Oxidative stress, antioxidant defences and aging

Article type: Research Article

Authors: Lenaz, Giorgio^; | Cavazzoni, Marika | Genova, Maria Luisa | D’Aurelio, Marilena | Pich, Milena Merlo | Pallotti, Francesco | Formiggini, Gabriella | Marchetti, Mario | Castelli, Giovanna Parenti | Bovina, Carla

Affiliations: Dipartimento di Biochimica “G. Moruzzi”, Università di Bologna, Via Irnerio 48, 40126 Bologna, Italy

Note: [] Corresponding author: Prof. Giorgio Lenaz, Dipartimento di Biochimica “G. Moruzzi”, Università di Bologna, Via Irnerio 48, 40126 Bologna, Italy. Tel.: +39 51 351229; Fax: +39 51 351217; E‐mail: [email protected].

Abstract: Apoptosis and aging share common mechanisms in oxidative stress and mitochondrial involvement. Treatment of cultured neuroblastoma cells with a radical initiator induced apoptosis; raise in hydrogen peroxide and release of cytochrome c from mitochondria preceded collapse of mitochondrial potential and cell death. In rat hepatocytes treated with adriamycin incubation with exogenous Coenzyme Q_{10 } counteracted the drug‐induced increase of hydrogen peroxide and the fall of the mitochondrial potential, thus demonstrating the quinone antioxidant effect. Complex I activity and its rotenone sensitivity decreased in brain cortex non‐synaptic mitochondria from old rats; a 5 kb mitochondrial DNA deletion was found only in the old rats. A similar behavior was found in human platelets from old individuals. The postulated energy decline was confirmed by the inhibitor sensitivities of platelet aggregation and lactate production. The lack of the 5 kb deletion in platelets throws doubts on mitochondrial DNA lesions as the only causes of mitochondrial dysfunction in aging.

Journal: Biofactors, vol. 8, no. 3-4, pp. 195-204, 1998