Utilization of lithium incorporated mesoporous silica for preventing necrosis and increase apoptosis in different cancer cells

There are many molecules used as a drug carrier. TUD-1 is a newly synthesized mesoporous silica (SM) molecule possess two important features; consists of mesoporous so it is very suitable to be drug carrier in addition to that it has the ability to induce apoptosis in cancer cells. However, the effect of TUD-1 appears to act as cell death inducer, regardless of whether it is necrosis or apoptosis. Unfortunately, recent studies indicate that a proportion of cells undergo necrosis rather than apoptosis, which limits the use of TUD-1 as a secure treatment. On the other hand, lithium considered as necrosis inhibitor element. Hence, the current study based on the idea of producing a new Li-TUD-1 by incorporated mesoporous silica (TUD-1 type) with lithium in order to produce a new compound that has the ability to activate apoptosis by mesoporous silica (TUD-1 type) and at the same time can inhibit the activity of necrosis by lithium. Herein, lithium incorporated in TUD-1 mesoporous silica by using sol-gel technique in one-step synthesis procedure. Moreover, lithium incorporated in TUD-1 with different loading in order to form different active sites such as isolated lithium ions, nanoparticles of Li2O, and bulky crystals of Li2O. The ability of the new compounds to induce apoptosis and prevent necrosis was evaluated on three different types of cancer cell lines, which are; liver HepG-2, breast MCF-7, and colon HCT116. The obtained results show that Li-TUD-1 has the ability to control necrosis and thus reduce the side effects of treatments containing silica in the case of lithium added to them, especially in chronic cases. This opinion has demonstrated by the significant increase in the IC50 value and cell viability compared to control groups. Consequently, the idea is new, so it needs more develop and test with materials that have a more apoptotic impact than silica to induce apoptosis without induction of necrosis.