The aim of this research was to study the influence of aging on inflammation and oxidative stress in heart from SAM-P8 and SAM-R1 mice, and to investigate the effect of chronic administration of melatonin on these parameters. Mice of 2 and 10 months of age were used (n=60). Animals were divided into eight groups, two old groups, two young groups and four melatonin groups, of both strains. Melatonin was provided in two different dosages (1mg/kg/day- 10mg/kg/day) in the drinking water. After treatment (30 days) the expression of tumor necrosis factor-a (TNFa), interleukin 1 and 10 (IL-1, IL-10), endothelial and inducible nitric oxide synthases (eNOS, iNOS) and heme oxygenases 1 and 2 (HO-1, HO-2), were measured by real-time reverse transcription polymerase chain reaction. Age increased the expression of TNFa, IL-1, HO-1 and iNOS (p<0.05) in old SAM-P8 mice, as compared with young controls. In old SAM-R1 mice increases in HO-1 and iNOS (p<0.05) were found, compared to young mice. Levels of eNOS and IL-10 (p<0.05) were decreased in old SAM-P8 mice vs young animals. A similar situation was observed in SAM- R1 mice. The expression of HO-2 in SAM-P8 were practically identical, but lower than in SAM-R1 animals. After treatment with melatonin, the inflammatory and oxidative status were partially reverted, specially, with the highest dose. Our results suggest that inflammation and oxidative status could contribute to the alterations of the cardiovascular system associated with aging and that chronic treatment with melatonin during aging, may exert beneficial effects. Acknowledgments: RETICEF-RD06/0013, SAF200766878- C02-01, CONICYT Fellowship-Chile.