Carbonyl stress and oxidatively modified proteins in chronic renal failure

Oxidative stress is commonly observed in chronic renal failure patients resulting from an umbalance between overproduction of reactive oxygen species and impairement of defense mechanisms. Proteins appear as potential targets of uremia-induced oxidative stress and may undergo qualitative modifications. Proteins could be directly modified by reactive oxygen species which leads to amino acid oxydation and cross-linking. Proteins could be indirectly modified by reactive carbonyl compounds produced by glycoxidation and lipo-peroxidation. The resulting post-traductional modifications are known as carbonyl stress. In addition, thiols could be oxidized or could react with homocystein leading to homocysteinylation. Finaly, tyrosin could be oxidized by mycloperoxidase leading to advanced oxidative protein products (AOPP). Oxidatively modified proteins are increased in chronic renal failure patients and may contribute to exacerbate the oxidative stress/ inflammation syndrome. They have been involved in long term complications of uremia such as amyloidosis and accelerated atherosclerosis.