Changes in proHB-EGF expression after functional activation of the immune system cells

Abstract

The intensity of oxidative stress, protein expression of antiapoptotic Bcl-2 as well as antioxidant enzymes manganese superoxide dismutase (MnSOD) and glutathione peroxidase (GPx) and their regulator p53 were studied in the mitochondria of rat heart. Sessions of repeated hypoxia/reoxygenation ((h/r) A large body of experimental data indicates that reactive oxygen species (ROS) play a fundamental role in hypoxia/reoxygenation injury of cells and subcellular structures [1]. Mitochondria are considered an important locus of ROS production mainly at the level of complexes I and III of the respiratory chain and hence a potential contributor to cells damage during hypoxia [2]. At the same time, mitochondria could be major targets of ROS attack. These events result in mitochondrial dysfunction with superoxide leakage, the formation of other aggressive ROS which attack lipids, proteins and other cell constituents, lead to energy and metabolic disorders, deplete of cellular antioxidant defense, and induce the apoptotic cascade [1,2].In general, mitochondrial oxidative stress is determined by the balance between ROS generation and their elimination by antioxidants [3]. The antioxidants and free radical scavenging enzymes, including MnSOD, peroxiredoxin 3 and 5, thioredoxin, glutathione, and glutathione peroxidase, not only constitute the first line of defense against oxidative damage within the mitochondria but also are essential for maintaining the critical cellular redox balance and play key role in modulating cellular responses to external stimuli [4]. MnSOD and GPxthe key antioxidant defense enzymes that function in concert to prevent ROS reactions in response to oxidative stress [5]. There are plenty of reports concerning the role of MnSOD and GPx in the cellular redox homeostasis involved in the adaptive responses against oxidative stress [6][7][8][9], although the mechanisms associated with protein expression and specific activity of MnSOD as well as GPx during H/R of different duration are not fully understood.

Intermittent Hypoxia Prevents Myocardial Mitochondrial Ca2+ Overload and Cell Death during Ischemia/Reperfusion: The Role of Reactive Oxygen Species

“…However, the enzyme activity of CAT and GPx increased (Figure 2C). CAT and GPx mRNA expression was probably time-dependent [43]. It has been reported that mRNA half-lives were about several minutes to several hours.…”