תפריט נגישות
ניגודיות עדינהניגודיות גבוהה
מונוכרום
הדגשת קישורים
חסימת אנימציה
פונט קריא
סגור
איפוס הגדרות נגישות
להורדת מודול נגישות חינם תפריט נגישותניגודיות עדינהניגודיות גבוההמונוכרוםהדגשת קישוריםחסימת אנימציהפונט קריאסגוראיפוס הגדרות נגישותלהורדת מודול נגישות חינםRivka Ofir - Dead Sea & Arava Science Center and Department of Microbiology & Immunology Ben-Gurion University of the Negev, Beer-Sheva, Israel
Elie Beit-Yannai -Department of Clinical Pharmacology, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer‑Sheva, Israel
Oxidative damage plays a pivotal role in the initiation and progress of many human diseases and also in the development of acute and chronic pathological conditions in brain tissue (Halliwell, 2006; Hyslop et al., 1995; Ischiropoulos & Beckman, 2003; Minghetti, 2005). Compared with other tissues, the brain is particularly vulnerable to oxidative damage due to its high rate of oxygen utilization and high contents of oxidizable polyunsaturated fatty acids (Floyd, 1999; Sastry, 1985). In addition, certain regions of the brain are highly enriched in iron, a metal that is catalytically involved in the production of damaging reactive oxygen species (ROS) (Hallgren & Sourander, 1958). Although ROS are critical intracellular signaling messengers (Schrecka & Baeuerlea, 1991), excess of free radicals may lead to peroxidative impairment of membrane lipids and, consequently, to disruption of neuronal functions, and apoptosis. Among the ROS that are responsible for oxidative stress, H2O2 is thought to be the major precursor of highly reactive free radicals, and is regarded as a key factor in both neuronal (Vaudry et al., 2002) and astroglial cell death (Ferrero-Gutierrez et al., 2008). H2O2 is normally produced in reactions predominantly catalyzed by superoxide dismutase (SOD) and monoaminoxidases (MAO) A and B in the brain (Almeida et al., 2006; Duarte et al., 2007).......
Rivka Ofir - Dead Sea & Arava Science Center and Department of Microbiology & Immunology Ben-Gurion University of the Negev, Beer-Sheva, Israel
Elie Beit-Yannai -Department of Clinical Pharmacology, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer‑Sheva, Israel
Oxidative damage plays a pivotal role in the initiation and progress of many human diseases and also in the development of acute and chronic pathological conditions in brain tissue (Halliwell, 2006; Hyslop et al., 1995; Ischiropoulos & Beckman, 2003; Minghetti, 2005). Compared with other tissues, the brain is particularly vulnerable to oxidative damage due to its high rate of oxygen utilization and high contents of oxidizable polyunsaturated fatty acids (Floyd, 1999; Sastry, 1985). In addition, certain regions of the brain are highly enriched in iron, a metal that is catalytically involved in the production of damaging reactive oxygen species (ROS) (Hallgren & Sourander, 1958). Although ROS are critical intracellular signaling messengers (Schrecka & Baeuerlea, 1991), excess of free radicals may lead to peroxidative impairment of membrane lipids and, consequently, to disruption of neuronal functions, and apoptosis. Among the ROS that are responsible for oxidative stress, H2O2 is thought to be the major precursor of highly reactive free radicals, and is regarded as a key factor in both neuronal (Vaudry et al., 2002) and astroglial cell death (Ferrero-Gutierrez et al., 2008). H2O2 is normally produced in reactions predominantly catalyzed by superoxide dismutase (SOD) and monoaminoxidases (MAO) A and B in the brain (Almeida et al., 2006; Duarte et al., 2007).......
