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Oxidative stress (OS) is a well-recognized etiologic agent of senescence and of several pathological conditions, such as heart failure, Duchenne's muscular dystrophy, Parkinson's disease, diabetic retinopathy and Crohn's disease (1). OS can be either intrinsic or extrinsic of biological systems, for instance originating from mitochondrial respiration, phagocytic cell activity, mechanical unloading, exposure to xenobiotics or even highly energetic radiations. OS consists in an unbalance between production and scavenging of pro-oxidant chemical species, which favors a pathological oxidized state of biomacromolecules, activates degenerative chain reaction processes, and disrupts fundamental redox signaling/control (2). Pro-oxidant chemical species are typical by-products of metabolism and accomplish complex regulatory functions (also with beneficial effects) that ultimately affect several cellular processes (3). However, if in large amount, they can for instance affect proteins by triggering opposite sign processes, that is a loss of normal folding and function or a gain of aberrant function, frequently related to protein misaggregation. Rich in contractile proteins, muscle tissue is particularly vulnerable to protein carbonylation. In this context, oxidation of myosin heavy chain was shown to decrease sliding velocity during contraction of both diaphragm and soleus muscle in rats, thus suggesting important functional impairment (4). Conditions that decrease gravity load for several days or weeks, such as prolonged bed rest or long space flights, cause the deterioration and weakening of the postural muscles, and this phenomenon has been shown to be tightly correlated with OS (5). Other evidences demonstrated that the administration of the antioxidant allopurinol presented protective effects on muscle under limb-lifting conditions, counteracting the contractile dysfunction of the soleus (6). Analogously, the absence of load on the respiratory muscles due to continuous mechanical ventilation-caused OS and subsequent contractile dysfunction, which were inhibited by systemic administration of the antioxidant Trolox (7). Due to the ubiquitous presence and the high diffusivity of several pro-oxidant chemical species in both intracellular and extracellular environments, complex and cross-talking antioxidant systems evolved to quench their detrimental effects on biomacromolecules. Among these, there are enzymatic and nonenzymatic defense mechanisms (the latter typically featuring low molecular weight). Superoxide dismutase and catalase are the main antioxidant enzymes involved in the depletion of exceeding pro-oxidants, whereas glutathione, ubiquinone, uric acid and other molecules of dietary intake (such as L-ascorbic acid, α-tocopherol and curcumin) are a...