Advances in Molecular Toxicology, Volume 2Advances in Molecular Toxicology features the latest advances in all of the subspecialties of the broad area of molecular toxicology. Toxicology is the study of poisons and this series details the study of the molecular basis by which a vast array of agents encountered in the human environment and produced by the human body itself manifest themselves as toxins. Not strictly limited to documenting these examples the series is also concerned with the complex web of chemical and biological events that give rise to toxin-induced symptoms and disease. The new technologies that are being harnessed to analyze and understand these events will also be reviewed by leading workers in the field. Advances in Molecular Toxicology will report progress in all aspects of these rapidly evolving molecular aspects of toxicology with a view toward detailed elucidation of both progress on the molecular level and on advances in technological approaches employed
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From inside the book
Results 6-10 of 79
Page 6
... oxidation can occur either at the deoxyribose sugar or at one of the four nucleic acid bases. Depending upon the site of oxidation, different lesions with differing mutagenic and toxic endpoints can be formed. 3.1.1. Sugar oxidation and ...
... oxidation can occur either at the deoxyribose sugar or at one of the four nucleic acid bases. Depending upon the site of oxidation, different lesions with differing mutagenic and toxic endpoints can be formed. 3.1.1. Sugar oxidation and ...
Page 7
... oxidation state formed during chromate reduction) were shown to nick and unwind supercoiled plasmid DNA [18,21,24,54]. In synthetic oligonucleotides, the formation of frank strand breaks during this process has shown little or no ...
... oxidation state formed during chromate reduction) were shown to nick and unwind supercoiled plasmid DNA [18,21,24,54]. In synthetic oligonucleotides, the formation of frank strand breaks during this process has shown little or no ...
Page 8
... oxidation products. 2 Nucleoside Sequence 1.5 Cr(IV)/(III) 1 T C A G GA GG 8-oxoG * Cr(V)/(III) GGG Cr(V)/(IV) 0.5 0 Figure 6 Reduction potentials of the four nucleobases, 8-oxoG, and guanine residues in DNA with consecutive runs ...
... oxidation products. 2 Nucleoside Sequence 1.5 Cr(IV)/(III) 1 T C A G GA GG 8-oxoG * Cr(V)/(III) GGG Cr(V)/(IV) 0.5 0 Figure 6 Reduction potentials of the four nucleobases, 8-oxoG, and guanine residues in DNA with consecutive runs ...
Page 9
... oxidation [65]. As illustrated in Figure 6, high-valent chromium species have reduction potentials adequate to ... oxidation is often difficult. Recent studies have shown that 8-oxoG is considerably more prone towards oxidation than the ...
... oxidation [65]. As illustrated in Figure 6, high-valent chromium species have reduction potentials adequate to ... oxidation is often difficult. Recent studies have shown that 8-oxoG is considerably more prone towards oxidation than the ...
Contents
1 | |
25 | |
Chapter 3 GlucuronidationDependent Toxicity and Bioactivation | 57 |
Chapter 4 Allergic Contact Dermatitis A Common Skin Disease Caused by Allergic Reactions to Chemicals in Our Environment | 87 |
Chapter 5 Inorganic Molecular Toxicology and Chelation Therapy of Heavy Metals and Metalloids | 123 |
Chapter 6 Pyrimidine Damage and Repair | 153 |
Chapter 7 Formation Persistence and Significance of DNA Adduct Formation in Relation to Some Pollutants from a Broad Perspective | 183 |
Subject Index | 241 |
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Common terms and phrases
A.T. Karlberg activity acyl glucuronide adduct levels allergy amines amino analogs aristolochic acid aromatic arsenic base bile bioactivation Biochem Biochemistry Biol biological biomarkers biotransformation BSEP buspirone cancer carcinogen Carcinogenesis cells cellular chelation Chem chemical cholestasis cholestatic chromate chromium clinical compounds contact allergens Contact Dermatitis covalent binding cytosine deamination diclofenac Dispos DNA adduct DNA damage DNA glycosylase dose Drug Metab effects electrophilic enzymes excretion exposure Figure gene genetic genotoxic genotype glucuronide glucuronide conjugates glutathione GSTM1 guanine hepatic hepatocytes hepatotoxicity human hydrogen hydroperoxides induced interactions intestinal irinotecan L.C. Sowers lesions liver mechanism mercury metabolism metabolites metal microsomes molecules Mrp2 mutagenic Mutat nefazodone Nucleic Acids nucleophilic oxidation pathway Pharmacol polymorphism potential protein pyrimidines radical rats reactions reactive metabolites role rosiglitazone selenium skin sensitization species structure studies substrate thymine tissue toxicity Toxicol Toxicology trazodone troglitazone tumour uracil vitro vivo workers
Popular passages
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