Surfactant-potentiated increases in intracranial pressure in a mouse model of Reye's syndrome

Crocker, John F. S.; Lee, S.H.S.; Love, J. A.; Malatjalian, D. A.; Renton, Kenneth W.; Rozee, K. R.; Murphy, Mary

doi:10.1016/0014-4886(91)90054-g

Cited by 11 publications

(4 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The two aspects of this detergent + FluB model that best reflect the human disease are the selective ultrastructural damage to hepatic mitochondria (Cracker et al, 1986), and the increases in intracranial pressure (ICI?) (Cracker et al, 1991). Neither effect is seen in animals exposed to detergent alone; virus infection alone does not affect the mitochondria, although it does produce moderate increases in ICI?.…”

Section: Surfactan T-dependen T Poten Tiation Of a Virus-initiated Diseasementioning

confidence: 96%

“…In recent studies in which we measured ICI? using a scaled-down method described for cats, we found that the mice treated with detergent plus FluB had significantly elevated values for ICP (Cracker et al, 1991). Our present focus is to determine whether there is a relationship between detergent exposure, lipid catabolism, and elevated ICI?.…”

Section: Surfactan T-dependen T Poten Tiation Of a Virus-initiated Diseasementioning

confidence: 97%

See 1 more Smart Citation

Animal Models for Reye’s Syndrome

Murphy

Digout

Crocker

1992

Animal Models of Neurological Disease, II

View full text Add to dashboard Cite

Section: Surfactan T-dependen T Poten Tiation Of a Virus-initiated Diseasementioning

confidence: 96%

Section: Surfactan T-dependen T Poten Tiation Of a Virus-initiated Diseasementioning

confidence: 97%

Animal Models for Reye’s Syndrome

Murphy

Digout

Crocker

1992

Animal Models of Neurological Disease, II

View full text Add to dashboard Cite

“…All forms of NOS, NOS 1 or nNOS, NOS 2 or iNOS, and NOS 3 or eNOS, are stimulated following ischemic insult (Crocker et al, 1991;Samdani et al, 1997). NO is a second messenger that activates soluble guanylyl cyclase and participates in a signal transduction pathway involving cyclic GMP.…”

Section: Glutamate In Ischemic Injurymentioning

confidence: 99%

Neurochemical Aspects of Excitotoxicity

2008

View full text Add to dashboard Cite

“…We examined the effect of the emulsifier Toximul, based on our previous observations that the surfactant potentiates virus-induced increases in intracranial pressure in mice (Crocker et al, 1991), and that surfactant is present in brains of children who died of RS in Atlantic Canada (Crocker et al, 1985). The data in Table I1 indicate that palmitate oxidation was inhibited in a dosedependent manner when the homogenates were exposed to increasing concentrations of Tox, with significant decreases apparent at levels of Tox 210 pg/ml.…”

Section: Effects Of Ammonia and Xenobiotic Agents On Fatty-acid Oxidamentioning

confidence: 99%

β‐Oxidation of [1‐¹⁴C]palmitic acid by mouse astrocytes in primary culture: Effects of agents implicated in the encephalopathy of Reye's syndrome

Murphy¹,

Jollimore²,

Crocker³

et al. 1992

J of Neuroscience Research

View full text Add to dashboard Cite

beta-Oxidation of [1-14C]palmitic acid was examined in homogenates of astrocytes cultured from neonatal mouse brain. Under optimal reaction conditions (< or = 50 micrograms protein, 10 min at 37 degrees C), oxidation increased as a function of palmitate concentration (15 microM to 2 mM) and reached a maximum rate of 1.98 +/- 0.29 nmol/min/mg protein (mean +/- SEM) at 0.2 mM substrate. Eadie-Hofstee analysis of data from four experiments yielded apparent values for Vmax of 1.87 nmol/min/mg protein, and for Km, 35-40 microM. There were no dramatic changes in the oxidation rate in cells between 10 and 36 days in culture. During the 10-min assays, less than 0.05% of the radioactivity was converted to 14CO2 by the astrocytes; water-soluble products accounted for 1-2% of the total substrate added. Studies with KCN indicated that 60-70% of the total activity occurred in the mitochondria. We have been studying the structural and functional changes associated with the cerebral encephalopathy of Reye's syndrome (RS). Three-week-old astrocytes exposed to serum from RS children for the final 7 days of culture exhibited minor mitochondrial pleomorphism and had increased numbers of other intracellular organelles. Examination of the effects of agents implicated in RS indicated that oxidation of [1-14C]palmitate was not altered by Na+ salicylate (1-3 mM), but was inhibited by the industrial surfactant, Toximul MP-8 (> or = 10 micrograms/ml), 4-pentenoic acid (> or = 0.1 microM), or with 4 days' exposure to ammonia (10 nM). The latter treatment also resulted in an increase in protein synthesis, cell volume, and malondialdehyde formation. These results suggest that some of the "toxins" implicated in RS inhibit fatty-acid oxidation in the astrocytes and produce other lipid-related abnormalities that could be related to encephalopathy.

show abstract

Surfactant-potentiated increases in intracranial pressure in a mouse model of Reye's syndrome

Cited by 11 publications

References 12 publications

Animal Models for Reye’s Syndrome

Animal Models for Reye’s Syndrome

Neurochemical Aspects of Excitotoxicity

β‐Oxidation of [1‐¹⁴C]palmitic acid by mouse astrocytes in primary culture: Effects of agents implicated in the encephalopathy of Reye's syndrome

Contact Info

Product

Resources

About

Surfactant-potentiated increases in intracranial pressure in a mouse model of Reye's syndrome

Cited by 11 publications

References 12 publications

Animal Models for Reye’s Syndrome

Animal Models for Reye’s Syndrome

Neurochemical Aspects of Excitotoxicity

β‐Oxidation of [1‐14C]palmitic acid by mouse astrocytes in primary culture: Effects of agents implicated in the encephalopathy of Reye's syndrome

Contact Info

Product

Resources

About

β‐Oxidation of [1‐¹⁴C]palmitic acid by mouse astrocytes in primary culture: Effects of agents implicated in the encephalopathy of Reye's syndrome