Mechanisms of Mitochondrial Defects in Gulf War Syndrome.

摘要

Gulf War syndrome (GWS) is associated with increased incidences of amyotrophic lateral sclerosis, pain syndromes, muscle complaints that include fatigue and myalgias, as well as other neurological symptoms. Approximately 100,000 individuals have medical complaints consistent with GWS. Clinical manifestations are similar to those identified in Chronic Fatigue Syndrome (CFS). Mitochondrial defects are identified pathologically, metabolically, and genetically in some patients with CFS. GWS has significant evidence for mitochondrial dysfunction with abnormalities in exercise physiology, abnormalities in mitochondrial morphology, biochemical defects in mitochondrial function, abnormalities in free radical generation affecting mitochondrial integrity, gene expression in genes affecting mitochondrial function, and mtDNA mutations (inherited, somatic, and sporadic during embryogenesis). Gene expression abnormalities in CFS show abnormalities in genes that are related to mitochondrial function. Hence, investigation of mitochondrial dysfunction in GWS is a priority.