Ceria-Doped Titania Nanoparticles as Drug Delivery System.

The development of new devices at the nanoscale level, as therapeutic support in medical practice, has facilitated the development of drug delivery systems (DDSs) based on nanoparticles. This enables the transport of an effective dose of therapeutic agents to target cells or tissues, with no collateral damage to healthy cells. Owing to their unique properties, nanoparticles doped with rare earths have demonstrated the potential of being used as a DDS of drug molecules to target cells or tissues. In the present work, ceria-doped titania nanoparticles (CeO2/TiO2NPs) were used to form the DNR-CeO2/TiO2NPs complex as a DDS of daunorubicin (DNR), which was tested in a B-lymphocyte cell culture. The CeO2/TiO2NPs were synthesized via the sol-gel process in a microemulsion of reverse micelle. In general, the results indicated that the nanoparticles presented good biocompatibility and load efficiency superior to that reported in other investigations for pure titania nanoparticles, suggesting that the CeO2/TiO2NPs increased intracellular accumulation of the drug. These results indicate that a delivery strategy using CeO2/TiO2NPs is a promising approach in the medical field, particularly in anticancer therapies.

Colloidal synthesis of biocompatible iron disulphide nanocrystals.

The aim of this research was to synthesis biocompatible iron disulphide nanocrystals at different reaction temperatures using the colloidal synthesis methodology. Synthesis was conducted at the 220-240 °C range of reaction temperatures at intervals of 5 °C in an inert argon atmosphere. The toxicity of iron disulphide nanocrystals was evaluated in vitro using mouse fibroblast cell line. Two complementary assays were conducted: the first to evaluate cell viability of the fibroblast via an MTT assay and the second to determine the preservation of fibroblast nuclei integrity through DAPI staining, which labels nuclear DNA in fluorescence microscopes. Through TEM and HRTEM, we observed a cubic morphology of pyrite iron disulphide nanocrystals ranging in sizes 25-50 nm (225 °C), 50-70 nm (230 °C) and >70 nm (235 °C). Through X-ray diffraction, we observed a mixture of pyrite and pyrrohotite in the samples synthesized at 225 °C and 240 °C, showing the best photocatalytic activity at 80% and 65%, respectively, for the degradation of methylene blue after 120 minutes. In all experimental groups, iron disulphide nanocrystals were biocompatible, i.e. no statistically significant differences were observed between experimental groups as shown in a one-way ANOVA and Tukey's test. Based on all of these results, we recommend non-cytotoxic semiconductor iron sulphide nanocrystals for biomedical applications.

Peroxisome proliferator-activated receptors: role of isoform gamma in the antineoplastic effect of iodine in mammary cancer.

Peroxisome proliferator-activated receptors (PPAR) are ligand-activated transcription factors. Three subtypes--PPAR alpha, PPAR beta, and PPAR gamma--have been identified and are differentially expressed in tissues. Originally, they were described as molecular regulators of lipid metabolism; recently, it has been shown that they are also involved in regulating the cell cycle and apoptosis in both normal and tumoral cells. In fact, some synthetic PPAR ligands are used to treat dyslipidemia, metabolic diseases, and type 2 diabetes. Here, we review the role of PPAR gamma (PPARγ) in tumor initiation and progression, emphasizing the relationship between this isoform and the cellular and molecular mechanisms involved in the antineoplastic effect of iodine on mammary cancer.

A complex between 6-iodolactone and the peroxisome proliferator-activated receptor type gamma may mediate the antineoplastic effect of iodine in mammary cancer.

Recently we and other groups have shown that molecular iodine (I(2)) exhibits potent antiproliferative and apoptotic effects in mammary cancer models. In the human breast cancer cell line MCF-7, I(2) treatment generates iodine-containing lipids similar to 6-iodo-5-hydroxy-eicosatrienoic acid and the 6-iodolactone (6-IL) derivative of arachidonic acid (AA), and it significantly decreases cellular proliferation and induces caspase-dependent apoptosis. Several studies have shown that AA is a natural ligand of the peroxisome proliferator-activated receptors (PPARs), which are nuclear transcription factors thought to participate in regulating cancer cell proliferation. Our results show that in MCF-7 cells: (1) 6-IL binds specifically and with high affinity to PPAR proteins (EMSA assays), (2) 6-IL activates both transfected (by transactivation assays) and endogenous (by lipid accumulation) peroxisome proliferator response elements, and (3) 6-IL supplementation increases PPAR gamma and decreases PPAR alpha expression. These results implicate PPARs in a molecular mechanism by which I(2), through formation of 6-IL, inhibits the growth of human breast cancer cells.