15 Estimation of serum creatinine
2.18.16 Estimation of Triglycerides in the serum
2.18.17 Estimation of Cholesterol in serum
2.18.17.1 Estimation of HDL - and LDL - Cholesterol
2.18.18 Estimation of total proteins and albumin in serum
2.18.19 Estimation of serum bilirubin
2.18.20 Estimation of serum urea
2.18.21 Determination of haemoglobin
2.18.22 Determination of total count of leukocyte
2.19 Statistical analysis
3. Antioxidant activity of Emblica officinalia
3.1 Introduction
3.2 Material and method
3.2.1 Determination of superoxide scavenging activity
3.2.1.1 Riboflavin photo reduction method
3.2.1.2 Xanthine - xanthine oxidase method
3.2.2 Determination of hydroxyl radical scavenging activity
3.2.3 Determination of lipid peroxidation inhibiting activity
3.2.3.1 Induction by Fe2+ / ascorbate system
3.2.3.2 Induction by Fe3+ - ADP/ascorbate system
3.2.4 lnhibition of superoxide generation by macrophages activated with PMA
3.2.5 Determination of antiinflammatory activity
3.2.6 lnhibition of phase-l enzyme activity in vitro
3.2.6.1 Aniline hydroxylase activity
3.2.6.2 Aminopyrene - N - demethylase activity
3.2.7 Determination of effect of E.O. and CHY extracts on lipid peroxidation and hepatic enzymes in normal rats.
3.2.7.1 Biochemical Analysis
3.2.8 Determination of effect of E.0 and CHY extracts on phenobarbital induced hepatic enzymes
3.2.9 Isolation of active principle from Emblica officinalis
3.2.9.1 Preparation of extract
3.3. Results
3.3.1 Effect of E.0 and CHY extracts on superoxide generation in vitro
3.3.2 Effect of E.0 and CHY extracts on hydroxyl radical generation
3.3.3 Effect of E.0 and CHY extracts on lipid peroxidation
3.3.4 Effect of E.0 extract on the inhibition of PMA induced superoxide production
3.3.5 Antiinflammatory activity of E.0 extract
3.3.6 Effect of E.0 extract on aniline hydroxylase (AH) and arninopyrene-N-demethylase (AD) in vitro
3.3.7 Effect of E.0 and CHY extracts in normal rats
3.3.7.1 Effect of E.0 and CHY extracts on lipid peroxidation
3.3.7.2 Effect of E.0 and CHY extracts on endogenous antioxidant levels
3.3.7.3 Effect of E.0 and CHY extracts on carcinogen metabolizing enzymes
3.3.8 Effect of E.0 and CHY extracts on phenobarbital induced hepatic enzymes
3.3.9 Antioxidant activity of isolated material from E.0
3.4. Disscussion
4. Antitumour activity of Emblica offcinalis
4.1 Introduction
4.2 Materials and methods
4.2.1 Short term in vitro cytotoxicity of E.0 extract
4.2.2 Cytotoxicity of E.0 extract in tissue culture
4.2.3 Effect of E.0 and CHY extracts on ascites tumour development
4.2.4 Effect of E.0 and CHY extracts on solid tumour development
4.2.5 Effect of E. 0 extract on cell cycle division
4.3. Results
4.3.1 Cytotoxic activity of E.0 extract in vitro
4.3.2 Cytotoxicity of E.0 extract in tissue culture
4.3.3 Effect of E.0 and CHY extracts on ascites tumour development
4.3.4 Effect of E.0 and CHY extracts on solid tumour development
4.3.5 Effect of E.0 extract on cell cycle regulation
4.4. Discussion
5. Antimutagenic and anticarcinogenic activity of Emblica ofcinalis
5.1. Inroduction
5.2 Materials and Methods
5.2.1 Preparation of S9 fraction
5.2.2 Antimutagenicity Assay
5.2.3 Determination of DNA - adduct formation
5.2.4 Anticarcinogenic activity
5.2.4.1 20 - Methylcholanthrene induced sarcoma model
5.2.4.2 N - Nitrosodiethylamine (NDEA) induced hepatocarcinogenesis
5.2.4.3 Biochemical parameters
5.3. Results
5.3.1 Antimutagenic activity of E.0 extract
5.3.2 Effect of E.O extract on DNA - adduct formation
5.3.3 Effect of E.O and CHY extracts on 20-rnethylcholanthrene induced sarcoma
5.3.4 Effect of E.O and CHY extracts on N-nitrosodiethylamine (NDEA) induced hepatocarcinogenesis.
Fig. 5.3 Effect of E.O and CHY extract on morphology of NDEA treated liver
5.4 Disscussion
Fig. 5.4 Effect of E.O and CHY extract on NDEA induced hepatocarcinogenesis
6. Hepato protective effect of Emblica officinalis and Chyavanaprash
6.1. Introduction
6.2. Materials and methods
6.2.1 lnduction of acute hepatotoxicity by carbon tetrachloride
6.2.2 Induction of carbon tetrachloride (CCI4) induced liver fibrosis
6.2.3 Induction of chronic hepatotoxicity by Thioacetamide (TAA)
6.2.4 Biochemical analysis
6.2.5 Histopathological analysis
6.3. Results
6.3.1 Effect of E.O and CHY extracts on acute CCI4 administration
6.3.2 Effect of E.O and CHY extracts on chronic CCl4 administration
Fig. 6.1 Effect of E.O and CHY extracts on acute CCl4 administration.
6.3.3 Effect of E.0 and CHY extracts on chronic TAA administration
Fig. 6.2 Effect of E.O and CHY extracts on liver fibrosis induced by chronic CCI4 administration.
6.4. Disscussion
Fig. 6.3 Effect of E.O and CHY extracts on chronic TAA administration.
7. Radioprotective and chemoprotective effect of Emblica officinalis and Chyavanaprash
7.1 Introduction
7.2 Materials and methods
7.2.1 Radioprotective studies
7.2.2 Chemoprotective studies.
7.3. Results
7.3.1 Radioprotective effect of E.O and CHY extracts
Fig.7.1 Effect of E.O and CHY onradiation induced total WBC
Fig.7.2 Effect of E.O and CHY on radiation induced change in organ weight
7.3.2 Chernoprotective effect of E.O and CHY extracts
Fig. 7.3 Effect of E.O and CHY on cyclophosphamide induced total WBC count
7.4. Discussion
Fig.7.4 Effect of E.O. and CHY on cyclocyclophosphamide induced change in organ weight
8. Summary and Conclusion
BIBILIOGRAPHY
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