tine Des Rosiers. Decreased cardiac mitochondrial NADP-isocitrate dehydrogenase activity and expression: a marker of oxidative stress in

00378.2004.—Mitochondrial dysfunction subsequent to increased ox-idative stress and alterations in energy metabolism is considered to play a role in the development of cardiac hypertrophy and its pro-gression to failure, although the sequence of events remains to be elucidated. This study aimed at characterizing the impact of hyper-trophy development on the activity and expression of mitochondrial NADP-isocitrate dehydrogenase (mNADP-ICDH), a metabolic en-zyme that controls redox and energy status. We expanded on our previous finding of its inactivation through posttranslational modifi-cation by the lipid peroxidation product 4-hydroxynonenal (HNE) in 7-wk-old spontaneously hypertensive rat (SHR) hearts before hyper-trophy development (Benderdour et al. J Biol Chem 278: 45154– 45159, 2003). In this study, we used 7-, 15-, and 30-wk-old SHR and Sprague-Dawley (SD) rats with abdominal aortic coarctation. Com-pared with age-matched control Wistar-Kyoto (WKY) rats, SH