Physiological regulation of heart mitochondrial nitric oxide synthase

BOVERIS A; REPETTO M; BUSTAMANTE J; BOVERIS AD; VALDEZ LB

Free Radical Pathophysiology

Transworld Research Network

Lugar: Kerala, India; Año: 2007;

In 1985, Helmut Sies coined the concept of oxidative stress as a situation of imbalance with an excess of oxidants or a decrease of antioxidants that may lead to cell damage. The concept was immediately accepted and widely utilized to plan experimental research and to explain results. After more than 20 years the concept keeps its original strength, validity and applicability. Recently, a difference started to be made between oxidative stress as a reversible situation and oxidative damage as an irreversible situation, but the limit is not clear. The difference is similar to the one between reversible and irreversible cell injury in classic cell pathology. The objective is to link, phenomenological and kinetically, the biochemical events that lead from oxidative stress to cell death, either by apoptosis or by necrosis, with the morphological evidence of histochemistry and electron microscopy. Another difference is also made between cellular oxidative stress and systemic oxidative stress. In the last case, the oxidative stress markers are determined in blood and plasma and seem to reflect the rate of a free-radical mediated chain reaction in the vascular space or oxidative damage occurring in target organs. Phagocyte produced oxidants or lipid hydroperoxides absorbed from food provide the reactants for the initiation reactions. Neurological diseases, such as Parkinson’s and Alzheimer’s diseases and vascular dementia, are associated to systemic oxidative stress with increased plasma levels of thiobarbituric acid-reactive substances (TBARS), decreased plasma levels of total reactive antioxidant potential (TRAP) and increased tert-butyl-hydroperoxide initiated chemiluminescence (BOOH-CL) in erythrocytes.