We propose that an increase in oxidative stress in a model of ‘in utero programming and catch-up growth’, leads to abnormally high levels of telomere attrition in kidney (Jennings, 1999) and reduced longevity (Ozanne, 2004). Dysfunctional mitochondria are thought to be a major contributor to the production of reactive oxygen species (ROS). The aim of this study was to measure mitochondrial respiratory chain complex activity (I, II, III, II+III, IV) and reduced glutathione (GSH) in the kidney of 12 month male offspring. Wistar rats were fed on dietary regimes as described in Ozanne (2004): control group (C), n=12, 20% protein during pregnancy, 20% protein during lactation, and chow from weaning through to adulthood; recuperated group (R), n=14, 8% protein during pregnancy, 20% protein during lactation, and chow from weaning through to adulthood. Male offspring were humanely killed at 12 months, and kidney cortex and medulla separated. Mitochondrial complex I to IV and citrate synthase activities were measured as described in Bolanos (1995). Results were normalized as a ratio of protein content to compensate for mitochondrial enrichment. GSH was measured by reverse phase HPLC with electrochemical detection as described by Rieder (1989). In the cortex a significant down regulation in R of mitochondrial respiratory chain enzyme activity, citrate synthase enzyme activity and GSH was observed using a paired t-test in standardised results; citrate synthase; C (136±3.6) vs. R (119±3.4) p<0.01, complex II+III; C (41±3.1), R (24±1.3) p<0.001, complex II; C (93±3.9) vs. R (83±3.2) p<0.05, complex IV; C (3.2±0.3) vs. R (2.4±0.1) p<0.01, GSH; C (1.1±0.04) vs. R (0.7±0.05) p<0.001. In the medulla a significant reduction was only observed in GSH measurements; C (0.8±0.03) vs. R (0.6±0.03) p<0.001, data means±S.E.M. We conclude that in utero protein restriction leads to mitochondrial abnormalities, which could conceivably precede and be a contributory factor in telomere shortening and premature death in these animals.