Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.6.5.4 (SOR)
 720 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have used a model of dietary deficiency that leads to a chronic oxidative stress to evaluate responses that are adaptations invoked to boost cellular defense systems. Long-Evans hooded rats were fed with a diet lacking vitamin E (E) and selenium (Se) for 7 wk from weaning leading to animals deficient in both nutrients (-E -Se). In the absence of an electron donor, liver plasma membranes from these rats were more sensitive to lipid peroxidation, although they contained 40% greater amounts of ubiquinone than the plasma membranes from rats consuming diets with sufficient vitamin E and Se (+E +Se). The incubation of plasma membranes with NAD(P)H resulted in protection against peroxidation, and this effect was more pronounced in -E -Se membranes. Deficiency was accompanied by a twofold increase in redox activities associated with trans plasma membrane electron transport such as ubiquinone reductase and ascorbate free radical reductase. Staining with a polyclonal antibody against pig liver cytochrome b5 reductase, which acts as one ubiquinone reductase in the plasma membrane, showed an increased expression of the enzyme in membranes from -E -Se rats. Little DT-diaphorase activity was measured in +E +Se plasma membranes, but this activity was dramatically increased in -E -Se plasma membranes. No such increase was found in liver cytosols, which contained elevated activity of calcium-independent phospholipase A2. Thus, ubiquinone-dependent antioxidant protection in +E +Se plasma membranes is based primarily on NADH-cytochrome b5 reductase, whereas additional protection needed in -E -Se plasma membranes is supported by the increase of ubiquinone levels, increased expression of the cytochrome b5 reductase, and translocation of soluble DT-diaphorase to the plasma membrane. Our results indicate that, in the absence of vitamin E and Se, enhancement of ubiquinone-dependent reductase systems can fulfill the membrane antioxidant protection.
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PMID:Vitamin E and selenium deficiency induces expression of the ubiquinone-dependent antioxidant system at the plasma membrane. 983 56

We have shown that exposure of rats to neonatal handling/maternal separation results in mossy fiber axon hypoplasia in field CA3 of the hippocampus. To better understand the molecular basis of this neuroanatomical alteration, the present study examined three developmentally regulated protein kinase C substrate mRNAs that are highly expressed in hippocampal granule cells during mossy fiber outgrowth: GAP-43, a presynaptic substrate implicated in axonal outgrowth, RC3 (neurogranin), a postsynaptic substrate implicated in calmodulin signaling, and MARCKS-like protein (MLP), which binds calmodulin and filamentous actin in neurons and glial cells. mRNA expression was examined by quantitative in situ hybridization in the developing [postnatal day 7 (P7), P13, P21, and P90] hippocampus (CA1, CA3, granule cells) in Long-Evans hooded rats: (1) reared under normal animal facility (AFR) conditions, (2) subjected to brief (15 min/day, HMS15), or (3) subjected to moderate (180 min/day) handling/maternal separation (HMS180) on P2-14. RC3 mRNA expression was consistently elevated in all of the hippocampal cell fields in HMS180 rats relative to HMS15 and/or AFR rats over postnatal development, but did not differ from HMS15 rats in adulthood. In contrast, neither GAP-43 mRNA nor MLP mRNA expression differed among AFR, HMS15, or HMS180 rats at any postnatal time point. Elevations in RC3 expression would be predicted to perturb calcium-calmodulin signaling that may, in turn, impair the formation and/or maintenance of mossy fiber-CA3 synapses during postnatal development.
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PMID:Postnatal maternal separation elevates the expression of the postsynaptic protein kinase C substrate RC3, but not presynaptic GAP-43, in the developing rat hippocampus. 1269 86

Women are more susceptible than men to stress-related mental disorders. However, few animal studies have been conducted on females. Given the interactions between gonadic hormones and the hypothalamo-pituitary-adrenal (HPA) axis, we hypothesized that the effects of early stress may be different between males and females depending on the state of their estrous cycle. Using adult Long-Evans rats of both genders, the effects of maternal deprivation were investigated on the estrous cycle length, corticosterone levels after food deprivation or restraint stress procedures, and the negative feedback efficiency of dexamethasone on the HPA axis. The individual length of the estrous cycle was evaluated using vaginal smears. Non-deprived (AFR) females mainly exhibited regular 5-day cycles (40% of the population) and 4-5-day cycles (26%), with fewer 4-day cycles (18%) and irregular cycles (16%). Comparatively, deprived (D) females displayed a significant decrease of 5-day cycles (24%) and a significant increase of irregular cycles (28%). After the restraint stress procedure, D females exhibited higher corticosterone level than AFR females during proestrous. After the food deprivation procedure, D and AFR females maintained dose-response sensitivity to the negative feedback induced by dexamethasone but only during proestrous. No differences were observed between D and AFR males under these experimental conditions. These data highlight the importance of early environmental factors in regulating the spontaneous pattern of the estrous cycle as well as gender- and stressor-dependent sensitivity of the HPA axis according to steroid levels.
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PMID:Early stress leads to effects on estrous cycle and differential responses to stress. 2105 66