, 2001). It is also reported that the mistletoe extract inhibited

protein synthesis in malignant cells and the lectins isolated from this extract (ML-I, ML II, and ML-III) dissociated into catalytic subunits before they translocated across the membrane and entered the cytoplasm. The involvement of caspases cascade and their effects on U937 cells, by lectin ML-II, explains its cytotoxicity and apoptosis induction ( Kim et al., 2000), as well as the lectin ML-I ( Lyu et al., 2001). Along with confirming pre-existing data for ConA, the present results show that legume lectins ConA and ConBr promoted apoptosis (Figs. 4A,B and 5A–D). Even though these lectins have slight structural differences, they have specificity for the same type of carbohydrate (glucose/mannose) and show a similar effect on the tumor cell lines MOLT-4 and HL-60. Nonetheless, in each trial, Y27632 it was noticeable that lectin ConA was more potent in its effects. This confirms the idea that the cytotoxicity exhibited by the lectins ConA and ConBr on ABT-199 order tumor cells was caused mainly by induction of cell death via apoptosis, but also by necrosis when they are at higher concentrations. Thus, the cytotoxic agent may induce either apoptosis or necrosis depending on the concentrations and time of contact with the substance. Generally, apoptosis induction in tumor cells is a beneficial effect for chemotherapy

treatment of cancer. The lectins may promote apoptosis via two mechanisms. One possibility is by interacting with the cell surface, being endocytosed, and then reaching the mitochondria. This possibility would occur directly through the intrinsic pathway, as with ConA in some cell lines and other lectins such as WGA ( Chang et isothipendyl al., 2007, Gastman et al., 2004 and Suen et al., 2000). A second possibility is by binding to glycosylated portions of death receptors and then leading to its activation and apoptotic signal transduction through the extrinsic pathway. It is expected that this cytotoxicity will be mediated by the carbohydrate-binding site of the lectins. These sites should specifically recognize membrane glycoreceptors on the cell surfaces of both HL-60 and

MOLT-4 leukemic cells. Data from this study has shown the in vitro antitumor potential of legume lectins ConA and ConBr in breast tumor MCF-7 cells ( Faheina-Martins et al., 2011). This is in agreement with existing literature on ConA and other lectins known for their cytotoxic potential, such as that obtained from mistletoe ( Pryme et al., 2007). In summary, ConA and ConBr lectins induce cell death in leukemic cells and promote apoptosis with DNA fragmentation, mitochondrial depolarization and increased production of ROS. Apoptosis plays a critical role in the molecular pathogenesis of cancer and can influence the outcome of chemotherapy and radiotherapy. Because of this, dietary compounds such as plant lectins should be considered promising for cancer treatment.