Catechin and epicatechin reduce mitochondrial dysfunction and oxidative stress induced by amiodarone in human lung fibroblasts

Abstract

BackgroundAmiodarone (AMD) and its metabolite N-desethylamiodarone can cause some adverse effects, which include pulmonary toxicity. Some studies suggest that mitochondrial dysfunction and oxidative stress may play a role in these adverse effects. Catechin and epicatechin are recognized as important phenolic compounds with the ability to decrease oxidative stress. Therefore, the aim of this study was to evaluate the potential of catechin and epicatechin to modulate mitochondrial dysfunction and oxidative damage caused by AMD in human lung fibroblast cells (MRC-5).MethodsMitochondrial dysfunction was assessed through the activity of mitochondrial complex I and ATP biosynthesis. Cell viability was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Superoxide dismutase and catalase activity were measured spectrophotometrically at 480 and 240 nm, respectively. Lipid and protein oxidative levels were determined by thiobarbituric reactive substances and protein carbonyl assays, respectively. Nitric oxide (NO) levels were evaluated using the Griess reaction method.ResultsAMD was able to inhibit the activity of mitochondrial complex I and ATP biosynthesis in MRC-5 cells. Lipid and protein oxidative markers increased along with cell death, while superoxide dismutase and catalase activities and NO production decreased with AMD treatment. Both catechin and epicatechin circumvented mitochondrial dysfunction, thereby restoring the activity of mitochondrial complex I and ATP biosynthesis. Furthermore, the phenolic compounds were able to restore the imbalance in superoxide dismutase and catalase activities as well as the decrease in NO levels induced by AMD. Protein and lipid oxidative damage and cell death were reduced by catechin and epicatechin in AMD-treated cells.ConclusionsCatechin and epicatechin reduced mitochondrial dysfunction and oxidative stress caused by AMD in MRC-5 cells.

(–)-Epicatechin Modulates Mitochondrial Redox in Vascular Cell Models of Oxidative Stress

“…Here, we observed a suppression of AA-induced mitochondrial superoxide at the higher concentration of EPICAT, albeit not significant, and significant lowering effect of EPI-CAT on HG-induced superoxide, confirming previous studies suggesting that EPICAT is an antioxidant [22,[24][25][26][27][28][29][30][31]38].…”

“…In plasma and urine, EPI-CAT promotes the activity of superoxide dismutase (SOD) and glutathione peroxidase [30]. In human lung fibroblasts, EPICAT restored SOD activity and complex I expression dampened by damaged mitochondria [31]. Despite this consistent antioxidant paradigm in numerous models and tissues, EPICAT's mechanism(s) at the cellular level remain largely unverified.…”

Characterization of the Omija (Schisandra chinensis) Extract and Its Effects on the Bovine Sperm Vitality and Oxidative Profile during In Vitro Storage

“…Furthermore, it was found that schisandrins balanced the energy metabolism and enhanced the mitochondrial antioxidant status, as assessed by the levels of reduced glutathione, alpha-tocopherol, and superoxide dismutase [ 62 ]. At the same time, catechin and quercetin found in our extract have the ability to modulate the activity of complex I of the electron transport chain, leading to an increased ATP production and a reduced oxidative damage [ 20 ]. Last but not the least, Parihar et al [ 63 ] and Semaming et al [ 64 ] reported that gallic and protocatechuic acid can act as electron acceptors at the mitochondrial complex I, resulting in an increased ATP production and regulation of energy metabolism in mammalian cells.…”

Separation of Active Compounds from Food by-Product (Cocoa Shell) Using Subcritical Water Extraction

“…Catechin and epicatechin, as flavonoid compounds, represent extremely important cocoa shell products. Beside their high antioxidant activity, they have ability to decrease oxidative stress [ 28 ] and improve cardiovascular function [ 29 ].…”