Particulate Matter Induces Tissue OxInflammation: From Mechanism to Damage

Significance: Oxidative stress and oxidative damage are central hypothetical mechanisms for the adverse effects of airborne particulate matter (PM). Activation of inflammatory cells capable of generating reactive oxygen and nitrogen species is another proposed damage pathway. Understanding the interplay between these responses can help us understand the adverse health effects attributed to breathing polluted air. Recent Advances: The consequences of PM exposure on different organs are oxidative damage, decreased function, and inflammation, which can lead to the development/exacerbation of proinflammatory disorders. Mitochondrial damage is also an important event in PM-induced cytotoxicity. Critical Issues: Reactive oxygen species (ROS) are generated during phagocytosis of the particles, leading to enhancement of oxidative stress and triggering the inflammatory response. The activation of inflammatory signaling pathways results in the release of cytokines and other mediators, which can further induce ROS production by activating endogenous enzymes, leading to a positive feedback loop, which can aggravate the effects triggered by PM exposure. Future Directions: Further research is required to elucidate the exact mechanisms by which PM exposure results in adverse health effects, in terms of the relationship between the redox responses triggered by the presence of the particles and the inflammation observed in the different organs, so the development/exacerbation of PM-associated health problems can be prevented

Editorial: Angiogenesis and Nutraceuticals

Angiogenesis is the formation of new capillary blood vessels from pre-existing arteries, veins and capillaries. This process involves proliferation, migration and differentiation of vascular endothelial cells following the stimulation by specific angiogenic factors. Angiogenesis is a hallmark of several physiological and pathological conditions. It contributes to tissue repair, expansion, and remodeling in physiological processes such as wound healing, ovulation and embryo development. Nevertheless, when dysregulated, angiogenesis contributes to disease progression in different pathologies including cancer, atherosclerosis, cerebrovascular diseases and chronic inflammation. Many of these conditions share the same characteristics, including the occurrence of hypoxia, inflammation or oxidative stress, recruitment of inflammatory cells, angiogenic growth factor production, basement membrane degradation, endothelial cell migration, proliferation and differentiation and modulation of vascular support cells

Band structure and magnetic properties of cubic crystals In_xGa_1-xN: Ab initio calculations

Band structure of solid solutions InxGa1-xN with sphalerite structure and with considerable percentage of indium (x = 0,25; 0,5; 0,6; 0,7; 0,75; 0,9; 0,95; 0,97; 0,99; 1,0 ) is calculated using the density-functional theory (DFT) and the cluster version of the local coherent potential method within the frame of the multiple scattering theory. The electron structure of the ternary solutions of InxGa1-xN in sphalerite crystallographic modification is compared; the interpretation of their features is given. The concentration dependence on the energy gap for the entire variation range of the indium content in the solution is obtained. The spin polarization effect of the states of In, Ga, and N for the alloys with the considerable percentage of In, as well as the transition of the ternary solutions of In0.75Ga0.25N into the of magnetic semiconductor state is found out. The magnetic moments of In, Ga, and N atoms, and the saturation magnetization in InxGa1-xN semiconductor system are determined

Modulation of cutaneous scavenger receptor B1 levels by exogenous stressors impairs "in vitro" wound closure

6noScavenger receptor B1 (SR-B1) is a trans-membrane protein, involved in tissue reverse cholesterol transport. Several studies have demonstrated that SR-B1 is also implicated in other physiological processes, such as bacteria and apoptotic cells recognition and regulation of intracellular tocopherol and carotenoids levels. Among the tissues where it is localized, SR-B1 has been shown to be significantly expressed in human epidermis. Our group has demonstrated that SR-B1 levels are down-regulated in human cultured keratinocytes by environmental stressors, such as cigarette smoke, via cellular redox imbalance. Our present study aimed to investigate whether such down-regulation was confirmed in a 3D skin model and under other environmental challengers such as particulate matter and ozone. We also investigated the association between oxidation-induced SR-B1 modulation and impaired wound closure. The data obtained showed that not only cigarette, but also the other environmental stressors reduced SR-B1 expression in epidermal cutaneous tissues and that this effect might be involved in impaired wound healing.reservedmixedMuresan, Ximena Maria; Sticozzi, Claudia; Belmonte, Giuseppe; Savelli, Vinno; Evelson, Pablo; Valacchi, GiuseppeMuresan, Ximena Maria; Sticozzi, Claudia; Belmonte, Giuseppe; Savelli, Vinno; Evelson, Pablo; Valacchi, Giusepp

Alterations in oxygen metabolism are associated to lung toxicity triggered by silver nanoparticles exposure

Along with the AgNP applications development, the concern about their possible toxicity has increasingly gained attention. As the respiratory system is one of the main exposure routes, the aim of this study was to evaluate the harmful effects developed in the lung after an acute AgNP exposure. In vivo studies using Balb/c mice intranasally instilled with 0.1 mg AgNP/kg b.w, were performed. 99mTc-AgNP showed the lung as the main organ of deposition, where, in turn, AgNP may exert barrier injury observed by increased protein content and total cell count in BAL samples. In vivo acute exposure showed altered lung tissue O2 consumption due to increased mitochondrial active respiration and NOX activity. Both O2 consumption processes release ROS triggering the antioxidant system as observed by the increased SOD, catalase and GPx activities and a decreased GSH/GSSG ratio. In addition, increased protein oxidation was observed after AgNP exposure. In A549 cells, exposure to 2.5 μg/mL AgNP during 1 h resulted in augment NOX activity, decreased mitochondrial ATP associated respiration and higher H2O2 production rate. Lung 3D tissue model showed AgNP-initiated barrier alterations as TEER values decreased and morphological alterations. Taken together, these results show that AgNP exposure alters O2 metabolism leading to alterations in oxygen metabolism lung toxicity. AgNP-triggered oxidative damage may be responsible for the impaired lung function observed due to alveolar epithelial injury

Oxidative metabolism in the cardiorespiratory system after an acute exposure to nickel-doped nanoparticles in mice

There is an increasing concern over the harmful effects that metallic nanoparticles (NP) may produce on human health. Due to their redox properties, nickel (Ni) and Ni-containing NP are particularly relevant. Hence, the aim of this study was to establish the toxicological mechanisms in the cardiorespiratory oxidative metabolism initiated by an acute exposure to Ni-doped-NP. Mice were intranasally instilled with silica NP containing Ni (II) (Ni-NP) (1 mg Ni (II)/kg body weight) or empty NP as control, and 1 h after exposure lung, plasma, and heart samples were obtained to assess the redox metabolism. Results showed that, NP were mainly retained in the lungs triggering a significantly increased tissue O2 consumption rate, leading to Ni-NP-increased reactive oxygen species production by NOX activity, and mitochondrial H2O2 production rate. In addition, an oxidant redox status due to an altered antioxidant system showed by lung GSH/GSSG ratio decreased, and SOD activity increased, resulting in an increased phospholipid oxidation. Activation of circulating polymorphonuclear leukocytes, along with GSH/GSSG ratio decreased, and phospholipid oxidation were found in the Ni-NP-group plasma samples. Consequently, in distant organs such as heart, Ni-NP inhalation alters the tissue redox status. Our results showed that the O2 metabolism analysis is a critical area of study following Ni-NP inhalation. Therefore, this work provides novel data linking the redox metabolisms alterations elicited by exposure to Ni (II) adsorbed to NP and cardiorespiratory toxicity