Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.4.37 (CNPase)
539 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Iron deficiency in early life is associated with hypomyelination; however, the role which iron plays in myelinogenesis is not clearly established. In this study, we examined the effect of preweaning [postnatal days (PND) 4-14 and PND 4-21] and postweaning (PND 21-63) iron deficiency on hindbrain 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase) activity (marker of oligodendrocyte metabolic activity) and myelin basic protein (MBP) concentrations. Both CNPase activity and concentrations in the cerebrum and hindbrain were significantly lower in pre- and postweaning iron-deficient rats. Similarly, MBP concentrations were also reduced (25-35%) in all three groups of iron-deficient animals. Iron-deficient animals also had significant alterations in the fatty acid composition of individual phospholipids within the hindbrain as well as changes in cytochrome oxidase activities. These studies show that postnatal iron deficiency, for as little as 10 days, can significantly alter the production of myelin and oligodendrocyte functioning. Importantly, postweaning iron deficiency was still associated with a decrease in CNPase activity and MBP concentrations despite occurring well past a likely key sensitive period of peak myelinogenesis at PND 8-12. This suggests that iron deficiency in later life, as well as during early postnatal growth, can effect the production and maintenance of myelin.
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PMID:Pre- and postweaning iron deficiency alters myelination in Sprague-Dawley rats. 1461 57

Preterm brain injury is partly associated with hypoxia-ischemia starting before birth. Excessive nitric oxide production during HI may cause nitrosative stress, leading to cell membrane and mitochondrial damage. We therefore tested the hypothesis that therapy with a new, selective neuronal nitric oxide synthase (nNOS) inhibitor, JI-10 (0.022mg/kg bolus, n=8), given 30min before 25min of complete umbilical cord occlusion was protective in preterm fetal sheep at 101-104day gestation (term is 147days), compared to saline (n=8). JI-10 had no effect on fetal blood pressure, heart rate, carotid and femoral blood flow, total EEG power, nuchal activity, temperature or intracerebral oxygenation on near-infrared spectroscopy during or after occlusion. JI-10 was associated with later onset of post-asphyxial seizures compared with saline (p<0.05), and attenuation of the subsequent progressive loss of cytochrome oxidase (p<0.05). After 7days recovery, JI-10 was associated with improved neuronal survival in the caudate nucleus (p<0.05), but not the putamen or hippocampus, and more CNPase positive oligodendrocytes in the periventricular white matter (p<0.05). In conclusion, prophylactic nNOS inhibition before profound asphyxia was associated with delayed onset of seizures, slower decline of cytochrome oxidase and partial white and gray matter protection, consistent with protection of mitochondrial function.
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PMID:Partial neuroprotection by nNOS inhibition during profound asphyxia in preterm fetal sheep. 2412 Apr 36