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Cytotoxicity, oxidative stress and inflammatory responses induced by fly ash particles in human lung epithelial cells.
No full textTossicità di inquinanti ambientali correlati ai processi di incenerimento dei rifiuti solidi urbani: studio dei meccanismi molecolari su cellule del tratto respiratorio
Full text linkThe demands of our society generate wastes that tend to increase in quantity as the standard of living increases. The most effective means of dealing with this problem is to reduce the amount of wastes generated (McKay, 2002). Solid waste incinerators reduce the volume and the mass of wastes, but emissions could contain highly toxic components. Major problems regarding the operation of incineration are by-products, especially the lightest fraction (Fly Ash), that contains the highest amount of volatile heavy metals, such as Cd, Pb and Zn, and polychlorinated dibenzo-p-dioxins and dibenzofurans (Yao et al., 2012).
Particulate air pollution (PM) is an important environmental health risk factor for many different diseases. This is indicated by numerous epidemiological studies on associations between PM exposure and occurrence of acute respiratory infections, lung cancer and chronic respiratory and cardiovascular diseases (de Kok et al., 2006).
The pulmonary epithelium represents a primary barrier preventing the entry of inhaled compounds into the body. As a consequence, lung epithelial cells are also a primary target of many inhaled noxious substances (Ovrevik et al., 2009).
Fly Ash collected from the electrostatic precipitator of Bozen’s municipal solid waste incinerator was taken as an example for real particles with complex composition released into the atmosphere to study the mechanism of early biological responses of BEAS-2B and A549 human lung epithelial cells. Furthermore, some different air samples were collected in Bozen area and their cellular effects were studied.
Chemical and physical analysis identified and quantified the pollutants, and in vitro cellular assays were used to estimate some toxic effects of Fly Ash (Total Fraction) and air samples. The studies include also the effects of Water-soluble, Water-insoluble and DMSO-soluble Fractions of the Fly Ash.
The Total Fraction induced a concentration-dependent reduction on cell viability (mostly on BEAS-2B cells, as compared with A549 cells) and increased ROS generation. The Fly Ash-induced oxidative stress was correlated with diminution of tGSH content and induction of heme oxygenase-1. Data confirmed a strong correlation between samples’ composition and their biological effects, in fact Total and Water-insoluble Fractions were the most toxic and responsive, instead Water and DMSO-soluble Fractions were less active.
Fly Ash was also able to induce inflammatory responses through NF-kB activation, followed by enhancement of IL-6 and IL-8 levels.
ROS generation, tGSH reduction and IL secretion were markedly inhibited by preincubation of the cells with the anti-oxidant N-acetylcysteine, which confirmed the involvement of oxidative stress in Fly Ash toxicity.
The study of the toxicity of air samples revealed that there was a significant diminution of cellular viability only after 72 hours of exposition. The sample containing the incinerator’s chimney emissions increased ROS production and IL-6 and IL-8 secretion. This underlined that oxidative stress was probably related to the inflammatory responses and cleared how the cellular response is closely linked with the content of toxic substances of the samples
In vitro evaluation of the toxicological effects induced by fly ash particles in human airway epithelial cells
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Atypical Antipsychotics induce lysosomal regeneration rescuing dysbindin-dependent astrocytes death
No full textA Drosophila loss of function model to study the effects of Atypical Antipsychotic drugs
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Naringenin Ameliorates Drosophila ReepA Hereditary Spastic Paraplegia-Linked Phenotypes
Full text linkDefects in the endoplasmic reticulum (ER) membrane shaping and interaction with other organelles seem to be a crucial mechanism underlying Hereditary Spastic Paraplegia (HSP) neurodegeneration. REEP1, a transmembrane protein belonging to TB2/HVA22 family, is implicated in SPG31, an autosomal dominant form of HSP, and its interaction with Atlastin/SPG3A and Spastin/SPG4, the other two major HSP linked proteins, has been demonstrated to play a crucial role in modifying ER architecture. In addition, the Drosophila ortholog of REEP1, named ReepA, has been found to regulate the response to ER neuronal stress. Herein we investigated the role of ReepA in ER morphology and stress response. ReepA is upregulated under stress conditions and aging. Our data show that ReepA triggers a selective activation of Ire1 and Atf6 branches of Unfolded Protein Response (UPR) and modifies ER morphology. Drosophila lacking ReepA showed Atf6 and Ire1 activation, expansion of ER sheet-like structures, locomotor dysfunction and shortened lifespan. Furthermore, we found that naringenin, a flavonoid that possesses strong antioxidant and neuroprotective activity, can rescue the cellular phenotypes, the lifespan and locomotor disability associated with ReepA loss of function. Our data highlight the importance of ER homeostasis in nervous system functionality and HSP neurodegenerative mechanisms, opening new opportunities for HSP treatment
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