Neuronal nitric oxide synthase and N-methyl-d-aspartate neurons in experimental carbon monoxide poisoning

Thom, Stephen R.; Fisher, Donald; Zhang, Jie; Bhopale, Veena M.; Cameron, Bruce A.; Buerk, Donald G.

doi:10.1016/j.taap.2003.09.017

Cited by 55 publications

(35 citation statements)

References 42 publications

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“…Rats were anesthetized, and brain tissue was processed for Western blotting as described in ref. 10. In brief, after decapitation and isolation, brains were frozen in liquid nitrogen, homogenized in 5 ml of chloroform:methanol (2:1 vol͞vol), and then diluted with chloroform:methanol to obtain a ratio of 1 g of brain to 19 ml of ice-cold chloroform:methanol.…”

Section: Methodsmentioning

confidence: 99%

“…Cognitive function was examined by using an eight-arm radial maze according to methods we described in ref. 10. In brief, familiarization and testing procedures were performed every other day, 3 days per week.…”

Section: Assessment Of Mda-reacted Substances In Brain Fractions Withmentioning

confidence: 99%

“…Cognitive function of rats was assessed as the ability to learn to maneuver in an eight-arm radial maze, according to our published methods (10). Control rats exhibited progressive improvement in ''entry-to-repeat'' scores ( Fig.…”

Section: Mda-mbp Adducts and Mbp Charge Isomersmentioning

confidence: 99%

“…However, because carboxyhemoglobin values correlate poorly with clinical outcomes, additional pathophysiological mechanisms for delayed sequelae are thought to exist (2)(3)(4). Damage to brain related to excitatory amino acids and oxidative stress has been demonstrated in several animal models (5)(6)(7)(8)(9)(10). Experimental CO poisoning causes activation of N-methyl-D-aspartate neurons, and subsequent overactivity of neuronal nitric oxide synthase gives rise to perivascular changes that cause neutrophil sequestration͞activation (10)(11)(12)(13)(14).…”

mentioning

confidence: 99%

“…Damage to brain related to excitatory amino acids and oxidative stress has been demonstrated in several animal models (5)(6)(7)(8)(9)(10). Experimental CO poisoning causes activation of N-methyl-D-aspartate neurons, and subsequent overactivity of neuronal nitric oxide synthase gives rise to perivascular changes that cause neutrophil sequestration͞activation (10)(11)(12)(13)(14). Reactive O 2 species produced by activated neutrophils, mitochondria, and xanthine oxidase cause brain lipid peroxidation, but how these events trigger delayed neurological injuries is not understood (8)(9)(10)(11)(12)(13)(14).…”

mentioning

confidence: 99%

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Delayed neuropathology after carbon monoxide poisoning is immune-mediated

Thom

Bhopale²,

Fisher³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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234

165

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The neuropathological sequelae of carbon monoxide (CO) poisoning cannot be explained by hypoxic stress alone. CO poisoning also causes adduct formation between myelin basic protein (MBP) and malonylaldehyde, a reactive product of lipid peroxidation, resulting in an immunological cascade. MBP loses its normal cationic characteristics, and antibody recognition of MBP is altered. Immunohistochemical evidence of degraded MBP occurs in brain over days, along with influx of macrophages and CD-4 lymphocytes. Lymphocytes from CO-poisoned rats subsequently exhibit an autoreactive proliferative response to MBP, and there is a significant increase in the number of activated microglia in brain. Rats rendered immunologically tolerant to MBP before CO poisoning exhibit acute biochemical changes in MBP but no lymphocyte proliferative response or brain microglial activation. CO poisoning causes a decrement in learning that is not observed in immunologically tolerant rats. These results demonstrate that delayed CO-mediated neuropathology is linked to an adaptive immunological response to chemically modified MBP. myelin basic protein ͉ malonylaldehyde ͉ lymphocyte activation ͉ CD-40 ͉ microglia

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Section: Methodsmentioning

confidence: 99%

Section: Assessment Of Mda-reacted Substances In Brain Fractions Withmentioning

confidence: 99%

Section: Mda-mbp Adducts and Mbp Charge Isomersmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Delayed neuropathology after carbon monoxide poisoning is immune-mediated

Thom

Bhopale²,

Fisher³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

234

165

View full text Add to dashboard Cite

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Inorganic Compounds of Carbon, Nitrogen, and Oxygen

Leikauf,

Bein,

Prows

2023

Patty's Toxicology

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This chapter reviews the toxicology of some of the most commonly encountered chemicals in environmental and occupational settings. Although these chemicals are often generated by industrial processes such as combustion, several are generated by natural processes including endogenous production within the body. These substances are basic to the biological process and therefore life itself. Nonetheless, excessive exposures can be life‐threatening and must be controlled. This chapter is modeled after the excellent, previous chapter in this series written by Michael J. Lipsett, Dennis J. Shusterman, and Rodney R. Beard.

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Inorganic Compounds of Carbon, Nitrogen, and Oxygen

Leikauf¹,

Prows²

2012

Patty's Toxicology

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Neuronal nitric oxide synthase and N-methyl-d-aspartate neurons in experimental carbon monoxide poisoning

Cited by 55 publications

References 42 publications

Delayed neuropathology after carbon monoxide poisoning is immune-mediated

Delayed neuropathology after carbon monoxide poisoning is immune-mediated

Inorganic Compounds of Carbon, Nitrogen, and Oxygen

Inorganic Compounds of Carbon, Nitrogen, and Oxygen

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