We have previously shown that the proliferative response of T cells to antigenic or mitogenic stimulus decreased with age and that caloric resection (CR) attenuated the age-related decline in proliferation and IL-2 expression. Because activation-induced apoptosis is known to regulate cell proliferation and eliminate the high number of activated cells during an immune response, it was of interest to determine what effect aging or CR has on activation-induced apoptosis in T cells. Splenic T cells isolated from young (6-month) and old (25-month) mice fed ad libitum (control group) and from old (24-month) mice fed a restricted diet (40% caloric restriction) that began at 6 weeks of age. T cells were stimulated with superantigen staphylococcal enterotoxin B (SEB) or anti-CD3 antibody (primary stimulus) for 72 to 96 h, followed by restimulation with anti-CD3 (secondary stimulus). Activation-induced apoptosis was assessed by DNA fragmentation assay and the expression Fas/CD95 and Fas-ligand (Fas-L) was measured by flow cytometry. We found that the amount of DNA fragmentation was significantly (p<0.05) increased in the stimulated and restimulated T cells from old control mice and old caloric restricted mice compared to young control mice. The increase in DNA fragmentation with age was paralleled with an increase in the proportion of the cells expressing Fas and Fas-L. However, CR had no significant effect on the age-related increase in DNA fragmentation, Fas, or Fas-L expression. We also measured the Bcl-2 and Bax protein level and found that the level of Bcl-2 decreased and Bax increased with age and that CR had no effect on the age-related changes in the level of Bcl-2 or Bax protein. These results demonstrate that aging but not CR alters activation-induced apoptosis in mice T cells.