Aim: Evaluation of the biocompatibility and radiosensitizer potential of citrate-coated cobalt (cit-CF) and nickel (cit-NF) ferrite nanoparticles (NPs). Materials & methods: Normal fibroblast and b... Graphical abstract

Magnetic hyperthermia can complement traditional cancer treatments by exploiting the greater heat sensitivity of tumor cells. This approach allows for localized action, increasing its therapeutic effectiveness. In this study, MCF-7 breast cancer cell radiosensitization, induced by the magnetic hyperthermia of PEGylated nickel ferrite magnetic nanoparticles (PEG-NiF MNPs), was evaluated by exposing the cells in the presence of MNPs to an alternating magnetic field followed by ⁶⁰Co gamma irradiation. Superparamagnetic PEG-NiF MNPs (25.6 ± 0.5 nm) synthesized via the hydrothermal method exhibited a hydrodynamic size below 150 nm, a saturation magnetization of 53 emu·g⁻¹, biocompatibility of up to 100 µg·mL⁻¹, selectivity for breast cancer cells, and an up-to-fivefold increase in therapeutic efficacy of radiation. When combined with magnetic hyperthermia, this increase reached up-to-sevenfold. These results indicate that PEG-NiF MNPs are suitable thermal radiosensitization agents for breast cancer cells.

Technetium-99m (99mTc) has been the radionuclide of choice for nuclear medicine procedures and experimental research. Because of its optimal nuclear properties, 99mTc is suitable for high efficiency detection with the advantage of reduced radiological waste. Crotalus venom (CV) has been shown to reduce tumors in clinical studies and tissue distribution studies are very important for clinical use. The goal of this work was to obtain CV labeled with 99mTc which preserves its biological activity. After labeling, biological activity was assessed by hemolytic activity evaluation. Labeled and crude venom caused indirect hemolysis provided that the incubation medium contained an exogenous source of lecithin. High yield radiolabeled-CV was obtained and biological activity was preserved. The results suggest that 99mTc-CV can be a useful tool for biodistribution studies.

Vitamin D (VD) is a steroid hormone with multiple biological functions in the body and its activity requires the binding to the receptor named VDR. VDR polymorphisms seems to be involved in the development of several types of cancer. Herein we performed the genotyping of two VDR polymorphisms (Fok I and Taq I) in MCF-7 breast cancer and U87-MG glioblastoma (GBM) cell lines and investigated the antiproliferative effect of the VD analog cholecalciferol. Polymorphisms were identified by PCR-RFLP and the effect of VD was determined by viability and clonogenic assays. VD inhibited the growth of both tumor cells in vitro. MCF-7 cells were more sensitive than U87-MG cells at concentrations ranging from 0.1nM to 1000nM. The same primer pairs used for PCR amplification of VDR gene in MCF-7 failed to amplify a fragment of expected size in the U87-MG cell line. VDR Fok I and Taq I polymorphisms in breast cancer MCF-7 cells were characterized as FF (CC) and TT respectively. The absence of amplification of VDR gene fragment in U87-MG suggests a possible chromosomal rearrangement and/or impairment of gene expression of VDR which could interfere in the sensitivity of this cell line to vitamin D.

Pituitary adenomas constitute about 6-18% of brain tumours in adults. Activation of voltage gated calcium currents can account for growth hormone oversecretion in some GH-secreting pituitary adenomas that produce an acromegaly appearance and increase mortality. Ca2+ ions, as mediators of intracellular signalling, are crucial for the development of apoptosis. However, the role of [Ca2+] in the development of apoptosis is ambiguous. In this study, the effects of low-dose ionising gamma radiation (60Co) on rat pituitary adenoma cells survival and proliferation and the role of calcium channels on the apoptosis radio-induced were evaluated. Doses as low as 3 Gy were found to inhibit GH3 cell proliferation. Even though there was a significant number of live cells,168 hours following irradiation, they were not able to proliferate. The results indicate that the blockade of extracellular calcium influx through these channels does not interfere in the radiation-induced apoptosis in GH3 cells.