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Selenium causes growth inhibition and apoptosis in human brain tumor cell lines
N Sundaram1, A K Pahwa, M D Ard
1Department of Neurosurgery, University of Mississippi Medical Center, Jackson 39216-4505, USA.
Abstract:
We examined the effect of the trace element selenium on human glioma cell lines: T98G, U373MG, and U87MG, in addition to dermal fibroblast cells. Cultures were incubated with sodium selenite, 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 using the MTT (tetrazolium salt reduction) assay. 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. Selenium also induced mitochondrial damage as shown by MTT assay in two brain tumor cell lines and in minimally passaged fibroblasts, but it had little effect upon the high-passage fibroblasts. 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 adverse effects of selenium on mitochondrial function, inhibition of cell growth, and apoptosis and shows that selenium similarly affects three different brain tumor cell lines and minimally passaged fibroblasts. Further, the results with fibroblasts show that some types of cells after repeated passages can develop resistance to selenium damage.
Insights
Selenium inhibits human glioma cell growth and damages mitochondria, inducing apoptosis. However, high-passage fibroblasts show resistance, suggesting acquired tolerance to selenium toxicity.
Area of Science:
- Cell Biology
- Toxicology
- Oncology
Background:
- Trace elements like selenium play crucial roles in cellular processes.
- Understanding selenium's impact on cancer cells versus normal cells is vital for therapeutic development.
- Glioma cell lines and fibroblasts serve as models to study cellular responses to xenobiotics.
Purpose of the Study:
- To investigate the effects of selenium on human glioma cell lines and dermal fibroblasts.
- To assess selenium's impact on cell growth, mitochondrial function, and apoptosis.
- To determine if cell passage number influences sensitivity to selenium.
Main Methods:
- Cell cultures of T98G, U373MG, and U87MG glioma lines, plus dermal fibroblasts.
- Treatment with sodium selenite.
- Assays for cell viability, mitochondrial function (MTT assay), and apoptosis (electron microscopy).
Main Results:
- Selenium significantly inhibited glioma cell growth and induced mitochondrial damage and apoptosis.
- Minimally passaged fibroblasts showed sensitivity, while high-passage fibroblasts exhibited resistance.
- Ultrastructural analysis revealed electron-dense inclusions in mitochondria post-selenium treatment.
Conclusions:
- Selenium exhibits potent anti-cancer effects against glioma cells by impairing mitochondrial function and inducing apoptosis.
- Cellular resistance to selenium can develop with repeated passaging, particularly in fibroblasts.
- These findings highlight selenium's differential effects based on cell type and passage history, with implications for its therapeutic use.
