Effects of chronic sodium azide on brain and muscle cytochrome oxidase activity: A potential model to investigate environmental contributions to neurodegenerative diseases

Citation
Jd. Berndt et al., Effects of chronic sodium azide on brain and muscle cytochrome oxidase activity: A potential model to investigate environmental contributions to neurodegenerative diseases, J TOX E H A, 63(1), 2001, pp. 67-77
Citations number
34
Categorie Soggetti
Environment/Ecology,"Pharmacology & Toxicology
Journal title
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A
ISSN journal
15287394 → ACNP
Volume
63
Issue
1
Year of publication
2001
Pages
67 - 77
Database
ISI
SICI code
1528-7394(20010511)63:1<67:EOCSAO>2.0.ZU;2-E
Abstract
Deficits in oxidative phosphorylation have been implicated in many neurodeg enerative diseases. In this study, cytochrome oxidase activity was inhibite d following a 28-d systemic administration of nonlethal sodium azide via su bcutaneous osmotic pumps. Quantitative enzyme histochemistry was performed on tissue sections from brain, skeletal muscle, and heart to localize cytoc hrome oxidase activity both globally and in regions within each tissue Sign ificant decreases of cytochrome oxidase activity were found in the brain an d skeletal muscle but not heart. In addition, regions within each tissue we re also analyzed, such as cortex and striatum in the brain and red and whit e fibers in skeletal muscle. The tissue specific inhibition of cytochrome o xidase by sodium azide could serve as a positive control for studies of oth er mitochondrial toxins in aerobically compromised cells. Therefore, chroni c nonlethal sodium azide administration may provide a potential rat model f or the study of mitochondrial dysfunction and the role of environmental pol lutants in brain and muscle tissues affected in certain neurodegenerative d iseases.