Over the last few years, it has been clearly established that normal plasma contains low levels of oxidized polypeptides, and that these accumulate in tissues during several age-related pathologies. In contrast, normal mammalian aging, contrary to conventional dogma, is not clearly associated with enhanced levels of oxidized proteins, except in extracellular connective tissues, whose proteins can, for example, be oxidized by the neutrophil oxidative burst. Since mildly oxidized proteins are susceptible to accelerated degradation in most experimental systems, the question arises as to how the accumulation of oxidized proteins can take place. Such accumulation requires an excess of production (or deposition) over removal, which might reflect alterations in capacity or rate of production or removal. This chapter discusses our presently limited knowledge of rates and control of proteolysis of oxidized proteins in two pathologies, cataractogenesis and atherogenesis. It commences with a brief summary of current understanding of the mechanisms of protein oxidation, and of the observed accumulation of oxidized proteins in several pathologies.
Proteolytic 'defences' and the accumulation of oxidized polypeptides in cataractogenesis and atherogenesis
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Jeremy Saklatvala, Hideaki Nagase, Guy Salvesen, Roger T. Dean, Rachael Dunlop, Peter Hume, Ken J. Rodgers; Proteolytic 'defences' and the accumulation of oxidized polypeptides in cataractogenesis and atherogenesis. Biochem Soc Symp 1 September 2003; 70 135–146. doi: https://doi.org/10.1042/bss0700135
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