Telomeres and Oxidative Stress

Abstract

Stroke is a heterogeneous syndrome caused by multiple disease mechanisms, resulting in a disruption of cerebral blood flow with subsequent tissue damage. Stroke remains the third leading cause of death and the leading cause of disability in adults. In 25–40% of patients with ischemic stroke, neurological symptoms progress during the initial hours. Early clinical deterioration results in increased mortality and functional disability. The molecular mechanisms underly- ing early clinical worsening are still not well clarified. There is considerable evidence that reactive oxygen species (ROS), reactive nitrogen species (RNS), and oxidative state are important mediators to tissue injury in cerebral ischemia. In normal conditions, free radical levels are controlled by cellular endogenous antioxidants. In fact, oxidative stress occurs when there is an impairment or inability to balance antioxidant production with ROS and RNS levels. The brain is highly susceptible to oxidative stress because of its high consumption of body oxygen (20%) to produce energy and free radicals, which in turn can cause damage to the main components of cells (DNA, lipids, proteins). In this chapter we focus our attention on the evidence of oxidative stress in ischemic stroke; particular attention is given to the current knowledge about the biomarkers of oxidative stress that can possibly be used to monitor the severity and outcome of stroke.