In this study, an increase was demonstrated by us in caspase 3 and 8 like actions after incubation of Jurkat cells with the trypsin inhibitors. variegata Kunitz AP26113 trypsin inhibitor didn’t. On another hand, SBTI was proven to suppress ovarian cancer cell invasiveness by blocking urokinase upregulation while Bowman? Birk soybean trypsin inhibitor did not. We formerly demonstrated that PDTI and SBTI trigger rat lymphoma cell apoptosis and the present study reports that both inhibitors also induce human leukemic cell apoptosis. To achieve some understanding on the mechanism with this cell death, many features of apoptosis were investigated. A characteristic feature of apoptosis could be the cleavage of genomic DNA in to oligonucleosomal fragments. DNA fragmentation was quantified by flow cytometry after propidium iodide staining, providing proof of apoptosis induction by these trypsin Papillary thyroid cancer inhibitors, that is not linked to cell cycle arrest. The service of a number of caspases plays a major role in apoptosis in many systems, both in the original and in the execution stages and they are responsible for many of the biochemical and morphological features connected with apoptosis. Caspases may be triggered either by signaling through cell surface death receptors, TRAIL R2) or by stimuli that specifically target the mitochondria evoking the release to the cytosol of mitochondrial pro apoptotic components. Effector caspases, such as caspases3, 6, and 7, activated by initiator caspases cleave intracellular substrates, such as poly polymerase. In keeping with these results, pan caspase inhibitor and caspase 8 inhibitor protected Jurkat cells Imatinib Gleevec from PDTI induced apoptosis. Nevertheless, SBTI induced apoptosis appears not to be entirely determined by caspase 8 activity because caspase 8 inhibitor did not completely protect cells from apoptosis. Another finding was that the apoptotic process wasn’t connected to caspase 9 activation, demonstrated by the possible lack of LEHD AFC bosom together with the failure of caspase 9 inhibitor to stop cell death. Active caspase 8 may possibly induce apoptosis often straight activating other caspases or indirectly following cleavage of cytosolic facets resulting in involvement of mitochondria and release of cytochrome c. We considered the release of mitochondrial cytochrome c, and observed no significant differences with the control, to further examine the process of PDTI or SBTIinduced Jurkat mobile apoptosis. This effect, together with the fact that caspase 9 is not activated by PDTI or SBTI, recommend that the intrinsic mitochondrial pathway is not predominant in the apoptotic process. In the death receptor pathway, membrane receptors, such as Fas, trimerize and then recruit an molecule, such as FADD, and the procaspase 8, forming the death inducing signaling complex.