Figure 6

Figure 6

Sub-lethal HHcy linked malfunctional ETC impairs mitochondrial respiration of endothelial cells. (A) OCR curves showing drastic reduction in endothelial mitochondrial respiration upon 2 mM Hcy treatment for 24 h as measured by an extracellular flux analyzer. (B–D) Respective bar graphs demonstrating that in comparison to untreated cells, there is significant decrease in basal respiration, ATP production and maximal respiration of endothelial cells with sub-lethal HHcy. (E) OCR curves showing no restoration of sub-lethal HHcy-induced mitochondrial respiration defect in presence of TUDCA. (F–H) Bar plots respectively showing no significant improvement in the reduction in basal respiration, ATP production and maximal respiration upon TUDCA pre-treatment, compared with sub-lethal Hcy treated endothelial cells. (I) Targeted metabolomics mediated quantification exhibiting significant elevation of metabolites of TCA cycle in sub-lethal Hcy treated endothelial cells compared with untreated control cells. AUC, area under the curve. (J) Bar plot showing that sub-lethal HHcy in endothelial cells causes significant reduction in enzymatic activity of COX, the terminal electron acceptor of ETC. Data are shown as Mean ± SEM with n ≥ 3. * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001 and ns is non-significant (p > 0.05).