ABSTRACT In the early twentieth century, the “ rate-of-living hypothesis ” was derived from observations that animals with higher metabolic rates were characterized by shorter life spans, implying that a species ’ metabolic rate ultimately determines its life expectancy. In 1956, Denham Harman proposed a “ free radical theory ” that endogenous oxygen radicals were generated in cells over time, resulting in cumulative cellular damage targeting DNA, protein, lipids, and other components of the cell [1]. Human body is a constant source of reactive oxygen species (ROS) and oxidative stress arises when the antioxidant capacity of cells to scavenge the excess production of ROS falls short. In health conditions, pro-oxidants engage in useful signaling pathways that are important for growth and cellular health. Normally, antioxidants counteract the activity of pro-oxidants to retain cellular homeostasis and therefore a state of health. Overstimulation of signaling pathways leads to sustained pro-oxidant production in the form of ROS that disrupt cellular structures and impair function leading to disease [2] (Table I). The importance of oxidative stress injury depends on the molecular target, the severity of the stress, and the mechanism by which the oxidative stress is imposed. Cardiovascular disease (CVD) is associated with a series of risk factors which may be classifi ed into fi xed and modifi able. Fixed risk factors include genetic composition, age, menopausal status, and gender. The modifi able factors are a series of environmental cues and lifestyle choices including (but not limited to) diet, smoking, status of concurrent diseases (e.g. diabetes), exercise, and ethanol consumption [3]. When considering these risk factors, it is noteworthy that many, if not all, contribute to disease progression at least in part via oxidative stress. An higher prevalence of cardiovascular disease is seen also in patients aff ected by chronic renal failure (CRF) compared with other population: cardiovascular disease is the major cause of morbidity and mortality in patients with CRF [4,5]. Although CRF is strongly associated with risk factors for atherosclerosis, the excessive high cardiovascular risk seen in this cohort of patients is not fully accounted for by the traditional cardiovascular risk factors [6]. One particular example of an extra risk factor that may accelerate atherogenesis in CRF is oxidative stress. CRF is associated with oxidative stress, and its presence is evidenced by an imbalance between pro- and antioxidant systems [7], which probably makes a signifi - cant contribution to the excess cardiovascular burden in CRF patients [8]. In this review, we aim at focusing on oxidative stress in CVD and CRF. We address both the genesis of oxidative stress in general and its detrimental eff ects in patients with cardiovascular and renal dysfunction.

Oxidative stress in patients with cardiovascular disease and chronic renal failure

POPOLO, Ada;AUTORE, Giuseppina;PINTO, Aldo;MARZOCCO, STEFANIA
2013-01-01

Abstract

ABSTRACT In the early twentieth century, the “ rate-of-living hypothesis ” was derived from observations that animals with higher metabolic rates were characterized by shorter life spans, implying that a species ’ metabolic rate ultimately determines its life expectancy. In 1956, Denham Harman proposed a “ free radical theory ” that endogenous oxygen radicals were generated in cells over time, resulting in cumulative cellular damage targeting DNA, protein, lipids, and other components of the cell [1]. Human body is a constant source of reactive oxygen species (ROS) and oxidative stress arises when the antioxidant capacity of cells to scavenge the excess production of ROS falls short. In health conditions, pro-oxidants engage in useful signaling pathways that are important for growth and cellular health. Normally, antioxidants counteract the activity of pro-oxidants to retain cellular homeostasis and therefore a state of health. Overstimulation of signaling pathways leads to sustained pro-oxidant production in the form of ROS that disrupt cellular structures and impair function leading to disease [2] (Table I). The importance of oxidative stress injury depends on the molecular target, the severity of the stress, and the mechanism by which the oxidative stress is imposed. Cardiovascular disease (CVD) is associated with a series of risk factors which may be classifi ed into fi xed and modifi able. Fixed risk factors include genetic composition, age, menopausal status, and gender. The modifi able factors are a series of environmental cues and lifestyle choices including (but not limited to) diet, smoking, status of concurrent diseases (e.g. diabetes), exercise, and ethanol consumption [3]. When considering these risk factors, it is noteworthy that many, if not all, contribute to disease progression at least in part via oxidative stress. An higher prevalence of cardiovascular disease is seen also in patients aff ected by chronic renal failure (CRF) compared with other population: cardiovascular disease is the major cause of morbidity and mortality in patients with CRF [4,5]. Although CRF is strongly associated with risk factors for atherosclerosis, the excessive high cardiovascular risk seen in this cohort of patients is not fully accounted for by the traditional cardiovascular risk factors [6]. One particular example of an extra risk factor that may accelerate atherogenesis in CRF is oxidative stress. CRF is associated with oxidative stress, and its presence is evidenced by an imbalance between pro- and antioxidant systems [7], which probably makes a signifi - cant contribution to the excess cardiovascular burden in CRF patients [8]. In this review, we aim at focusing on oxidative stress in CVD and CRF. We address both the genesis of oxidative stress in general and its detrimental eff ects in patients with cardiovascular and renal dysfunction.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11386/4029253
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