Chapter 2: Transition Metals and Other Forms of Oxidative Protein Damage in Renal Disease (CROSBI ID 42775)
Prilog u knjizi | ostalo
Podaci o odgovornosti
Monnier, M. Vincent ; Nemet, Ina ; Sell, R. David ; Weiss, F. Miriam
engleski
Chapter 2: Transition Metals and Other Forms of Oxidative Protein Damage in Renal Disease
Oxidative and carbonyl stresses are dramatically increased in chronic renal disease, whereby an inverse relationship usually exists between renal clearance and the accumulation of low molecular weight compounds ultimately responsible for the damage to plasma constituents. Damage to proteins results from primary attack to protein residues by reactive oxygen species with or without metal catalyst, or via myeloperoxidase and hypochlorous acid. Secondary, indirect forms of damage result from oxoaldehydes and lipid peroxidation products involved in glycation and glycoxidation reactions with nucleophilic residues. The chemical oxidative pathways responsible for protein damage and its biological and clinical significance are discussed, emphasizing end stage renal disease. Interventions that improve or worsen oxidant stress, such as intravenous iron therapy, are reviewed.
Oxidative stress, Carbonyl stress, Glycation, Catalytic metals, Myeloperoxidase, Methylglyoxal, Ascorbic acid
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Podaci o prilogu
25-50.
objavljeno
Podaci o knjizi
Oxidative Stress in Applied Basic Research and Clinical Practice
Miyata, T. ; Eckardt, K.-U. ; Nagaku, M.
New York (NY): Springer
2011.
978-1-60761-856-0