Markers of oxidant stress that are clinically relevant in aging and age-related disease

Abstract

Despite the long held hypothesis that oxidant stress results in accumulated oxidative damage to cellular macromolecules and subsequently to aging and age-related chronic disease, it has been difficult to consistently define and specifically identify markers of oxidant stress that are consistently and directly linked to age and disease status. Inflammation because it is also linked to oxidant stress, aging, and chronic disease also plays an important role in understanding the clinical implications of oxidant stress and relevant markers. Much attention has focused on identifying specific markers of oxidative stress and inflammation that could be measured in easily accessible tissues and fluids (lymphocytes, plasma, serum). The purpose of this review is to discuss markers of oxidant stress used in the field as biomarkers of aging and age-related diseases, highlighting differences observed by race when data is available. We highlight DNA, RNA, protein, and lipid oxidation as measures of oxidative stress, as well as other well-characterized markers of oxidative damage and inflammation and discuss their strengths and limitations. We present the current state of the literature reporting use of these markers in studies of human cohorts in relation to age and age-related disease and also with a special emphasis on differences observed by race when relevant.

Figure 1. The role of oxidant stress in aging and age-related disease

Both non-modifiable risk factors (age, race, genotype) and modifiable risk factors (diet, socioeconomic status, environment) have the propensity to interact with and affect the inflammatory processes and affect and be affected by oxidant stress. The interaction of all of these parameters can result in oxidative modifications of cellular macromolecules DNA, RNA, lipid and proteins. These oxidative modifications alone or in association with other biologic factors can lead to epigenetic changes, changes in both gene expression and DNA repair capacity, or mitochondrial and membrane dysfunction.