Abstract
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.
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Acknowledgments
This work was supported by grants from NIA (AG18436) to VMM, NIDDK/NIH DK57733 and DK45619 to MAF, from the National Institute of Environmental Health Sciences (MAF) grant ES11461, and from the Leonard B. Rosenberg Renal Research Foundation of the Center for dialysis Care, Cleveland Ohio.
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Monnier, V.M., Nemet, I., Sell, D.R., Weiss, M.F. (2011). Transition Metals and Other Forms of Oxidative Protein Damage in Renal Disease. In: Miyata, T., Eckardt, KU., Nangaku, M. (eds) Studies on Renal Disorders. Oxidative Stress in Applied Basic Research and Clinical Practice. Humana Press. https://doi.org/10.1007/978-1-60761-857-7_2
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Publisher Name: Humana Press
Print ISBN: 978-1-60761-856-0
Online ISBN: 978-1-60761-857-7
eBook Packages: Biomedical and Life SciencesBiomedical and Life Sciences (R0)