Reactive oxygen species and energy machinery: an integrated dynamic model

Abstract

The role of several important reactive oxygen species (ROS) on the Krebs cycle, the electron transport chain (ETC) and the two important shuttles has been modelled. Major part of the ROS is produced during oxygen reduction in the ETC, which has been kinetically simulated, and the changes in the final concentrations of several important metabolites were found. The simulation is based on chemical kinetics equation, and the associated set of differential equations was solved by the ordinary differential equation package in Octave. The validity of the model is checked by comparing the experimental results available in the literature with the simulations when a part of the ETC is blocked (80%) in the script. The present approach is versatile and flexible and has potential applications in various simulations. It is easy to study the change in concentrations of various metabolites when a particular enzyme or pathway is blocked (say by a drug). The Octave script is presented in the text.

Protective effects of pterostilbene against hepatic damage, redox imbalance, mitochondrial dysfunction, and endoplasmic reticulum stress in weanling piglets

“…Consistent with the present findings, animal models of cerebral ischemia-reperfusion injury show that PT can alleviate mitochondrial free radical accumulation and oxidative insults by increasing the activities of ETC complexes I and IV (Yang et al, 2016). Increases in mitochondrial complex activities, and particularly complexes I and III, may reduce the leakage of electrons from the ETC, thereby decreasing the reaction between free electrons and molecular oxygen and the resulting formation of superoxide anion (Korla, 2016). PT also has the potential to prevent the collapse of the mitochondrial membrane potential and inhibit the translocation of cytochrome c from the mitochondria to the cytoplasm, thereby conferring protection to mitochondrial homeostasis under adverse situations (Yang et al, 2017).…”

Cardiac Oxidative Signaling and Physiological Hypertrophy in the Na/K-ATPase α1s/sα2s/s Mouse Model of High Affinity for Cardiotonic Steroids

“…Using the Reactome database (Figure 4c), a similar trend was noted for downregulated pathways involving the extracellular matrix, and upregulated pathways related to energy production, such as citric acid cycle, respiratory electron transport, and mitochondrial fatty acid β-oxidation. The increased energetic metabolism suggested by RNA-seq analysis is consistent with hypertrophic growth, but also increased the levels of reactive oxygen species (ROS) [43][44][45]. Consistently, increased sensitivity to CTS would be expected to stimulate the NKA α1 oxidant amplification loop [36,46], which prompted us to explore redox signaling in α1 s/s α2 s/s mouse hearts.…”

Oxidative Stress Evaluation in Ischemia Reperfusion Models: Characteristics, Limits and Perspectives

“…In the last two decades, due to the specific characteristics and importance of the -SH group in cell redox status, a growing number of MS studies have targeted thiol-based systems (e.g., GSH, thioredoxin, peroxiredoxin) [30,31], and the "cysteine redoxome" concept has been coined [29]. Most recently, in order to both quantitatively and dynamically reproduce dedicated or bibliographical experimental data, MS studies have implemented redox processes, in multi-compartment/multi-dynamic approaches, such as: production and elimination kinetics of H 2 O 2 [105,111], coupling between redox metabolism and energetic metabolism [107,112,113]; quantitative and MS analysis of the modulation of cell signaling by redox processes [114]; MS description of redox processes and metabolism in single cells, such as the erythrocyte [115] or micro-organisms [116]. Higher integrated levels of ROS and redox-related pathophysiological issues are also addressed through the MS paradigm [93].…”