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Increased 3‐nitrotyrosine in both sporadic and familial amyotrophic lateral sclerosis
Author(s) -
Beal M. Flint,
Ferrante Robert J.,
Browne Susan E.,
Matthews Russell T.,
Kowall Neil W.,
Brown Robert H.
Publication year - 1997
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410420416
Subject(s) - peroxynitrite , amyotrophic lateral sclerosis , nitrotyrosine , pathogenesis , oxidative stress , nitric oxide , medicine , superoxide dismutase , pathology , superoxide , chemistry , nitric oxide synthase , biochemistry , enzyme , disease
The pathogenesis of neuronal degeneration in both sporadic and familial amyotrophic lateral sclerosis (ALS) associated with mutations in superoxide dismutase may involve oxidative stress. A leading candidate as a mediator of oxidative stress is peroxynitrite, which is formed by the reaction of superoxide with nitric oxide. 3‐Nitrotyrosine is a relatively specific marker for oxidative damage mediated by peroxynitrite. In the present study, biochemical measurements showed increased concentrations of 3‐nitrotyrosine and 3‐nitro‐4‐hydroxyphenylacetic acid in the lumbar and thoracic spinal cord of ALS patients. Increased 3‐nitrotyrosine immunoreactivity was observed in motor neurons of both sporadic and familial ALS patients. Neurologic control patients with cerebral ischemia also showed increased 3‐nitrotyrosine immunoreactivity. These findings suggest that peroxynitrite‐mediated oxidative damage may play a role in the pathogenesis of both sporadic and familial ALS.