Relation Between Mitochondrial Membrane Potential and ROS Formation

Abstract

Mitochondria are considered as the main source of reactive oxygen species (ROS) in the cell. For this reason, they have been recognized as a source of various pathological conditions as well as aging. Chronic increase in the rate of ROS production is responsible for the accumulation of ROS-associated damages in DNA, proteins, and lipids, and may result in progressive cell dysfunctions and, in a consequence, apoptosis, increasing the overall probability of an organism's pathological conditions. The superoxide anion is the main undesired by-product of mitochondrial oxidative phosphorylation. Its production is triggered by a leak of electrons from the mitochondrial respiratory chain and the reaction of these electrons with O(2). Superoxide dismutase (MnSOD, SOD2) from the mitochondrial matrix as well as superoxide dismutase (Cu/ZnSOD, SOD1) present in small amounts in the mitochondrial intramembrane space, convert superoxide anion to hydrogen peroxide, which can be then converted by catalase to harmless H(2)O. In this chapter, we describe a relation between mitochondrial membrane potential and the rate of ROS formation. We present different methods applicable for isolated mitochondria or intact cells. We also present experiments demonstrating that a magnitude and a direction (increase or decrease) of a change in mitochondrial ROS production depends on the metabolic state of this organelle.

Dimethyl Sulfoxide Damages Mitochondrial Integrity and Membrane Potential in Cultured Astrocytes

“…Astrocytes exposed to DMSO at concentrations of 1.0% also increases Cyt c release and activated caspase 3 expression, and decreases anti-apoptotic protein Bcl-2 expression, supporting the review that rupture of mitochondria is an initial trigger of apoptotic cascades [28], [35]. Furthermore, the present results indicated that DMSO dose-dependently increases mitochondria-derived ROS production, which is consistent with the notion that degenerated mitochondria are the primary site of ROS production [32]. Taken together, these results reveal that mitochondrial impairment is a primary event in the astrocyte toxicity of DMSO.…”

“…It has been demonstrated that decreased ΔΨm reduces aerobic metabolism and increases ROS generation [31], [32]. Thus, the generation of mitochondrial ROS in DMSO-treated astrocytes was assessed by detection of MitoSOX-Red, a highly selective detector of superoxide in live cell mitochondria, using the flow cytometry.…”

Deoxyelephantopin Induces Reactive Oxygen Species-Mediated Apoptosis and Autophagy in Human Osteosarcoma Cells

“…Previous studies showed that ROS generation was closely related to MMP changes [13, 14]. Thus, we measured the MMP levels in MG-63 and U2OS cells using fluorescent JC-1.…”

Farm animal models of organic dust exposure and toxicity

“…Beneficial actions of nitric oxide (NO), presumably derived from inducible nitric oxide synthase (iNOS), include enhanced cilia motility [83] and airway smooth muscle relaxation, which have been shown to improve symptoms of hyperreactive asthmatic airways in a guinea pig model [82]. However, elevated levels of ROS/RNS, as seen in obstructive airway diseases [85], have been shown to mediate fibroblast activation, mucus hypersecretion, cell injury and production of pro-inflammatory mediators by epithelial cells, and damage macromolecules DNA, lipids and proteins [84,85,86**,87-91]. Oxidative and nitrative stress is associated with loss of superoxide dismutase activity and downstream events characteristic of asthma, including apoptosis, shedding of the airway epithelium, hyperresponsiveness and diminished antioxidant activity [90,92].…”