The Other Side of the Coin: Beneficiary Effect of 'oxidative Burst' Upsurge with T11TS Facilitates the Elimination of Glioma Cells

Free radicals and allied molecules are the potential threats for the cellular components when they are produced in excess amount and cause different pathophysiological disorders including aging. Contrary to their detrimental effects, these molecules, in the other hand, can be utilized by the Phagocytic cells to destroy the abnormal cells and cellular components. Generation of reactive oxygen species (ROS) and nitric oxide (NO) are used as important effector molecules by Phagocytic macrophage/microglia to eliminate neoplastic cells in glioma bearing rat model. The glycoprotein T11TS/SLFA-3, by binding with CD2 receptor of macrophage/microglia, induces the generation of these reactive species when applied in three consecutive doses in glioma bearing animals. The CR3 family receptor CD11b is also correlated with the Phagocytic activity of the cells. The 'controlled' and directed production of ROS and NO by phagocytes induce cell death signals to the glioma cells and resulted in phagocytic destruction and apoptosis. The death signals generated by the free radicals and associated molecules resulted in accumulation of p53 proteins in the glioma cells. This oxidative stress induced p53 protein accumulation in neoplastic cells direct them to die by apoptosis. Therefore, the same oxidative stress causing pathophysiological problems, are used here to destroy the glioma cells by the macrophage/microglia in the delicate CNS tissue.