Mitochondrial Impairment Induced by Sub-Chronic Exposure to Multi-Walled Carbon Nanotubes

Giuseppa Visalli, Alessio Facciolà, Monica Currò, Pasqualina Laganà, Vincenza La Fauci, Daniela Iannazzo, Alessandro Pistone and Angela Di Pietro
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Giuseppa Visalli: Department of Biomedical and Dental Sciences and Morphofunctional Imaging. University of Messina, 98125 Messina, Italy
Alessio Facciolà: Department of Clinical and Experimental Medicine, Unit of Infectious Diseases, University of Messina, 98125 Messina, Italy
Monica Currò: Department of Biomedical and Dental Sciences and Morphofunctional Imaging. University of Messina, 98125 Messina, Italy
Pasqualina Laganà: Department of Biomedical and Dental Sciences and Morphofunctional Imaging. University of Messina, 98125 Messina, Italy
Vincenza La Fauci: Department of Biomedical and Dental Sciences and Morphofunctional Imaging. University of Messina, 98125 Messina, Italy
Daniela Iannazzo: Department of Electronic Engineering, Industrial Chemistry and Engineering, University of Messina, 98125 Messina, Italy
Alessandro Pistone: Department of Electronic Engineering, Industrial Chemistry and Engineering, University of Messina, 98125 Messina, Italy
Angela Di Pietro: Department of Biomedical and Dental Sciences and Morphofunctional Imaging. University of Messina, 98125 Messina, Italy

IJERPH, 2019, vol. 16, issue 5, 1-13

Abstract: Human exposure to carbon nanotubes (CNTs) can cause health issues due to their chemical-physical features and biological interactions. These nanostructures cause oxidative stress, also due to endogenous reactive oxygen species (ROS) production, which increases following mitochondrial impairment. The aim of this in vitro study was to assess the health effects, due to mitochondrial dysfunction, caused by a sub-chronic exposure to a non-acutely toxic dose of multi walled CNTs (raw and functionalised). The A549 cells were exposed to multi-walled carbon nanotubes (MWCNTs) (2 µg mL −1 ) for 36 days. Periodically, cellular dehydrogenases, pyruvate dehydrogenase kinase 1 (PDK1), cytochrome c release, permeability transition pore (mPTP) opening, transmembrane potential (Δψ m), apoptotic cells, and intracellular ROS were measured. The results, compared to untreated cells and to positive control formed by cells treated with MWCNTs (20 µg mL −1 ), highlighted the efficiency of homeostasis to counteract ROS overproduction, but a restitutio ad integrum of mitochondrial functionality was not observed. Despite the tendency to restore, the mitochondrial impairment persisted. Overall, the results underlined the tissue damage that can arise following sub-chronic exposure to MWCNTs.

Keywords: MWCNTs; oxidative stress; mitochondria (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2019
References: View complete reference list from CitEc
Citations: View citations in EconPapers (2)

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