Abstract
Nanoparticles have great potential for numerous applications due to their unique physicochemical properties. However, concerns have been raised that they may induce deleterious effects on biological systems. There is accumulating evidence that, like asbestos, inhaled nanomaterials of >5 μm and high aspect ratio (3:1), particularly rod-like carbon nanotubes, may inflict pleural disease including mesothelioma. Additionally, a recent set of case reports suggests that inhalation of polyacrylate/nanosilica could in part be associated with inflammation and fibrosis of the pleura of factory workers. However, the adverse outcomes of nanoparticle exposure to mesothelial tissues are still largely unexplored. In that context, the present review aims to provide an overview of the relevant pathophysiological implications involving toxicological studies describing effects of engineered nanoparticles on mesothelial cells and membranes. In vitro studies primarily emphasize on simulating cellular uptake and toxicity of nanotubes on benign or malignant cell lines. On the other hand, in vivo studies focus on illustrating endpoints of serosal pathology in rodent animal models. From a molecular aspect, some nanoparticle categories are shown to be cytotoxic and genotoxic after acute treatment, whereas chronic incubation may lead to malignant-like transformation. At an organism level, a number of fibrous shaped nanotubes are related with features of chronic inflammation and MWCNT-7 is the only type to consistently inflict mesothelioma.
Highlights
Nanoparticles are forms of matter with at least one dimension sized less than 100 nm
Proliferation/Increased MMP-2, PLAU, STAT-3, AKT1, VEGFA expression Internalization of all Carbon nanotubes (CNT)/150 nm resulted in most permeable membrane (29%) 15 nm resulted in greatest oxidative potential 150 nm or 80 nm induced autophagy Increased cell growth of MeT5A and invasiveness of both cell lines/Activation of H-Ras-ERK signaling/ERK mediated cortactin upregulation/Integrin AV upregulation Increased migration, spindled morphology after chronic exposure Hemoglobin or transferrin coated MWCNT-7 are internalized via TR1*, increase catalytic iron content and induce aggravated genotoxicity lysosomes contain MWCNTs/oxidative stress activates ERK1,2 that induces SOD-2 upregulation Increased proliferation, invasion/DNA lesions/Altered expression of Annexins 1, 2, 5, 6 may lead to DNA lesions and changes in molecular signaling owing to a combination of oxidant and non-oxidant mechanisms largely dependent on the nanotube class
Several issues concerning the in vivo experimental approaches need to be addressed. In this last part of the review we briefly summarize some important shortcomings with regards to in vitro and in vivo nanotoxicology investigations in mesothelial cells and membranes
Summary
Nanoparticles are forms of matter with at least one dimension sized less than 100 nm. A portion of genotoxicity is likely to be a consequence of direct physical contact between nanotubes and cellular components (Shvedova et al, 2012) In support of this contention, Pacurari et al reported that 81 nm, 8.19 μm MWCNT with low iron content did not significantly affect indices of oxidative stress despite inflicting cytotoxicity and DNA damage in mesothelial cells. Proliferation/Increased MMP-2, PLAU, STAT-3, AKT1, VEGFA expression Internalization of all CNT/150 nm resulted in most permeable membrane (29%) 15 nm resulted in greatest oxidative potential 150 nm or 80 nm induced autophagy Increased cell growth of MeT5A and invasiveness of both cell lines/Activation of H-Ras-ERK signaling/ERK mediated cortactin upregulation/Integrin AV upregulation Increased migration, spindled morphology after chronic exposure Hemoglobin or transferrin coated MWCNT-7 are internalized via TR1*, increase catalytic iron content and induce aggravated genotoxicity lysosomes contain MWCNTs/oxidative stress activates ERK1,2 that induces SOD-2 upregulation Increased proliferation, invasion/DNA lesions/Altered expression of Annexins 1, 2, 5, 6 may lead to DNA lesions and changes in molecular signaling owing to a combination of oxidant and non-oxidant mechanisms largely dependent on the nanotube class.
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