Comparative effects of boric acid and calcium fructoborate on breast cancer cells.

Recent studies suggested that boron has a chemo-preventive role in prostate cancer. In the present report, we investigated the effects of calcium fructoborate (CF) and boric acid (BA) on activation of the apoptotic pathway in MDA-MB-231 human breast cancer cells. Exposure to BA and CF inhibited the proliferation of breast cancer cells in a dose-dependent manner. Treatment with CF but not BA resulted in a decrease in p53 and bcl-2 protein levels. Furthermore, after the treatment with CF, augmentation of pro-caspase-3 protein expression, cytosolic cytochrome c level, and caspase-3 activity were observed, indicating apoptotic cell death induction. This was also demonstrated by terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick-end-labeling assay. In conclusion, our data provide arguments to the fact that both BA and CF inhibited the growth of breast cancer cells, while only CF induced apoptosis. Additional studies will be needed to identify the underlying mechanism responsible for the observed cellular responses to these compounds and to determine if BA and CF may be further evaluated as chemotherapeutic agents for human cancer.

Osteoblast cell behavior on the new beta-type Ti-25Ta-25Nb alloy.

Among metallic materials used as bone substitutes, ß titanium alloys gain an increasing importance because of their low modulus, high corrosion resistance and good biocompatibility. In this work, an investigation of the in vitro cytocompatibility of a recently new developed ß-type Ti-25Ta-25Nb alloy was carried out by evaluating the behavior of human osteoblasts. The metallic Ti-6Al-4V biomaterial, which is one of representative α+ß type titanium alloys for biomedical applications, and Tissue Culture Polystyrene (TCPS), were also investigated as reference Ti-based material and control substrate, respectively. Both metallic surfaces were analyzed by X-ray diffraction, atomic force microscopy and X-ray photoelectron spectroscopy. The cellular response was quantified by assessments of viability, cell attachment and spreading, cell morphology, production and extracellular organization of fibronectin and cell proliferation. Polished surfaces from both materials having an equiaxed grain microstructure and nanometre scale surface roughness elicited an essentially identical osteoblast response in terms of all analyzed cellular parameters. Thus, on both surfaces the cells displayed high survival rates, good cell adhesion and spreading, a dense and randomly dispersed fibronectin matrix and increasing cell proliferation rates over the incubation time. Furhermore, the enhanced biological performance of Ti-25Ta-25Nb was highly supported by the results obtained in comparison with TCPS. These findings, together with previously shown superelastic behavior, low Young's modulus and high corrosion resistance, recommend Ti-25Ta-25Nb as good candidate for applications in bone implantology.

In vitro effects of calcium fructoborate upon production of inflammatory mediators by LPS-stimulated RAW 264.7 macrophages.

The present study is supported by our previous findings suggesting that calcium fructoborate (CF) has anti-inflammatory and antioxidant properties. Thus, we investigated the effects of CF on a model for studying inflammatory disorders in vitro represented by lipopolysaccharide (LPS)-stimulated murine macrophage RAW 264.7 cells. This investigation was performed by analyzing the levels of some mediators released during the inflammatory process: cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukins IL-1beta and IL-6 as well as cyclooxygenase-2 (COX-2), the main enzyme responsible for endotoxin/LPS-induced prostaglandin synthesis by macrophages. We also measured production of nitric oxide (NO) that plays an important role in the cytotoxicity activity of macrophages towards microbial pathogens. After CF treatment of LPS-stimulated macrophages we found an up-regulation of TNF-alpha protein level in culture medium, no significant changes in the level of COX-2 protein expression and a decrease in NO production as well as in IL-1beta and IL-6 release. Collectively, this series of experiments indicate that CF affect macrophage production of inflammatory mediators. However, further research is required in order to establish whether CF treatment can be beneficial in suppression of pro-inflammatory cytokine production and against progression of endotoxin-related diseases.