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Outdoor Air Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Two-photon imaging of live mice through a closed cranial window has since permitted the direct observation of CSF movement through the intact brain. This technique revealed that CSF is exchanged rapidly with interstitial fluid (ISF) in the brain by a highly organized, brain-wide pathway that consists of three serial elements: a para-arterial CSF influx route, a paravenous ISF clearance route, and an intracellular trans-astrocytic path that couples the two extracellular paravascular routes.7 Specifically, CSF passes through the para-arterial space that surrounds arteries; the space is bound by the abluminal surface of the blood vessel and the apical processes of astrocytes. Water channels called aquaporin 4 (AQP4) on the vascular endfeet of astrocytes8 facilitate convective flow out of the para-arterial space and into the interstitial space (Figure 2.1).
The effect of experimentally-induced diabetes on rat hippocampus and the potential neuroprotective effect of Cerebrolysin combined with insulin. A histological and immunohistochemical study
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Doaa El-Adli, Salwa A. Gawish, Amany AbdElFattah Mohamed AbdElFattah, Mona Fm. Soliman
As regards Cerebrolysin, it has been reported to activate TrKB receptor via brain derived neurotrophic factor (BDNF). TrKB is associated with anti-apoptotic signaling pathways [55]. Moreover, it has been stated that Cbl decreases the gene expression of pro-inflammatory factors and increases the gene expression of anti-inflammatory factors [56]. Also, Cbl has been presumed to activate Shh signaling cascade which is an essential modulator of anti-oxidation and anti-inflammation [12,57]. Furthermore, Cbl has been postulated to increase the expression of synaptic proteins and to promote formation of new synapses [58,59]. The authors also stated that neurotropic drugs enhance and regulate the expression of growth-associated phosphoprotein (GAP43) which is a crucial component of the axon and presynaptic terminals. Moreover, astrocytes migration and proliferation are suggested to be affected by Aquaporin-4 channel, water-selective membrane transport protein, which is regulated by Cbl as it can inhibit its activity [60,61].
Environmental transformation and nano-toxicity of engineered nano-particles (ENPs) in aquatic and terrestrial organisms
Published in Critical Reviews in Environmental Science and Technology, 2020
Qumber Abbas, Balal Yousaf, Habib Ullah, Muhammad Ubaid Ali, Yong Sik Ok, Jörg Rinklebe
Mammals including human-beings are the ultimate recipient of the ENPs distributed in different compartments of the environment either through dermal absorption, inhalation or ingestion with the consumption of contaminated food. A summary of different carbon-based, metal and metal oxide ENPs toxicological effects to mammals is presented in Table 4. Intravenous administration of ultra-small superparamagnetic-Fe3O4 (0.4, 2 and 10 μg kg−1) and diesel exhaust (400 μg kg−1) ENPs to mice increased the levels of oxidative stress-related biomarkers (lipid peroxidation, ROS, SOD) and induced DNA damage (Nemmar et al., 2015). The author speculated that small size particles specifically responsible for biological response due to their deep cellular penetration capacity. When mice were exposed to ultrafine Cu (15.7 nm) atmosphere containing 3.5 mg m−3 Cu ENPs, these ENPs were redistributed in the animal body. These ENPs caused pulmonary inflammation with increased activity of neutrophils and different cytokines/chemokines. Moreover, the expression levels of several immune responsive genes including Th1/Th2 were also altered in the spleen of Cu ENPs treated mice as compared to the control (Adamcakova-Dodd, Monick, Powers, Gibson-Corley, & Thorne, 2015). Co-exposure of ENPs can either have additive or antagonistic effects on the organisms. Tsugita, Morimoto, and Nakayama (2017) have observed the drastic lung inflammation in C57BL/6 N female mice with caspase-1 inflammasome activation and secretion of interleukin-1β (IL-1β) cytokine under the synergistic influence of widely used TiO2 and SiO2 ENPs. In order to study the genotoxic and mutagenic effects of ENPs, Åkerlund et al. (2018) have treated the human bronchial epithelial cell line (HBECL) and mouse embryonic stem cell line (MECL) with Ni ENPs, NiO and soluble Ni chloride. Hypoxanthine phosphoribosyl transferase (HPRT) and comet assays confirmed the only NiO ENPs mediated mutation and DNA damage through oxidative stress and protein unfolding (Åkerlund et al., 2018). Moreover, Al2O3 ENPs triggered up-regulation of genes associated with cell cycle retardation at the G2/S stage and ultimately cell death in human lung adenocarcinoma cell line (A549) (Li, Zhang, et al., 2016). Omics approach also detected the perturbations in normal cellular functioning in the response to alumina ENPs (Li, Zhang, et al., 2016). Carbon black ENPs induced neurotoxicity in the mice offsprings through the over-expression of the glial fibrillary acidic protein (GFAP) and aquaporin-4 after maternal exposure to ENPs in dose-dependent manner (Onoda, Takeda, & Umezawa, 2017).