Abstract

This dataset contains data from the evaluation of the effect of melatonin on isolated mitochondria from porcine heart and on a hypoxia/reoxygenation (H/R) model of porcine aortic endothelial cells (pAECs). The aim of the research was to verify the effect of melatonin on mitochondrial bioenergetics by performing structure/activity correlation studies, on its antioxidant effect towards anion superoxide (SOX) production, on the phenomenon of mitochondrial permeability transition pore (mPTP) opening involved in regulated cell death processes and the protective effect on H/R-induced damage towards bioenergetic parameters in an in vitro model on pAECs. The results, reported in “Melatonin_mitochondria_pAECs_Dataset.xlsx”, showed that melatonin has an inhibitory effect on Mg2+-activated F1FO-ATPase at low temperatures (“Different T_Arrhenius_Mg” sheet) and not at 37°C, the physiological temperature. However, in this latter condition melatonin exerts an inhibitory effect on the enzymatic activity of Ca2+-activated F1FO-ATPase (as reported in “Titration curves” sheet), a molecular condition related to mPTP opening. Uncompetitive inhibition (“Inhibition kinetics_Ca” sheet) is exerted by binding to a site in the hydrophilic F1 portion of the enzyme (“F1-ATPase” and “Mutual exclusion_NBD_Ca” sheets). Consistently, mPTP opening was also desensitized by melatonin (“CRC” sheet). Its inhibitory effect was confirmed on the oxidative phosphorylation (“OXPHOS Site I” and “OXPHOS Site II” sheets) process when mitochondria were energized from the first phosphorylation site (Complex I). Its antioxidant effect was confirmed on SOX production (“ROS_Site I” and “ROS_Site II” sheets), in isolated mitochondria, induced from phosphorylation site I (Complex I) and site II (Complex II). pAEC viability was impaired by melatonin starting at a dose of 5 mM. After hypoxia/reoxygenation (H/R) treatment, cells appeared detached and phenotypically modified and the presence of 1 mM melatonin during H/R restored the adherent monolayer and cell viability was not different from normoxia control cells (“pAEC viability” sheet). The damage induced by the H/R process is reflected in mitochondrial bioenergetic parameters and increased SOX production; melatonin exerts a protective effect, improving bioenergetic parameters and reducing SOX levels (“Metab_ROS pAEC_H_R” sheet).