Curcumin, a phytochemical derived from the rhizome of Curcuma longa, is a very potent inducer of cancer cell death. It is believed that cancer cells are more sensitive to curcumin treatment than normal cells. Curcumin has been shown to act as a prooxidant and induce DNA lesions in normal cells. We were interested in whether curcumin induces DNA damage and the DNA damage response (DDR) signalling pathway leading to apoptosis in normal resting human T cells. To this end, we analyzed DNA damage upon curcumin treatment of resting human T cells (CD3+) and in proliferating leukemic Jurkat cells by fluorimetric detection of alkaline DNA unwinding (FADU assay) and immunocytochemical detection of -H2AX foci. We showed that curcumin-treated Jurkat cells and resting T cells show neither DNA lesions nor activated key proteins in DDR signalling pathway, such as phospho-ATM, and phospho- p53. However, both types of cells were equally sensitive to curcumin-induced apoptosis and displayed activation of caspase-8, but not of DNA-damage dependent caspase-2. Altogether, our results revealed that curcumin can induce apoptosis of normal resting human T cells which is not connected with DNA damage.