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

Clinical and pathological studies have revealed that in multiple sclerosis (MS) the involvement of the optic tracts is much more frequent than that of the olfactory tracts. To investigate the possible reasons for this difference in involvement of these two adjacent structures, both containing a central type myelin, we have studied optic and olfactory tracts obtained at autopsy from 7 adult males ranging in age from 54 to 64 years. White matter from the frontal poles of the same individuals was used for reference. These tissues were compared with respect to the relative content of a) water, b) soluble proteins, c) 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNP) activity, and d) immunologically precipitable basic protein (BP). Homogenates from these tissues were further compared by disc gel electrophoresis in two systems; phenolformic acid-water and SDS-urea gels. Results indicate that while the optic tracts and the frontal pole white matter were similar with respect to their water, total protein content and BP content, the optic tracts had lower CNP activity than the frontal poles. The olfactory tracts contained more water and less BP and the CNP activity of these structures was lower than that of the frontal pole white matter. Assuming the CNP activity and the BP content are true measures of the total myelin content of a given tissue, it appears that olfactory tracts have smaller amounts of myelin. On the other hand, the optic tracts contain only half as much CNP-activity with a disproportionately greater amount of BP. The possible significance of these findings is discussed.
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PMID:Biochemical and immunological studies with human optic and olfactory tracts. 8 54

When freeze-dried brain was extracted at -4-0degrees C with dry chloroform/methanol (2:1 v/v), four of the five enzymes examined were recovered in the diethyl ether-washed residue without inactivation. By contrast, extraction with chloroform/methanol (2:1 v/v) in the presence of water destroyed activities of all the enzymes examined. The amounts of major lipids extracted were similar whether extraction was done in the absence or presence of water. The study was carried out with special interest in 2':3'-cyclic nucleotide 3'-phosphodiesterase (EC 3.1.4.37), which is firmly bound to the membrane structures of brain white matter.
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PMID:The use of non-aqueous chloroform/methanol extraction for the delipidation of brain with minimal loss of enzyme activities. 19 93

Male Wistar rats were given o-cresol in their drinking water (0.3 g/l) for 20 weeks. The ingested cumulative dose exceeded the acute LD50 at the fourth week of the experiment. O-cresol induced an increased drinking rate initially which decreased significantly below the drinking rate of the controls at the end of the experiment. The biochemical effects in the cerebral homogenate were inconspicuous, and they included increased RNA content initially, and reduced glutathione concentration and azoreductase activity at the end of experiment. Glial cells displayed significant increases in the acid proteinase and 2',3'-cyclic nucleotide 3'-phosphohydrolase activities at the 20th week of exposure.
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PMID:Toxic effects of peroral o-cresol intake on rat brain. 49 19

The neurochemical effects of maternally administered cadmium (50 ppm through drinking water from 0 day of pregnancy) on the whole brain of offsprings exposed during gestation were studied in 7, 14 and 21 days old rats. The developmental pattern of body weight, protein, DNA and RNA contents in brain were not affected in Cd exposed pups of any age group. Brain weights were significantly reduced in exposed pups of postnatal age of 7 and 14 days but were comparable to controls in 21 days old pups. The content of Cd increased significantly in the brain of gestationally exposed pups of 7 days and remained almost stationary throughout the experimental period. The activity of Acetylcholinesterase, Na+, K(+)-ATPase, CNPase, 5'-Nucleotidase in the brain increased significantly from 7 to 21 days of age in control animals. In experimental pups, the activity of most of the enzymes was almost comparable to controls at 7 days of age except succinate dehydrogenase, which was significantly inhibited at 7, 14 and 21 days compared to controls. The activity of other enzymes was also significantly inhibited in the brain of experimental pups compared to controls of 21 days of age indicating marked retardation in the development of these enzymes. However, these changes had no correlation with the accumulation of Cd in the brain. These studies indicate that in utero exposure to Cd may retard the development of certain neurochemicals which may have long term implications on the brain functions.
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PMID:Gestational cadmium exposure and brain development: a biochemical study. 188 99

To study the effect of paternal chronic ethanol consumption on fetal development, an experimental rat model was established and compared to the fetal alcohol syndrome. Male and female Wistar rats were divided into 30% ethanol (E) and control groups. Before mating and during pregnancy the ethanol group and control group received E and water, respectively. Pregnancies were terminated on gestational day 21. The body weight, liver weight, blood glucose, serum insulin and cerebral CNPase activity were decreased in alcoholic males. The adverse effect of maternal chronic ethanol on fetal development was shown clearly and was not related to paternal ethanol. The adverse effect of paternal alcoholism on the fetus was shown in decreased litter size, or decreased body weight, cerebral weight and cerebral DNA, RNA and leucine incorporation into protein without a decrease in the litter size. The former finding was observed in the fetuses of aged male and female rats and latter in the fetuses of young female rats. In conclusion, both observations in our study indicate the adverse effect of paternal alcoholism on the fetal development.
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PMID:Experimental studies on the influence of male alcoholism on fetal development. 703 89

Lead poisoning is known to cause myelin defects. Galactolipids are the major lipid components of myelin and myelin-competent oligodendrocytes. The present study examines the cellular activity of enzymes involved in the galactolipid pathway, tissue concentrations of galactolipids, and the cellular activity of 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase) in rat pups exposed to lead in utero and subsequently through maternal milk from exposed mothers and in drinking water following weaning. Pups from control and lead-treated groups (500 or 2000 ppm lead in the drinking water) were euthanized by decapitation on postnatal day 7, 14, 21, 35, or 56. Lead decreased levels of galactolipids and the oligodendrocyte marker CNPase in the brain to a similar degree. The ratios of galactocerebrosides/sulfatides and nonhydroxy fatty acid/hydroxy fatty acid forms of the galactolipids were not altered by lead treatment. In contrast, the activities of the galactolipid metabolic enzymes were reduced to a degree significantly greater than that of CNPase or galactolipids. These results are consistent with previously obtained data indicating that in vitro cultured oligodendroglial progenitor cells are a target for Pb toxicity. Chronic Pb exposure may impact on brain development by impairing timely myelin production due to perturbation of the early developmental commitment of oligodendroglial progenitors. It is further suggested that perturbation of the galactolipid pathway during the developmental maturation of oligodendrocytes may represent a contributing mechanism for Pb-induced neurotoxicity.
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PMID:Lead exposure affects levels of galactolipid metabolic enzymes in the developing rat brain. 1129 96

The present study investigated the sensitivity of rats cerebral myelin to prolonged toxicity of lead (Pb) that imitates environmental exposure to this metal. The results indicated that 90 days exposure of young adult rats to lead in drinking water affects the morphology of myelin sheaths, expressed in disintegration of its multilamellar structure. Both, the protein content and the activity of the myelin-specific enzyme CNPase (2',3'-cyclic nucleotide 3-phosphodiesterase), were lowered. The Michaelis-Menten kinetic for CNPase in myelin obtained from control and Pb-treated rats was different. Km increased and Vmax decreased when compared to controls. Observed disturbances in enzyme activity may be one of the potential reasons of the ultrastructural changes. It is thus tempting to speculate that Pb may be considered as a one of the factors contributing to demyelinating diseases.
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PMID:CNPase activity in myelin from adult rat brains after prolonged lead exposure in vivo. 1553 87

In the present study, we assessed whether concurrent treatment with low doses of cilostazol and donepezil effectively improve memory deficits in association with amelioration of the pathological changes in the white matter of rats subjected to permanent ligation of bilateral common carotid arteries (BCCAL). The escape latency in Morris water maze test was significantly increased at 7, 14 and 21 days in rats subjected to BCCAL. At 21 days after ligation, the white matter lesions including vacuole formation with rarefaction were increased in the optic tract and corpus callosum accompanied by a large increase in glial fibrillary acidic protein (GFAP) immunoreactivity with significantly decreased CNPase-positive oligodendrocytes, all of which were significantly alleviated by the combination therapy with suboptimal doses of cilostazol (30 mg/kg orally) and donepezil (0.3 mg/kg intraperitoneally). The phosphorylated cyclic AMP response element-binding protein (p-CREB)- and Bcl-2-positive cells were significantly decreased following BCCAL, which were completely restored by the combination therapy, whereas the monotherapy with cilostazol or donepezil showed marginal effect. In conclusion, concurrent treatment with cilostazol and donepezil effectively prevented the occurrence of neuropathological alterations in the white matter by activation of p-CREB and Bcl-2, thereby resulting in improvement of spatial learning memory in rats subjected to chronic cerebral hypoperfusion.
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PMID:Concurrent administration of cilostazol with donepezil effectively improves cognitive dysfunction with increased neuroprotection after chronic cerebral hypoperfusion in rats. 1793 28

"Dirty-appearing white matter" (DAWM) in multiple sclerosis (MS) is defined as a region(s) with ill-defined borders of intermediate signal intensity between that of normal-appearing white matter (NAWM) and that of plaque on T(2)-weighted and proton density imaging. To delineate the histopathology of DAWM, four formalin-fixed cerebral hemisphere slices of three MS patients with DAWM were scanned with T(2)- weighted and proton density sequences. The myelin water fraction (MWF) was obtained by expressing the short T(2) component as a fraction of the total T(2) distribution. Hemispheric sections were then stained with Luxol fast blue (LFB) for myelin phospholipids, for myelin basic protein (MBP) and 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNP) for myelin; Bielschowsky silver impregnation for axons; and for glial fibrillary acidic protein (GFAP) for astrocytes. Compared to NAWM, DAWM showed reduction in MWF, corresponding to a reduction of LFB staining. DAWM also showed reduced Bielschowsky staining. Quantitatively, the change in MWF in DAWM most consistently correlated with the change in LFB staining. The findings of this preliminary study suggest that DAWM is characterized by loss of myelin phospholipids, detected by the short T(2) component, and axonal reduction.
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PMID:Dirty-appearing white matter in multiple sclerosis: preliminary observations of myelin phospholipid and axonal loss. 2697 93

Squirrel monkeys (Saimiri spp) are one of the most consistently used New World primates in biomedical research and are increasingly being used in neuroscience research, including models of drug abuse and addiction. Spontaneous neurologic disease in the squirrel monkey is uncommonly reported but includes various infectious diseases as well as cerebral amyloidosis. Hypernatremia is an extremely serious condition of hyperosmolarity that occurs as a result of water loss, adipsia, or excess sodium intake. Neurologic effects of hypernatremia reflect the cellular dehydration produced by the shift of water from the intracellular fluid space into the hypertonic extracellular fluid space. Severe hypernatremia may result in cerebrocortical laminar necrosis (polioencephalomalacia) in human patients as well as in a number of domestic species, including pigs, poultry, and ruminants. We report the clinical, histopathologic, and immunohistochemical findings of polioencephalomalacia in 13 squirrel monkeys. Polioencephalomalacia in these animals was associated with hypernatremia that was confirmed by serum levels of sodium greater than 180 mmol/L (reference range, 134.0-154.0 mmol/L [mEq/L]). All animals had concurrent diseases or experimental manipulation that predisposed to adipsia. Immunohistochemical investigation using antibodies to neuronal nuclei (NeuN), CNPase, Iba-1, and CD31 revealed necrosis of predominantly cerebral cortical layers 3, 4, and 5 characterized by neuronal degeneration and loss, oligodendrocytic loss, microglial proliferation, and vascular reactivity. The squirrel monkey is exquisitely sensitive to hyperosmolar metabolic disruption and it is associated with laminar cortical necrosis.
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PMID:Polioencephalomalacia secondary to hypernatremia in squirrel monkeys (Saimiri sciureus). 2604 82


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