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Effects of catechins on cellular energy supply in the heart
Author(s) -
Kopustinskiene Dalia,
Bernatoniene Jurga
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.04369
Subject(s) - mitochondrion , oxidative phosphorylation , chemistry , biochemistry , respiration , reactive oxygen species , carnitine , substrate (aquarium) , proanthocyanidin , biology , antioxidant , polyphenol , anatomy , ecology
Main cocoa catechins (‐)‐epicatechin and its derived dimer procyanidin B2 are effective antioxidants capable to protect cardiovascular system from reactive oxygen species (ROS) damage although their detailed mechanism of action has not been fully clarified yet. Mitochondria are not only the central players in the regulation of cell energy homeostasis but also the main sites of ROS generation as byproducts of oxidative phosphorylation. The essential role of mitochondria in oxidative stress imply that they could be also the potential targets of catechins in the cell. In this work we evaluated the direct effects of (‐)‐epicatechin and procyanidin B2 on the functions of cardiac mitochondria. Our results showed that (‐)‐epicatechin starting from 0.2 mg/mL in a concentration‐dependent manner significantly increased the substrate‐driven respiration rate of isolated rat heart mitochondria with all tested substrates ‐ pyruvate and malate, palmitoyl‐L‐carnitine and succinate. Procyanidin B2 from 0.7 ng/mL to 3.5 ng/mL also increased the substrate‐driven respiration rate of isolated rat heart mitochondria, the highest effect was observed with succinate, then with pyruvate and malate, and the lowest – with palmitoyl‐L‐carnitine as substrates. Thus, (‐)‐epicatechin and procyanidin B2 stimulated substrate‐driven mitochondrial respiration and phosphorylation at lower concentrations, whereas they inhibited the respiratory chain at higher concentrations. As the substrate‐driven mitochondrial respiration rate mainly depends on the passive proton flux through the mitochondrial inner membrane, our results show that both (‐)‐epicatechin and procyanidin B2 in a concentration‐dependent manner could uncouple oxidative phosphorylation in cardiac mitochondria. Furthermore, (‐)‐epicatechin‐reduced the release of apoptosis marker ‐ cytochrome c from mitochondria supporting the evidence of membrane stabilizing properties of this flavonol. Since catechins are weak acids of hydrophobic character, they could directly transfer protons through the inner mitochondrial membrane. As the mild mitochondrial uncoupling is implicated to be a highly effective in vivo antioxidant strategy, catechins could serve as potential compounds for further studies on the development of novel cardioprotective agents. Furthermore, the catechin‐rich diet could help to improve cardiac mitochondrial functions thus ddecreasing the risk of cardiovascular diseases.