Oxidative Stress and Diseases

JULIANA C. FANTINELLI; CLAUDIA CALDIZ; ALVAREZ. M. CECILIA.; CAROLINA D. GARCIARENA; GLADYS E. CHIAPPE DE CINGOLANI ; SUSANA M. MOSCA

InTech

Año: 2012 p. 624

978-953-51-0552-7

The spontaneously hypertensive rat (SHR) is a laboratory model of naturally developinghypertension and heart failure that appears to be similar in many aspects to essentialhypertension in humans (Trippodo & Frohlich, 1981). Systolic blood pressure in SHRrapidly increases during 5 to 10 weeks of age and develops cardiac hypertrophy between 9and 12 weeks of age (Shimamoto et al., 1982). Increasing evidence from differentexperimental models supports the concept that oxidative stress contributes to thepathogenesis of myocardial hypertrophy and in the process of myocardial remodelingleading to heart failure (Yücel et al., 1998; Lasségue & Griendling, 2004).The oxidative stress is the result of an increase of reactive oxygen species (ROS) and/orinadequate antioxidant defense mechanisms. It has been shown that an increase in theactivity and expression of myocardial NAD(P)H oxidase (NOX) is the main source of ROS incardiac hypertrophy (Bendall et al., 2002; Griendling et al., 2000; Xiao et al et al., 2002).However, existing data about the antioxidant status in hypertension are inconsistent. Somestudies have shown that the activities of one or more antioxidant enzymes are lower (Ito etal, 1995; Newaz & Nawal, 1999), higher (Czonka et al., 2000) or without changes (GómezAmoreset al., 2006; Girard et al, 2005) compared with normotensive controls. Although theunderlying causes of these discrepancies are unknown, it may be possibly due to the use ofdifferent hypertension models, animals at different hypertensive stages and/or differentexperimental preparations.On the other hand, ROS are thought to be a key mechanism in the aging process (Beckman& Ames, 1998; Colavitti & Finkel, 2004; Harman, 1988) and there are arguments that NOX-derived ROS may lead to cellular senescence (Ago et al., 2010a; Ago et al., 2010b; Imanishi etal., 2005). Thus, lipid peroxidation and oxidative modification of proteins by ROS likeperoxynitrite-the product of combination of superoxide (O2?.) and nitric oxide (NO)- areimplicated in the pathogenesis of hypertrophy (Nadruz et al., 2004) and in cardiac normalaging (Beal, 2002).The aim of this study was to assess the oxidative stress in hearts from young and old SHRcompared to age-matched Wistar rats.