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Abstract
This study presents the impact of carbon nanotubes (CNTs) on mitochondrial oxygen mass flux (Jm) under three experimental conditions. New experimental results and a new methodology are reported for the first time and they are based on CNT Raman spectra star graph transform (spectral moments) and perturbation theory. The experimental measures of Jm showed that no tested CNT family can inhibit the oxygen consumption profiles of mitochondria. The best model for the prediction of Jm for other CNTs was provided by random forest using eight features, obtaining test R-squared (R2) of 0.863 and test root-mean-square error (RMSE) of 0.0461. The results demonstrate the capability of encoding CNT information into spectral moments of the Raman star graphs (SG) transform with a potential applicability as predictive tools in nanotechnology and material risk assessments.
Highlights
Carbon nanotubes (CNTs) have attracted great interest for their promising applications in the fields of biomaterials and nano-biotechnology
A default experimental concentration of 5 μ g/mL for all CNTs was established to assess the different contribution of the remaining physical–chemical parameters in the no-observed-adverse-effect level (NOAEL) for the oxygen mass flux measurement of oxygen mass flux after exposure with different CNTs
The current study presented a mixture of experimental and predictive methodologies to study the effect of different CNTs on the mitochondrial oxygen mass flux
Summary
Carbon nanotubes (CNTs) have attracted great interest for their promising applications in the fields of biomaterials and nano-biotechnology. Some in vitro studies have demonstrated that CNTs exhibit cytotoxicity after their accumulation in the mitochondria matrix and/or by affecting the function of mitochondrial respiratory complexes of the inner membrane [2,3] It is still not known which bio-energetic mechanisms (the inhibition of adenosine diphosphate/adenosine triphosphate (ADP/ATP)-transport, uncoupling effects on oxidative phosphorylation, the induction of mitochondrial permeability transition pores, etc.) are responsible for the initiation of CNT mitochondrial damage [4,5,6,7,8,9]. Mitochondrial oxygen mass flux regulates the mitochondrial volume linked to the Ca2+ induction of mitochondrial permeability transition pores (MPTP) and to the increase of the mitochondrial reactive oxygen species (ROS-levels) based on the partial reduction of molecular oxygen in the mitochondrial respiratory complexes (complex IV) The latter have been extensively characterized and associated with several chronic pathological processes, such as neurodegenerative diseases (Alzheimer, Parkinson, Epilepsy), cardiac ischemia, and cancer. These diseases have currently high levels of morbidity and mortality, and mitochondrial dysfunction based on oxygen mass flux mechanisms has been indirectly or directly involved
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