By Trevor M. Penning, J. Mark Petrash
content material: part 1: common review ; 1. advent and assessment of the Aldo-Keto Reductase (AKR) Superfamily ; part 2: AKRS AND ENDOGENOUS TOXICANTS ; 2. Aldo-Keto Reductase-Catalyzed Detoxication of Endogenous Aldehydes linked to Diabetic problems ; three. Aldose Reductase Detoxifies Lipid Aldehydes and Their Glutathione Conjugates ; four. function of Aldose Reductase within the detoxing of Oxidized Phospholipids ; part three: AKRS AND EXOGENOUS TOXICANTS: TOBACCO comparable cancer causing agents ; five. Competing Roles of Reductases within the detoxing of the Tobacco-Specific Nitrosamine Ketone NNK ; 6. Aldo-Keto Reductases and the Metabolic Activation of Polycyclic fragrant Hydrocarbons ; 7. Molecular Cloning and Characterization of Dihydrodiol Dehydrogenase from Mouse ; eight effective Synthesis of the energetic Metabolites of Carcinogenic Polycyclic fragrant Hydrocarbons ; nine. Chemistry of PAH o-Quinones Generated through the AKR Pathway of PAH Activation ; 10. research of Etheno-2'-Deoxyguanosine Adducts as Dosimeters of AKR Mediated Oxidative tension ; part four: AKRS AND EXOGENOUS TOXICANTS: MYCOTOXINS, ALDEHYDES AND KETONES ; eleven. Aflatoxin Aldehyde Reductases ; 12. Competing Reactions of Aflatoxin B1-Dialdehyde: Enzymatic aid vs Adduction with Lysine ; thirteen. using mammalian mobilephone strains to enquire the function of aldo-keto reductases within the detoxication of aldehydes and ketones ; part five: AKRS, the tension reaction AND telephone SIGNALING ; 14. Aldose Reductase and the strain reaction ; 15. Aldose Reductase Regulates Reactive Oxygen Species Mediated-Inflammatory indications ; sixteen. Aldo-Keto Reductases within the pressure reaction of the Budding Yeast Saccharomyces cerevisiae
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M. Metabolism 1979, 38, 431-438. Brownlee, M . Annual Rev. Med. 1995, 46, 223-234. ; Wells-Knecht, K. ; Blackledge, J. ; Lyons, T. ; Thorpe, S. R; Baynes, J. W. Diabetes 1994, 43, 676-683. 5. Grandee, S. ; Monnier, V . M . J. Biol. Chem. 1991, 266, 11649-11653. 6. Nagaraj, R. ; Sell, D. ; Prabhakaram, M . ; Ortwerth, B. M. Proc. Natl. Acad. Sci. 1991, 88, 10257-10261. 7. ; Wells-Knecht, K. ; Thorpe, S. ; Baynes, J. W. Biochemistry. 1991, 34, 10872-10878. ; ACS Symposium Series; American Chemical Society: Washington, DC, 2003.
These observations suggest that metabolism via A R could be a potential mechanism for the detoxification of oxidized phospholipids generated during pathological oxidative stress. ; ACS Symposium Series; American Chemical Society: Washington, DC, 2003. ch004 50 Oxidative stress has been implicated in the etiology of several cardiovascular diseases including atherosclerosis, isehemia-reperfusion, and heart failure. Extensive investigations have shown that the pivotal step in the development of atherosclerosis is the oxidation of low-density lipoproteins (LDL) (1,2).
Ch003 42 different modification is observed when AR is treated with reagents that cause protein S-nitrosylation. When incubated with NO donors such as SNAP and NONOate the maximal A R activity is increased several fold (28). This change appears also to be due to the modification of Cys-298, but in this case it is linked to the formation of an S-nitrosothiol rather than a mixed disulfide (24). Because S-nitrosylation introduces only a small molecule (NO) at the active site cysteine, the enzyme remains active and substrate access is not prevented.
Aldo-Keto Reductases and Toxicant Metabolism by Trevor M. Penning, J. Mark Petrash