Free radical generation and oxidative stress with ageing and exercise: Differential effects in the myocardium and liver

Reactive oxygen species and other oxidants are implicated in the mechanisms of biological ageing and exercise-induced tissue damage. The present study examined the effects of ageing and an acute bout of exercise on intracellu lar oxidant generation, lipid peroxidation, protein oxidation and glutathio ne (GSH) status in the heart and liver of young adult (8 month, N = 24) and old (24 month, N = 24) male Fischer 344 rats. Young rats ran on treadmill at 25 m min(-1), 5% grade until exhaustion (55.4 +/- 2.7 min), whereas old rats ran at 15 m min(-1). 5% until exhaustion (58.0 +/- 2.7 min). Rate of d ichlorofluorescin (DCFH) oxidation, an indication of intracellular oxidant production, was significantly higher in the homogenates of aged heart and l iver compared with their young counterparts. In the isolated heart and live r mitochondria, ageing increased oxidant production by 29 and 32% (P < 0.05 ), respectively. Acute exercise increased oxidant production in the aged he art but not in the liver. When nicodinamide dinucleotide phosphate (reduced ), adenosine diphosphate and Fe3+ were included in the assay, DCFH oxidatio n rate was 47 and 34% higher (P < 0.05) in the aged heart and liver homogen ates, respectively, than the young ones. The age differences in the induced slate reached 83 and 140% (P < 0.01) in isolated heart and liver mitochond ria, respectively. Lipid peroxidation was increased in the aged liver and e xercised aged heart, whereas protein carbonyl content was elevated only in the aged heart (P < 0.05). Although our data using DCFH method probably und erestimated cellular oxidant production because of rime delay and antioxida nt competition, it is clear that oxidative stress was enhanced in both hear t and liver with old age. Furthermore, aged myocardium showed greater susce ptibility to oxidative stress after heavy exercise.