By Trevor M. Penning, J. Mark Petrash

content material: part 1: basic review ; 1. creation and evaluate 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 issues ; three. Aldose Reductase Detoxifies Lipid Aldehydes and Their Glutathione Conjugates ; four. function of Aldose Reductase within the cleansing of Oxidized Phospholipids ; part three: AKRS AND EXOGENOUS TOXICANTS: TOBACCO similar cancer agents ; five. Competing Roles of Reductases within the cleansing 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 by way of the AKR Pathway of PAH Activation ; 10. research of Etheno-2'-Deoxyguanosine Adducts as Dosimeters of AKR Mediated Oxidative rigidity ; 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 cellphone traces to enquire the position of aldo-keto reductases within the detoxication of aldehydes and ketones ; part five: AKRS, the strain reaction AND mobile SIGNALING ; 14. Aldose Reductase and the tension reaction ; 15. Aldose Reductase Regulates Reactive Oxygen Species Mediated-Inflammatory indications ; sixteen. Aldo-Keto Reductases within the tension reaction of the Budding Yeast Saccharomyces cerevisiae

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Liu, S. ; Runge, M. ; Bhatnagar, A. Arterioscler Thromb. 2000, 20, 1745-1752. ; ACS Symposium Series; American Chemical Society: Washington, DC, 2003. Chapter 4 Role of Aldose Reductase in the Detoxification of Oxidized Phospholipids 1 2 2 Sanjay Srivastava , Kota V. Ramana , Satish K. Srivastava , Stanley E. ch004 3 1 Departments of Medicine, Division of Cardiology and Physiology and Biophysics, University of Louisville, Louisville, KY 40202 Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston, TX 77555 1 3 2 Oxidation of phospholipids generates products in which unsaturated fatty acids at the sn-2 position are oxidized to short chain aldehydes or epoxides.

Tomlinson, D. ; Stevens, E. ; Diemel, L. T. Trends in Pharmacol. Sci. 1994, 15, 293-297. 11. ; Barlocco, D. Med Res Rev 1999, 19, 3-23. 12. Pfeifer, M . ; Schumer, M . P. Diabetes 1995, 44, 1355-1361. 13. Srivastava, S. ; Hair, G. ; Das, B. Proc. Natl. Acad. Sci. USA 1985 82, 7222-72226. 14. ; Srivastava, S. K. Diabetes 1985, 34, 1145-1151. 15. Srivastava, S. ; Petrash, J. ; Sadana, I. ; Ansari, N . ; Partridge, C. A. Curr. Eye Res. 1983, 2, 407-410. 16. ; Boss, G. ; Lane, M . F. 1987 Diabetologia 30, 222-227.

Treatment with AR inhibitors has been shown to prevent secondary complications of diabetes, however, the clinical efficiency of these drugs is limited due to generation of inhibitor-resistant forms of the enzyme in diabetic tissues. Our studies suggest that the development of inhibitor resistance is due to the induction of post-translational modifications of the enzyme mediated in part by concurrent changes in cellular glutathione and nitric oxide bioavailability. In addition, inhibition of the enzyme during diabetes could prevent the physiological functions of AR.

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