neuroprotection by radical avoidance search for suitable agents神经保护,彻底避免寻找合适的代理商.pdfVIP

Molecules 2009, 14, 5054-5102; doi:10.3390/molecule OPEN ACCESS molecules ISSN 1420-3049 /journal/molecules Review Neuroprotection by Radical Avoidance: Search for Suitable Agents Rüdiger Hardeland Johann Friedrich Blumenbach Institute of Zoology and Anthropology, University of Göttingen, Berliner str. 28, D-37073 Göttingen, Germany; E-Mail: rhardel@gwdg.de Received: 12 November 2009; in revised form: 30 November 2009 / Accepted: 4 December 2009 / Published: 7 December 2009 Abstract: Neurodegeneration is frequently associated with damage by free radicals. However, increases in reactive oxygen and nitrogen species, which may ultimately lead to neuronal cell death, do not necessarily reflect its primary cause, but can be a consequence of otherwise induced cellular dysfunction. Detrimental processes which promote free radical formation are initiated, e.g., by disturbances in calcium homeostasis, mitochondrial malfunction, and an age-related decline in the circadian oscillator system. Free radicals generated at high rates under pathophysiological conditions are insufficiently detoxified by scavengers. Interventions at the primary causes of dysfunction, which avoid secondary rises in radical formation, may be more efficient. The aim of such approaches should be to prevent calcium overload, to reduce mitochondrial electron dissipation, to support electron transport capacity, and to avoid circadian perturbations. L-Theanine