Antioxidant protection from HIV-1 gp120-induced neuroglial toxicity |
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| Authors: | Kimberley?A?Walsh,Joseph?F?Megyesi,John?X?Wilson,Jeff?Crukley,Victor?E?Laubach,Robert?R?Hammond mailto:rhammond@uwo.ca" title=" rhammond@uwo.ca" itemprop=" email" data-track=" click" data-track-action=" Email author" data-track-label=" " >Email author |
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| Affiliation: | (1) Department of Pathology, London Health Sciences Centre, University of Western Ontario, London, ON, Canada;(2) Department Clinical Neurological Sciences, London Health Sciences Centre, University of Western Ontario, London, ON, Canada;(3) Department Physiology, University of Western Ontario, London, ON, Canada;(4) Department of Surgery, University of Virginia Health System, Charlottesville, VA, USA |
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| Abstract: | ![]()
Background The pathogenesis of HIV-1 glycoprotein 120 (gp120) associated neuroglial toxicity remains unresolved, but oxidative injury has been widely implicated as a contributing factor. In previous studies, exposure of primary human central nervous system tissue cultures to gp120 led to a simplification of neuronal dendritic elements as well as astrocytic hypertrophy and hyperplasia; neuropathological features of HIV-1-associated dementia. Gp120 and proinflammatory cytokines upregulate inducible nitric oxide synthase (iNOS), an important source of nitric oxide (NO) and nitrosative stress. Because ascorbate scavenges reactive nitrogen and oxygen species, we studied the effect of ascorbate supplementation on iNOS expression as well as the neuronal and glial structural changes associated with gp120 exposure. |
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