24 research outputs found
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
Structurization of cement systems with nanodispersed silica stabilized with acetate ions
Insulin protects against hepatocyte ultrastructural damage induced by type 1 diabetes mellitus in rats
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