Oxidative stress is caused by an imbalance between the production of reactive species of oxygen
and nitrogen (RS) and the ability to either detoxify the reactive intermediates produced or repair the resulting
damage. Ultimately, oxidative stress conveys the alteration in cellular function caused by the reaction of RS
with cellular constituents. Oxidative stress has been extensively reported to participate in the progression of a
variety of human diseases including cancer, neurodegenerative disorders and diabetes. Oxidation of proteins
is thought to be one of the major mechanisms by which oxidative stress is integrated into cellular signal
transduction pathways. Thus, recent research efforts have been aimed to identify the role of specific oxidative
protein modifications in the signal transduction events mediating the etiology of human diseases progression.
The identification of these oxidative modifications has also raised the possibility of using this knowledge to
develop new methods to diagnose diseases before they are clinically evident. In this work, we summarize the
mechanisms by which RS generate distinct oxidative modifications. Furthermore, we also review the potential
of these oxidative modifications to be used as early biomarkers of human disease.
Keywords: Alzheimer’s disease, cancer, neurodegenerative diseases, oxidative post-translational modifications,
oxidative protein damage, oxidative stress, Parkinson’s disease, reactive oxygen species, redox proteomics, redox
signaling, RNS, ROS
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