Abstract

We investigated the relationship between mitochondrial production of reactive oxygen species (ROS) and mitochondrial energetics in various rat tissues with different contents of the reduced coenzyme Q (Q) pool (Q9 + Q10). Our results indicate that similar to the tissue level, mitochondrial H2O2 release under nonphosphorylating conditions was strongly dependent on the amount of the reduced Q pool. Namely, in brain and lung mitochondria, less H2O2 release corresponded to a less reduced Q pool, while in liver and heart mitochondria, higher H2O2 release corresponded to a more reduced Q pool. We can conclude that the differences observed in rat tissues in the size of the reduced Q pool reflect different levels of ROS production and hence may reflect different demands for reduced Q as an antioxidant. Moreover, differences in mitochondrial H2O2 release were observed in different types of rat mitochondria during the oxidation of succinate (complex II substrate), malate plus glutamate (complex I substrate), and their mixture under phosphorylating and nonphosphorylating conditions. Our results indicate the existence of a tissue-specific maximum respiratory chain capacity in ROS production, possibly related to the membrane potential-mediated control of oxidative phosphorylation. We propose the use of a new parameter for the study of isolated mitochondria, RCRROS, the ratio between the formation of mitochondrial ROS under nonphosphorylating and phosphorylating conditions, which represents the maximum factorial increase in mitochondrial ROS formation that can be achieved after all ADP is phosphorylated.

Highlights

  • Mitochondria are key organelles for cellular energy (ATP) production and reactive oxygen species (ROS) formation

  • As no procedures were performed using live animals and as they were sacrificed for scientific purposes, no approval was needed for our study according to the Polish Animal Welfare Act

  • The present study focuses on the relationship between mitochondrial ROS (mROS) generation and mitochondrial energetics in various rat tissues with different reduced Q pool contents

Read more

Summary

Introduction

Mitochondria are key organelles for cellular energy (ATP) production and reactive oxygen species (ROS) formation. The energy and ROS produced by mitochondria play an important role in various physiological and pathophysiological processes. Several sites that produce superoxide anion (O2 − ) and/or hydrogen peroxide (H2 O2 ) have been identified in mammalian mitochondria [1]. The predominant route of mitochondrial ROS (mROS). Production by the electron transport chain is the premature leakage of electrons from complexes I, II, and III. Coenzyme Q (Q) is a fat-soluble molecule present in all cell membranes, including the inner mito. Mitochondrial Q (mQ) plays a central role in the electron transport chain, transferring electrons between dehydrogenases and the oxidizing pathway (complex III and complex IV). MQ is involved in the formation of O2 −

Objectives
Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call