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Metals, Metal Oxides, and Their Composites—Safety and Health Awareness
Published in Vijay B. Pawade, Paresh H. Salame, Bharat A. Bhanvase, Multifunctional Nanostructured Metal Oxides for Energy Harvesting and Storage Devices, 2020
Some of the in-vitro examinations have reported the toxic potential of Ni and NiO NPs. In general, the NPs are more toxic than coarser particles, and moreover, Ni+2 ions released within cells is of vital importance. NiO NPs show cytotoxicity at high levels through cellular uptake and Ni2+ release within cells. As against this the cellular effect on fine NiO particles exposure was constrained because of a very small quantity of Ni2+ release. The investigation of toxicity observed in human lung epithelial A549 cells exposed to Ni NPs of size 65 nm with a concentration level of 25 μg/mL for a period of 24 and 48 hr was done. Different assays pertaining to oxidative stress and cell vitality were obtained. Ni NPs reduce cell vitality and enhance the oxidative stress to 2 μg/mL, which is a comparatively small level as against those employed in other in-vitro examinations. As far as the toxic potential of Ni NPs and that of Ni micrometer-sized particles is concerned, it was observed that soluble NiCl2 and NiO NPs almost had the same cytotoxicity; however, Ni metal NPs exhibited low toxicity while Ni micrometer-sized particles were not toxic on exposure to lung cells in humans. Both Ni and NiO NPs induced stability as well as nuclear translocation of the hypoxia-inducible transcription factor 1α (HIF-1α). Such an effect is not showcased by the micro-sized particles. HIF-1α is observed often in human cancers and help in the identification of cells showing resistance to hypoxia and tumor formation [384].
Anti-Cancer and Anti-Angiogenic Properties of Nano-Diamino-Tetrac, A Thyroid Hormone Derivative
Published in Shaker A. Mousa, Raj Bawa, Gerald F. Audette, The Road from Nanomedicine to Precision Medicine, 2020
Paul J. Davis, Shaker A. Mousa
Nanotetrac downregulates expression of 8 of 9 cyclin genes and one cyclin-dependent kinase gene [18] and more than 20 oncogenes. Thus, the agent acts at multiple points of vulnerability in the cancer cell. It promotes apoptosis, antagonizes anti-apoptotic (survival) defenses, disrupts control of the cell cycle, and interferes with function of the frequently mutated catenins [7, 18, 22]. As noted above in the review of angiogenesis, thyroid hormone and tetrac or its Nanotetrac formulation affect matrix metalloproteinase gene expression. T4 induces transcription of MMP-9 in myeloma cells [53] and tetrac prevents expression of this gene in response to thyroid hormone. The importance of this is that an intact metalloproteinase axis interferes with cell-cell interaction, resulting in tissue destabilization that supports cancer cell invasiveness and metastasis [76]. We would also note that thyroid hormone (T4) has protein trafficking action on integrin αvβ3, directing internalization of the membrane protein—without the hormone ligand—and nuclear uptake of the αv monomer, but not of β3. In the nuclear compartment, αv is a co-activator protein [73]. Among the cancer-relevant genes whose transcription is affected by this action of T4 is ERα, important to breast, ovarian, and certain lung cancers. The thyroid hormone-directed αv monomer also increases transcription of the HIF1α gene. HIF-1α protein is a cell survival factor that triggers angiogenesis and cellular conversion to anaerobic metabolism [77].
Anti-Cancer and Anti-Angiogenic Properties of Nano-Diamino-Tetrac, A Thyroid Hormone Derivative
Published in Shaker A. Mousa, Raj Bawa, Gerald F. Audette, The Road from Nanomedicine to Precision Medicine, 2019
Paul J. Davis, Shaker A. Mousa
Nanotetrac downregulates expression of 8 of 9 cyclin genes and one cyclin-dependent kinase gene [18] and more than 20 oncogenes. Thus, the agent acts at multiple points of vulnerability in the cancer cell. It promotes apoptosis, antagonizes anti-apoptotic (survival) defenses, disrupts control of the cell cycle, and interferes with function of the frequently mutated catenins [7, 18, 22]. As noted above in the review of angiogenesis, thyroid hormone and tetrac or its Nanotetrac formulation affect matrix metalloproteinase gene expression. T4 induces transcription of MMP-9 in myeloma cells [53] and tetrac prevents expression of this gene in response to thyroid hormone. The importance of this is that an intact metalloproteinase axis interferes with cell-cell interaction, resulting in tissue destabilization that supports cancer cell invasiveness and metastasis [76]. We would also note that thyroid hormone (T4) has protein trafficking action on integrin αvβ3, directing internalization of the membrane protein—without the hormone ligand—and nuclear uptake of the αv monomer, but not of β3. In the nuclear compartment, αv is a co-activator protein [73]. Among the cancer-relevant genes whose transcription is affected by this action of T4 is ERα, important to breast, ovarian, and certain lung cancers. The thyroid hormone-directed αv monomer also increases transcription of the HIF1α gene. HIF-1α protein is a cell survival factor that triggers angiogenesis and cellular conversion to anaerobic metabolism [77].
Detoxifying effects of optimal hyperoxia (40% oxygenation) exposure on benzo[a]pyrene-induced toxicity in human keratinocytes
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Yong Chan Kwon, Hyung Sik Kim, Byung-Mu Lee
In this study, HIF-1α was measured to assess O2 levels within the cell (Chandel and Budinger 2007). HIF-1α is a protein that is expressed dependent upon O2 concentrations. In particular, it is a protein that is commonly detected in hypoxic conditions. The expression of this protein was reduced with increasing O2 levels and did not appear to be markedly affected by the presence of B[a]P in HaCat cells (Figure 4b).
Effects of intermittent hypoxic training performed at high hypoxia level on exercise performance in highly trained runners
Published in Journal of Sports Sciences, 2018
Anthony M. J. Sanchez, Fabio Borrani
Chronic adaptations to altitude and normobaric hypoxic training include muscle remodeling and the modulation of central factors such as ventilation, haemodynamics or neural factors. The most recognized effects of training in hypoxia are growth of mitochondrial density, increased oxidative enzyme activity, enhanced capillary thickness, and generally a shift from fat and muscle glycogen to blood glucose combustion (Bailey & Davies, 1997; Böning, 1997; Flaherty et al., 2016). In addition, a transient increase in hemoglobin concentration and hematocrit can be observed, especially for acclimatisation to spending many weeks at altitude or in hypoxia (De Smet et al., 2017; Park et al., 2016; Wehrlin, Marti, & Hallén, 2016; Woods et al., 2017). However, the duration of hypoxic exposure appears too small to induce hematological adaptations in hypoxic training interventions (Constantini, Wilhite, & Chapman, 2017; Park, Nam, Tanaka, & Lee, 2016). From a molecular viewpoint, the hypoxia-inducible factor (HIF-1) induces transcription of the erythropoietin (EPO) gene and other molecules involved in angiogenesis in response to hypoxia (Prabhakar & Semenza, 2012), while it is quickly degraded by the ubiquitin-proteasome system in normoxia (Cheng, Kang, Zhang, & Yeh, 2007; Wilber, Stray-Gundersen, & Levine, 2007). HIF-1 is also involved in the improvement of tissue function during low oxygen availability through increased expression of glycolytic enzymes and glucose transporters. Furthermore, recent data strongly suggests that the HIF-1α response is blunted in response to long-term exercise training which promotes enhanced oxidative metabolism (Lindholm & Rundqvist, 2016). According to the degree of hypoxia and the duration of exposure, the effects of IHT on performance seem more related to skeletal muscle adaptations than to systemic responses (Hoppeler & Vogt, 2001; Lundby, Calbet, & Robach, 2009; Park et al., 2016; Villa et al., 2005; Vogt et al., 2001; Zoll et al., 2006). Moreover, with IHT, even if athletes are under hypoxic stress, the training-related stress is limited due to the diminution of training load. “IHNT” is an interval training modality where high-intensity exercise periods are conducted under hypoxia, while the recovery periods are in normoxia. Performing recoveries in normoxia during IHNT allows completion of greater workloads during the sessions (e.g. more repetitions), especially when the hypoxic stimulus is the key. However, to our knowledge, this variant of IHT has not yet been assessed in athletes. Previous studies have only shown that this method is successful in patients, especially among those with neurological disorders, but were completed with a lower hypoxic stimulus (Astorino, Harness, & White, 2015).