Introduction et But de l’étude. – Oxidative stress has been involved in the aging-associated mitochondrial dysfunctions, which may themselves contribute to the development of chronic metabolic diseases. In this study, we aimed at investigating the association between aging-associated oxidative stress and impairments in mitochondrial functionning.

Matériel et Méthodes. – Twelve month-old mice from the well characterized aging model senescence-accelerated mouse prone-8 strain, supplemented (P8-NAC) or not (P8) with 15 mg/d N-acetylcysteine, and their controls from the senescence-accelerated mouse resistant-1 strain (R1) were used for assessment of the oxidative status and mitochondrial function in skeletal muscle.

Résultats. – P8 mice displayed an oxidative stress evidenced by increased muscle carbonylated proteins content (+ 95 %), increased xanthine oxidase (+ 79 %) and decreased MnSOD (– 24 %) activities (p = 0,03, p = 0,03 and p = 0,02, respectively), both latter being reversed in P8-NAC (p = 0,029 and p = 0,02). Compared to R1, P8 group was characterized by lower enzymatic activity of mitochondrial complex 1 (p = 0,03). By contrast, respiration measurements in muscle-isolated mitochondria revealed higher glutamate/malate as well as succinate/rotenone, stimulated maximal respiration in P8 compared to R1 (+ 47 % and + 26 %, respectively). These strain differences in enzymatic activity and respiration were reversed in P8-NAC (p = 0,01 and p = 0,02, respectively).

Conclusion. – In this model of aging, mitochondrial enzymatic adaptation matches expected effect of subchronic oxidative stress. However, functional investigations reveal that respiratory activity is disconnected from these alterations. These intrinsical adaptations might be explained by differential expression of ubiquinone, a coenzyme involved in the transport of electrons and with antioxidant properties.