Options
Effect of resveratrol on the function of rat heart mitochondria
Date Issued | Volume | Issue | Start Page | End Page |
---|---|---|---|---|
2024-04-05 | 60 | Suppl. 1 | 142 | 142 |
Background. Resveratrol is a bioactive compound that directly or indirectly affects mitochondrial functions. It can both stimulate and inhibit mitochondrial functions. The hormetic (cytoprotective or cytotoxic) effects of resveratrol are due to the different concentrations of resveratrol used in in vitro and in vivo experiments. Aim. To evaluate the effect of resveratrol on the function of rat heart mitochondria. Methods. Mitochondria from rat hearts were isolated by differential centrifugation. Protein quantity was determined by the biuret method. The mitochondrial respiration (oxygen consumption) rates were measured using the high-resolution respirometry system Oxygraph-2k. Results. Resveratrol in the concentration range of 10–150 µM had no effect on the leak state of mitochondria oxidizing NAD-dependent substrate pyruvate + malate. However, higher concentrations of resveratrol (200–300 µM) resulted in a statistically significant increase in the rate of the leak state. Moreover, the effect of resveratrol (50 µM to 150 µM) on the rate of oxidative phosphorylation (State3) was investigated. In mitochondria oxidizing pyruvate + malate 50 µM of resveratrol inhibited the State3 rate by 53%, 100 µM – by 63%, and 150 – by 73% respectively. Conclusions.
- Resveratrol (10–150 µM) had no statistically significant effect on the leak state respiration rate of rat heart mitochondria oxidizing the substrates of complex C(I). Higher concentrations of resveratrol (200–300 µM) had a statistically significant increase in the leak state respiration rate.
- The effect of resveratrol on the rate of the State3 was concentration-dependent. Resveratrol (10 µM and 25 µM) had no statistically significant effect on the rate of the State3 with either the C(I) substrates. Resveratrol (50 µM to 150 µM) statistically significantly inhibited the State 3 respiration rate (oxidative phosphorylation) in rat heart mitochondria oxidizing the substrates of complex C(I).