Abstract
It has been established that the activity of recombinant human peroxiredoxins (Prx1, Prx2, Prx4 and Prx6) inhibits by natural dicarbonyls formed during free radical peroxidation of unsaturated lipids (malonic dialdehyde) and oxidative transformations of glucose (glyoxal, methylglyoxal). The possible role of peroxiredoxins activity decreasing under oxidative and carbonyl stress is discussed as an important factor that includes molecular mechanisms of vascular wall damage in atherosclerosis and diabetes mellitus.
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