Brain multiparametric responses to carbon monoxide exposure in the aging rat

Mendelman, Avivit; Zarchin, N.; Rifkind, Joseph M.; Mayevsky, Avraham

doi:10.1016/s0006-8993(00)02326-x

Cited by 12 publications

(3 citation statements)

References 20 publications

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“…CO, an endogenously derived gas formed from the breakdown of heme by the enzyme heme oxygenase (HO), exerts a beneficial effect in maintaining cardiovascular homeostasis in relation to NO availability. The vasodilatory (nonhypoxic) effects of CO on cerebral blood flow in adult rats were mediated by NO; aging rats exposed to CO and to air under the same conditions did not show significant changes in cerebral blood flow, indicating that the brain vasodilatory response to CO does not seem to be active in the aging rat (Mendelman et al, 2000). Intraperitoneal administration of the HO inhibitor zinc deuteroporphyrin 2,4-bis glycol had no effect on the resting cerebral blood flow in rats but increased hypothalamic NOS activity without changing cerebrospinal fluid cyclic GMP concentration.…”

Section: Influences Of Carbon Dioxide Oxygen and Carbon Monoxidementioning

confidence: 94%

Cerebral Blood Flow Regulation by Nitric Oxide: Recent Advances

Toda

Ayajiki²,

Okamura³

2009

Pharmacol Rev

328

248

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Section: Influences Of Carbon Dioxide Oxygen and Carbon Monoxidementioning

confidence: 94%

Cerebral Blood Flow Regulation by Nitric Oxide: Recent Advances

Toda

Ayajiki²,

Okamura³

2009

Pharmacol Rev

328

248

View full text Add to dashboard Cite

“…CO has been also identified as an important endogenous biological messenger in the brain [ 4 , 5 ], and it is a major component in the regulation of the cerebro-vascular circulation in newborns [ 6 ]. The central nervous system (CNS) is the most sensitive tissue to CO, and usually suffers the greatest lasting damage from CO poisoning [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Evidence for oxidative stress in the developing cerebellum of the rat after chronic mild carbon monoxide exposure (0.0025% in air)

et al. 2009

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Background: The present study was designed to test the hypothesis that chronic very mild prenatal carbon monoxide (CO) exposure (25 parts per million) subverts the normal development of the rat cerebellar cortex. Studies at this chronic low CO exposure over the earliest periods of mammalian development have not been performed to date. Pregnant rats were exposed chronically to CO from gestational day E5 to E20. In the postnatal period, rat pups were grouped as follows: Group A: prenatal exposure to CO only; group B: prenatal exposure to CO then exposed to CO from postnatal day 5 (P5) to P20; group C: postnatal exposure only, from P5 to P20, and group D, controls (air without CO). At P20, immunocytochemical analyses of oxidative stress markers, and structural and functional proteins were assessed in the cerebellar cortex of the four groups. Quantitative real time PCR assays were performed for inducible (iNOS), neuronal (nNOS), and endothelial (eNOS) nitric oxide synthases.

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“…The physiological vs. toxic effects of CO would be expected to depend on the pharmacodynamics of this molecule in the various tissues (Mendelman et al, 2000). The central nervous system is the most tissue sensitive to CO exposure and usually suffers the greatest lasting damage from CO poisoning (Koehler and Traystman, 2002).…”

mentioning

confidence: 99%

Mild carbon monoxide exposure diminishes selectively the integrity of the cochlea of the developing rat

López

Acuña

Webber

et al. 2003

J of Neuroscience Research

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Rat pups were chronically exposed to carbon monoxide (CO) concentrations (12 or 25 ppm) in air starting at day 8, through 22 days of age, to examine the changes in the peripheral auditory system. Gastrostomy-reared rat pups, with or without CO exposure, were used and compared with mother-reared pups. The organ of Corti and the neurons of the spiral ganglion were analyzed for their morphology by using immunochemical and histological techniques. The inner and outer hair cells in the organ of Corti of animals exposed to 12 and 25 ppm CO were not different from the controls. However, at 25 ppm CO exposure, the nerve terminals innervating the inner hair cells were swollen. The somata of neurons in the spiral ganglion showed mild changes in the cytoplasm, and signs of mild vacuolization were observed in myelin covering their central processes. Synaptophysin, a marker for synaptic vesicles, and choline acetyltransferase, a marker for cholinergic terminals, showed no difference in immunoreactivity in CO exposed animals at 12 and at 25 ppm when compared with their age-matched controls. Also, Na(+)K(+) ATPase immunoreactivity patterns were normal compared with controls. Three enzymes were significantly reduced at the 25 ppm CO exposure: Cytochrome oxidase, NADH-TR, and calcium ATPase were decreased in both the organ of Corti and the neurons of the spiral ganglion, and decreased immunostaining for the neurofilament and myelin basic proteins was found. We conclude that components of the cochlea are selectively affected by mild chronic CO exposure during development.

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Brain multiparametric responses to carbon monoxide exposure in the aging rat

Cited by 12 publications

References 20 publications

Cerebral Blood Flow Regulation by Nitric Oxide: Recent Advances

Cerebral Blood Flow Regulation by Nitric Oxide: Recent Advances

Evidence for oxidative stress in the developing cerebellum of the rat after chronic mild carbon monoxide exposure (0.0025% in air)

Mild carbon monoxide exposure diminishes selectively the integrity of the cochlea of the developing rat

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