The ability of selenium compounds and selenoproteins to regulate apoptosis is of interest to brain cancer researchers. As mentioned in the section describing anti-cancer mechanisms of selenium, apoptosis, or as it is often called, programmed cell death, is a normal event at the end of the life cycle of most cells, except brain, cardiac and cancer cells. Cancer cells are normal cells that have been ‘immortalized’ and continue to divide, because they have lost the restraints imposed by the cell’s normal life cycle. The controlling factor for the induction of cellular apoptosis is the mitochondrion. Selenium compounds can have a favorable action on the mitochondria to encourage apoptosis in cancerous brain cells.
In 1988, Philipov and Tzatchev measured the concentrations of serum selenium in 139 patients with tumors in cranium cavity. The data from patients were compared with those from a reference group of 294 healthy adult individuals. The serum concentrations of selenium was significantly decreased (p less than 0.001) in the patients with malignant tumors. The researchers discussed the possibilities for treatment of malignant tumors of central nervous system with selenium.
In 2006, S et al. examined the effect of selenium on human glioma cell lines. Cultures were incubated with selenium, and the following parameters were studied: cell growth, mitochondrial function, and ultrastructure. Cell growth was assayed by counting the number of viable cells after treatment with selenium. Mitochondrial function was analyzed. Apoptosis was determined by evaluating nuclear chromatin condensation by electron microscopy. The results indicated that selenium had a significant inhibitory effect on the growth of the tumor cells but had little effect upon dermal fibroblasts which had been passaged numerous times. Ultrastructurally, mitochondria had electron-dense inclusions resulting from selenium treatment. High rates of apoptosis were induced by selenium in the tumor cell lines and in the minimally passaged fibroblasts, whereas the fibroblasts with a high number of passages had some resistance to selenium treatment. This study correlates the effects of selenium on apoptosis and shows that selenium similarly affects three different brain tumor cell lines and minimally passaged fibroblasts.
In 2007, Rooprai et al. studied the effects of a range of concentrations (2-10 mcg/ml) of selenium were investigated in one low-passage culture of biopsy-derived glioma cells and a normal human brain cell culture. Results from 2 viability assays, consistently showed that the IC50 for selenium in the astrocytoma was approximately 5 mcg/ml whilst the normal brain cells were unaffected by selenium in the range of concentrations studied. Time-lapse video microscopy revealed that, while at 4 mcg/ml selenium, the time taken to achieve 100% cell death was 17 h, with increasing concentrations of selenium from 6 to 8 mcg/ml and finally at 10 mcg/ml the IPSB-18 cells rounded up and died much more quickly. The time taken to achieve 100% cell death was 7 h, 7 h and 6 h, respectively, suggesting that the effect was similar at higher concentrations. Flow cytometry indicated that cell death was by apoptosis. RT-PCR results showed downregulation of the gene expression of 6 matrix metalloproteases (MMP2, 9, 14, 15, 16, 24), their inhibitors, TIMPs and epidermal growth factor receptor, in IPSB-18 cells treated with 2, 4 and 8 mcg/ml of selenium. Collectively, the data in this study suggests that selenium not only induces tumor cell-specific apoptosis but also has anti-invasive potential.
 Philipov, P. and Tzatchev, K. Selenium concentrations in serum of patients with cerebral and extracerebral tumors. Zentralbl Neurochir. 1988:49;344-7.
 Sundaram, N., Pahwa, A.K., Ard, M.D., et al., Selenium causes growth inhibition and apoptosis in human brain tumor cell lines. J. Neurooncol. 2000:46;125-133
 Rooprai HK, Kyriazis I, Nuttall RK, et al. Inhibition of invasion and induction of apoptosis by selenium in human malignant brain tumour cells in vitro. Int J Oncol. 2007 May;30(5):1263-71.)