Induction of Nitric Oxide -- Dependent Apoptosis in Motor Neurons by Zinc-Deficient Superoxide Dismutase-Reference-Cited by-同舟云学术

Induction of Nitric Oxide -- Dependent Apoptosis in Motor Neurons by Zinc-Deficient Superoxide Dismutase

Published:1999-12-24 Issue:5449 Volume:286 Page:2498-2500
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Estévez Alvaro G.¹²,Crow John P.¹³²,Sampson Jacinda B.¹⁴²,Reiter Christopher¹⁴,Zhuang Yingxin¹,Richardson Gloria J.¹,Tarpey Margaret M.¹²,Barbeito Luis²⁵,Beckman Joseph S.¹⁴⁶²

Affiliation:

1. Departments of Anesthesiology,

2. Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, AL 35233, USA.

3. Pharmacology and Toxicology and the

4. Biochemistry and Molecular Genetics,

5. Sección Neurociencias, Facultad de Ciencias, Universidad de la República, Division Neurobiologı́a Celular y Molecular, Instituto de Investigaciones Biologicas Clemente Estable, Montevideo, 11600 Uruguay.

6. Neurobiology, and

Abstract

Mutations in copper, zinc superoxide dismutase (SOD) have been implicated in the selective death of motor neurons in 2 percent of amyotrophic lateral sclerosis (ALS) patients. The loss of zinc from either wild-type or ALS-mutant SODs was sufficient to induce apoptosis in cultured motor neurons. Toxicity required that copper be bound to SOD and depended on endogenous production of nitric oxide. When replete with zinc, neither ALS-mutant nor wild-type copper, zinc SODs were toxic, and both protected motor neurons from trophic factor withdrawal. Thus, zinc-deficient SOD may participate in both sporadic and familial ALS by an oxidative mechanism involving nitric oxide.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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