Obesity-Related Oxidative Stress: the Impact of Physical Activity and Diet Manipulation

Obesity-related oxidative stress, the imbalance between pro-oxidants and antioxidants (e.g., nitric oxide), has been linked to metabolic and cardiovascular disease, including endothelial dysfunction and atherosclerosis. Reactive oxygen species (ROS) are essential for physiological functions including gene expression, cellular growth, infection defense, and modulating endothelial function. However, elevated ROS and/or diminished antioxidant capacity leading to oxidative stress can lead to dysfunction. Physical activity also results in an acute state of oxidative stress. However, it is likely that chronic physical activity provides a stimulus for favorable oxidative adaptations and enhanced physiological performance and physical health, although distinct responses between aerobic and anaerobic activities warrant further investigation. Studies support the benefits of dietary modification as well as exercise interventions in alleviating oxidative stress susceptibility. Since obese individuals tend to demonstrate elevated markers of oxidative stress, the implications for this population are significant. Therefore, in this review our aim is to discuss (i) the role of oxidative stress and inflammation as associated with obesity-related diseases, (ii) the potential concerns and benefits of exercise-mediated oxidative stress, and (iii) the advantageous role of dietary modification, including acute or chronic caloric restriction and vitamin D supplementation

In vitro biocompatibility evaluation of surface-modified titanium alloys

The present work is aimed to evaluate the effects of a surface modification process on the biocompatibility of three vanadium-free titanium alloys with biomedical applications interest. Chemical composition of alloys investigated, in weight %, were Ti-7Nb-6Al, Ti-13Nb-13Zr, and Ti-15Zr-4Nb. An easy and economic method intended to improve the biocompatibiblity of these materials consists in a simple thermal treatment at high temperature, 750°C, in air for different times. The significance of modification of the surface properties to the biological response was studied putting in contact both untreated and thermally treated alloys with human cells in culture, Human Umbilical Vein Endothelial Cells (HUVEC) and Human Peripheral Blood Mononuclear Cells (PBMC). The TNF-α release data indicate that thermal treatment improves the biological response of the alloys. The notable enhancement of the surface roughness upon oxidation could be related with the observed reduction of the TNF-α levels for treated alloys. A different behavior of the two cell lines may be observed, when adhesion molecules (ICAM-1 and VCAM-1 in HUVEC, ICAM-1, and LFA-1 in PBMC) were determined, PBMC being more sensitive than HUVEC to the contact with the samples. The data also distinguish surface composition and corrosion resistance as significant parameters for the biological response.MIUR and Cassa di Risparmio di Firenze. Project CSD2007‐00041 of the Spanish MEC.Peer reviewe

Thermal oxidation of vanadium-freeTi alloys: An X-ray photoelectron spectroscopy study

In the present work, X-rayphotoelectronspectroscopy (XPS) was used to study the surface chemical composition of three alloys for biomedical applications: Ti–7Nb–6Al, Ti–13Nb–13Zr and Ti–15Zr–4Nb. The surface of these alloys was modified by annealing in air at 750 °C for different times with the aim of developing an oxide thick layer on top. The evolution of surface composition with annealing time was studied by XPS, and compared with the composition of the native oxide layer present on the samples before annealing. Two different oxidation trends were observed depending on the alloying elements and their corresponding diffusion kinetics, which give rise to different chemical species at the topmost layers. These results were linked with an evaluation of the biological response of the alloys by bringing them in contact with human peripheral blood mononuclear cells (PBMC).This work has been partially supported by the Spanish MEC under Projects MAT-2008-01497/NAN, MAT-2007-66719-C03-03, MAT-2006-13348 and CSD2007-00041, and by grants from Italian MIUR.Peer reviewe

New signalling pathway involved in the anti-proliferative action of vitamin D\u2083 and its analogues in human neuroblastoma cells. A role for ceramide kinase

1\u3b1,25-Dihydroxyvitamin D3 (1,25(OH)\u2082D\u2083), a crucial regulator of calcium/phosphorus homeostasis, has important physiological effects on growth and differentiation in a variety of malignant and non-malignant cells. Synthetic structural hormone analogues, with lower hypercalcemic side effects, are currently under clinical investigation. Sphingolipids appear to be crucial bioactive factors in the control of the cell fate: the phosphorylated forms, sphingosine-1-phosphate (S1P) and ceramide-1-phosphate (C1P), are mitogenic factors, whereas sphingosine and ceramide (Cer) usually act as pro-apoptotic agents. Although many studies correlate S1P function to impaired cell growth, the relevance of C1P/Cer system and its involvement in neuroblastoma cells remain to be clarified. Here, we demonstrated the anti-proliferative effect of 1,25(OH)\u2082D\u2083 as well as of its structural analogues, ZK156979 and ZK191784, in human SH-SY5Y cells, as judged by [\ub3H]thymidine incorporation, cell growth and evaluation of active ERK1/2 levels. The inhibition of ceramide kinase (CerK), the enzyme responsible for C1P synthesis, by specific gene silencing or pharmacological inhibition, drastically reduced cell proliferation. 1,25(OH)\u2082D\u2083 and ZK191784 treatment induced a significant decrease in CerK expression and C1P content, and an increase of Cer. Notably, the treatment of SH-SY5Y cells with ZK159222, antagonist of 1,25(OH)\u2082D\u2083 receptor, trichostatin A, inhibitor of histone deacetylases, and COUP-TFI-siRNA prevented the decrease of CerK expression elicited by 1,25(OH)\u2082D\u2083 supporting the involvement of VDR/COUP-TFI/histone deacetylase complex in CerK regulation. Altogether, these findings provide the first evidence that CerK/C1P axis acts as molecular effector of the anti-proliferative action of 1,25(OH)\u2082D\u2083 and its analogues, thereby representing a new possible target for anti-cancer therapy of human neuroblastoma