کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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5432274 | 1508832 | 2017 | 19 صفحه PDF | دانلود رایگان |
In the present study, different in vitro and electrochemical protocols were employed to determine the mitoprotective properties of carbon nanotubes family (pristine-CNT, oxidized-CNT) based on free radical scavenging ability against the most aggressive reactive oxygen species (ROS) as hydroxyl radical (·OH) formed by Fenton-Haber-Weiss reaction, which was experimentally induced on isolated rat-liver mitochondria through Fe2+ ions overload. The results suggest that the mitochondrial Fenton-inhibition response involves a significant reduction of (·OH) concentration linked to iron-complexing ability of CNT-family, following the order: carboxylated-CNT > pristine-CNT â¼Â hydroxylated-CNT, without affecting the electrochemical mitochondrial membrane potential in Fe2+-overloaded mitochondria.Besides, a new in silico dose-response QSPR-model was applied suggesting reliability for the CNT-dose-effect series predictions towards the mitochondrial Fenton ROS-inhibition with excellent linear behavior on the training set (R2 = 0.901; R2(adj.) = 0.901; Q2(LOO-CV) = 0.901) and test set (Q2F1 = 0.9008; Q2F2 = 0.9008; Q2F3 = 0.9009; MAE = 21.213) for internal and external validation respectively, with p < 0.05 for all regression coefficient for > 70,000 data points. Lastly, these experimental and theoretical evidences open a gate to the rational design of novel carbon nanomaterials toward mitochondrial nanomedicine based redox-targeting as an alternative of treatment of several chronic diseases where pathological Fenton-reaction mechanisms have been directly involved.
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Journal: Carbon - Volume 115, May 2017, Pages 312-330