Evaluation of the biological effect of Ti generated debris from metal implants: ions and nanoparticles.

Metallic implants placed in humans exhibit wear and corrosion that result in the liberation of metal-containing by-products. In the case of titanium (Ti) containing implants, the metal containing debris may exist in a number of states, including metallic particles produced by mechanical wear and the products of metal corrosion in biological environments, such as the joints and surrounding fluids and tissues. In addition, these constituents may dissolve in both intracellular and extracellular solutions generating Ti ions. Both species, ions and nanoparticles, show different cellular toxicities. In this work we have evaluated the possible evolution of TiO2 nanoparticles (NPs) into soluble Ti metal ions by contact with biological fluids. For this aim, an in vitro study to address quantitative Ti solubilisation from TiO2 nanoparticles (with a diameter of 21 nm) after incubation with human serum at different concentrations has been conducted. Total Ti determination revealed low solubilisation rates ranging from 0.53 to 0.82% after just one week of incubation in the serum. The incubated serum was then subjected to speciation analysis by anion exchange liquid chromatography using an inductively coupled plasma mass spectrometer (ICP-MS) as an elemental detector for Ti monitoring. The obtained results revealed a significant increase in the Ti signal associated with the fraction of the protein transferrin and preferentially with one of the metal binding sites of the protein, the N-lobe. Thus, the effect of Ti at the cellular level has been evaluated by considering that it can be present either as ions or as nanoparticles using two different cells lines: human enterocytes HT29 and murine osteoblasts MC3T3. Significant toxicity was found at the highest concentration assayed (50 µg mL(-1)) for both Ti species (ions and NPs) and slightly higher for the ionic species at lower concentrations (1 and 10 µg mL(-1)).

Aggravation by vanadium of magnesium deficiency in STZ-induced diabetic rats.

This study examined changes in the metabolism of magnesium (Mg), and related serum parameters, following treatment with vanadium (V) in streptozotocin-diabetic rats. Over a period of five weeks, four groups were examined: control, diabetic, diabetic-treated with 1 mg V/day or 3 mg V/day. The V was supplied in drinking water as bis(maltolato)oxovanadium(IV). The Mg levels were measured in food, faeces, urine, serum, muscle, kidney, liver, spleen, heart and femur. Albumin, uric acid, urea, total-cholesterol, LDL-cholesterol, triglycerides, aspartate-aminotransferase and alkaline-phosphatase were determined in serum. In the diabetic group, Mg retained and Mg content in serum and femur decreased, while levels of uric acid, urea, total-cholesterol, LDL-cholesterol, triglycerides and alkaline-phosphatase and aspartate-aminotransferase activity increased compared with control rats. In the diabetic group treated with 1 mg V/day, Mg retained, serum levels of Mg, urea and triglycerides, and alkaline-phosphatase activity remained unchanged, while levels of uric acid, total-cholesterol and LDL-cholesterol increased and the Mg content in femur and aspartate-aminotransferase activity decreased compared with the diabetic untreated group. In the diabetic rats treated with 3 mg V/day, food intake and glycaemia were normal. In this group, Mg content in serum, kidney and femur, levels of urea and aspartate-aminotransferase and alkaline-phosphatase activity decreased, whereas LDL-cholesterol increased, uric acid and total-cholesterol levels remained unchanged in comparison with untreated diabetic rats. In conclusion, although treatment with 3 mg V/day normalised the glycaemia, the hypomagnesaemia and tissue depletion of Mg seen in the diabetic rats, caused by the treatment with V, could have partially contributed to the fact that V did not normalise other serum parameters altered by the diabetes.