Abstract
High dose selenium acts as a cytotoxic agent, with potential applications in cancer treatment. However, clinical trials have failed to show any chemotherapeutic value of selenium at safe and tolerated doses (<90 μg/day). To enable the successful exploitation of selenium for cancer treatment, we evaluated inorganic selenium nanoparticles (SeNP), and found them effective in inhibiting ovarian cancer cell growth. In both SKOV-3 and OVCAR-3 ovarian cancer cell types SeNP treatment resulted in significant cytotoxicity. The two cell types displayed contrasting nanomechanical responses to SeNPs, with decreased surface roughness and membrane stiffness, characteristics of OVCAR-3 cell death. In SKOV-3, cell membrane surface roughness and stiffness increased, both properties associated with decreased metastatic potential. The beneficial effects of SeNPs on ovarian cancer cell death appear cell type dependent, and due to their low in vivo toxicity offer an exciting opportunity for future cancer treatment.
Highlights
Selenium (Se) is an essential trace element, obtained primarily through the diet as selenium containing amino acids,[1] it has a narrow safe range of exposure and becomes toxic at levels above the recommended dietary intake (30-90 μg/ day)
Characterization of selenium nanoparticles (SeNP) aggregation and charge demonstrated SeNP-BSA had a negative charge (-51.2 ± 15.8 mV) and an average size of 108 ± 30 nm and PDI of 0.123 ± 0.002 which was considered monodisperse, and the 30-100 nm size range confirmed by transmission electron microscopy (TEM) (Figure 1, A and B)
SeNP-chitosan had a positive charge of 16.4 ± 4.4 mV, an average size of 320 ± 221 nm and PDI of 0.220 ± 0.012 and was considered as polydisperse.[29]
Summary
Selenium (Se) is an essential trace element, obtained primarily through the diet as selenium containing amino acids,[1] it has a narrow safe range of exposure and becomes toxic at levels above the recommended dietary intake (30-90 μg/ day). Observational studies revealed that Se can inhibit cancer cell growth This effect occurs through increasing ROS-mediated necrosis in prostate cancer,[4] autophagy in colorectal cancer,[5] and apoptosis in skin, breast, and liver cancer.[6] a metaanalysis of randomized controlled trials, N25,000 patients, failed to show any significant effect of Se dietary supplementation in reducing the incidence of colorectal, skin, lung, bladder or prostate cancer.[7] High supplementation levels induced toxicity limiting the utility of Se containing compounds as potential chemotherapeutic agents.[8] To overcome the toxicity associated with soluble Se, Se-nanoparticles (SeNPs) have been synthesized and evaluated for their anticancer properties. Modifications to those networks influence cytoadherence, migration, invasion and tumor metastasis.[19,20]
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