Reactive oxygen species (ROS), as well as reactive nitrogen species (RNS) are known to exert either harmful or beneficial effects on biological systems. Beneficial effects of ROS include the defense against infectious agents and in the function of a number of cellular signaling pathways, such as apoptosis. Generally, physiological levels of ROS and RNS are eliminated by an efficient scavenging system, however an imbalance between their production and destruction can induce oxidative stress and/or nitrosative stress. The inability of cell to counteract oxidative damage, and the oxidative stressrelated damage to DNA, to proteins and to lipids has been proposed to play a key role in the pathological processes leading to cancer, aging, heart disease, and especially a group of metabolic disorders which are associated to the metabolic syndrome (MS). The MS consists of a cluster of metabolic alterations, between them dyslipidemia and insulin resistance. When these conditions combine with genetic susceptibility and obesity, became risk factors for type 2 diabetes, vascular inflammation, atherosclerosis, and nonalcoholic fatty liver disease. Several evidences indicate that a large part of disorders associated to MS are strongly associated by an increase of oxidative stress and consequent oxidative damage of cellular components. Here, we discuss the available evidence for the involvement of cellular oxidants in the maintenance of redox regulation during normal physiological functions, as well as an overview of the actual knowledge on the role of oxidative stress in MS and its associated disorders.

Redox status alterations and metabolic disorders

BALSANO, CLARA;
2009-01-01

Abstract

Reactive oxygen species (ROS), as well as reactive nitrogen species (RNS) are known to exert either harmful or beneficial effects on biological systems. Beneficial effects of ROS include the defense against infectious agents and in the function of a number of cellular signaling pathways, such as apoptosis. Generally, physiological levels of ROS and RNS are eliminated by an efficient scavenging system, however an imbalance between their production and destruction can induce oxidative stress and/or nitrosative stress. The inability of cell to counteract oxidative damage, and the oxidative stressrelated damage to DNA, to proteins and to lipids has been proposed to play a key role in the pathological processes leading to cancer, aging, heart disease, and especially a group of metabolic disorders which are associated to the metabolic syndrome (MS). The MS consists of a cluster of metabolic alterations, between them dyslipidemia and insulin resistance. When these conditions combine with genetic susceptibility and obesity, became risk factors for type 2 diabetes, vascular inflammation, atherosclerosis, and nonalcoholic fatty liver disease. Several evidences indicate that a large part of disorders associated to MS are strongly associated by an increase of oxidative stress and consequent oxidative damage of cellular components. Here, we discuss the available evidence for the involvement of cellular oxidants in the maintenance of redox regulation during normal physiological functions, as well as an overview of the actual knowledge on the role of oxidative stress in MS and its associated disorders.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11697/24288
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