In this study, lauric acid-coated, superparamagnetic, nanoparticle-based magnetic fluids of different ferrites (Fe(3)O(4), MnFe(2)O(4), and CoFe(2)O(4)) were prepared and compared in terms of heating ability and biocompatibility to evaluate the feasibility of use in hyperthermia treatment of cancer. All the magnetic fluids prepared had particles of average sizes 9-11 nm. Heating ability of these magnetic fluids was evaluated by calorimetric measurement of specific absorption rate (SAR) at 300 kHz frequency and 15 kA/m field. Fe(3)O(4) and MnFe(2)O(4) showed higher SAR (120 and 97 W/g of ferrite, respectively) than CoFe(2)O(4) (37 W/g of ferrite). In vitro study on BHK 21 cell lines showed dose-dependent cell viability for all the magnetic fluids. Threshold-biocompatible ferrite concentration for all the magnetic fluids was 0.1 mg/mL. Above 0.2 mg/mL, CoFe(2)O(4) was more toxic than the other magnetic fluids. On intravenous injection of different doses (50, 200, and 400 mg/kg body weight) of magnetic fluids in mice, no significant changes in hematological and biochemical parameters were observed for Fe(3)O(4) and MnFe(2)O(4). With CoFe(2)O(4), an increase in SGPT levels at a dose rate of 400 mg/kg body weight was observed, indicating its mild hepatotoxic effect. However, histology of different vital organs showed no pathological changes for all the three magnetic fluids. Further, long term in vivo evaluation of biocompatibility of the lauric acid-coated ferrites is warranted. This study shows that lauric acid-coated, superparamagnetic Fe(3)O(4) and MnFe(2)O(4) may be used for hyperthermia treatment and are to be preferred over CoFe(2)O(4).

The aqueous extract of the fruits of Emblica officinalis (T1), Terminalia chebula (T2) and Terminalia belerica (T3) and their equiproportional mixture triphala were evaluated for their in vitro antioxidant activity. gamma-Radiation induced strand break formation in plasmid DNA (pBR322) was effectively inhibited by triphala and its constituents in the concentration range 25-200 microg/mL with a percentage inhibition of T1 (30%-83%), T2 (21%-71%), T3 (8%-58%) and triphala (17%-63%). They also inhibited radiation induced lipid peroxidation in rat liver microsomes effectively with IC(50) values less than 15 microg/mL. The extracts were found to possess the ability to scavenge free radicals such as DPPH and superoxide. As the phenolic compounds present in these extracts are mostly responsible for their radical scavenging activity, the total phenolic contents present in these extracts were determined and expressed in terms of gallic acid equivalents and were found to vary from 33% to 44%. These studies revealed that all three constituents of triphala are active and they exhibit slightly different activities under different conditions. T1 shows greater efficiency in lipid peroxidation and plasmid DNA assay, while T2 has greater radical scavenging activity. Thus their mixture, triphala, is expected to be more efficient due to the combined activity of the individual components.

No abstract

Ionizing radiation-generated reactive oxygen species (ROS) resulting in oxidative damage to the cell membrane and its consequent role in the mechanism of apoptotic cell death have been receiving growing attention in cellular radiobiology. In recent years, evidence has accumulated to suggest that it is the damage to the cell membrane that contributes to the radiation cell killing. It has been demonstrated that degradation of membrane-bound sphingomyelinase (SMase) after irradiation of bovine endothelial cell produces ceramide, which initiates an apoptotic cascade, suggesting membrane-triggered events in the mechanism of cellular apoptosis. Fluorescence and electron spin resonance (ESR) studies from gamma-irradiation ofliposomal vesicles have shown that radiation-mediated lipid damage was modified by the inclusion of structure-modulating agents (e.g., cholesterol) and antioxidants (e.g., tocopherol, eugenol). The magnitude of the modification of the damage was found to be dependent on the concentration of these modifiers. Moreover, experiments on dipalmitoyl phosphatidyl choline (DPPC) unilamellar liposomes demonstrated a biphasic behavior of radiation damage, which was remarkably modified by ascorbic acid and alpha-tocopherol in a concentration-dependent fashion. The comparison of their protective effects showed that ascorbic acid was less effective than tocopherol against radiation damage to liposomes. Studies on irradiated mouse thymocytes employing FDA fluorescence probe have suggested post-irradiation time- and dose-dependent changes in membrane permeability. The determination of induction of apoptosis in irradiated thymocytes showed a time-dependent DNA fragmentation, suggesting that radiation-induced permeability changes and occurrence of apoptotic death in thymocytes were closely correlated. These results are discussed, with an emphasis on membrane-damage-mediated apoptotic death with relevance to improvement of cancer radiotherapy.