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131.
Twenty-four weanling male Wistar rats were divided into four groups fed diets containing adequate or deficient levels of selenium
(0.5 ppm [+ Se] or <0.02 ppm [−Se] and protein (15% [+Pro] or 5% [−Pro]), but adequate levels of all other nutrients for 4
wk to determine the effects of Se deficiency and protein deficiency on tissue Se and glutathione peroxidase (GSHPx) activity
in rats. Plasma, heart, liver, and kidney Se and GSHPx were significantly lower in Se-deficient groups in relation to Se-sufficient
groups. In Se-deficient groups, Se and GSHPx were significantly higher in −Se−Pro rats in heart, liver, and kidney. Data analysis
showed that there were significant interaction effects between dietary Se and protein on Se and GSHPx of rats. It is assumed
that under the condition of Se deficiency. a low level of protein may decrease Se and GSHPx utilization, increase GSHPx synthesis,
and result in Se redistribution. This could account for high levels of Se and GSHPx in the −Se−Pro rats compared to −Se+Pro
rats. 相似文献
132.
Lead effect on the oxidation resistance of erythrocyte membrane in rat triton-induced hyperlipidemia
L. Zimmermann N. Pages H. Antebi A. Hafi C. Boudene L. G. Alcindor 《Biological trace element research》1993,38(3):311-318
The anemia observed in severe chronic lead poisoning is in part attributable to alterations in the erythrocyte physicochemical
properties. Since they are partly related to the membrane lipid composition, the aim of the present study was to determine
the effects of a triton-induced hyperlipidemia on the resistance to oxidation of erythrocyte membranes in lead-treated Wistar
rats.
Our results showed that triton administration to lead-treated rats induced an increase in erythrocyte choline phospholipid
levels together with a significant decrease in the erythrocyte membrane lipid resistance to oxidation. These results led us
to suggest that anemia in lead poisoning is linked to interactions between lead present in the membrane and plasma phospholipids.
Their increase in rat hyperlipidemia induced by triton resulted in a decrease in the membrane resistance to oxidation and
finally in an erythrocyte fragility leading to their destruction. 相似文献
133.
Joan G. Fischer Randall L. Tackett E. W. Howerth Mary Ann Johnson 《Biological trace element research》1993,37(2-3):233-251
The hypothesis that copper (Cu) alters drug metabolizing enzymes and functions as an antioxidant nutrient in doxorubicin cardiotoxicity
was tested. Male Sprague-Dawley rats were fed Cu adequate (+Cu; 5 mg Cu/kg of diet), marginally Cu deficient (MCu; 1.2 mg Cu/kg of diet), or severely Cu deficient (−Cu; 0.5 mg Cu/kg of diet) diets for 6 wk. Doxorubicin (1, 2, or 4 mg/kg body wt) or saline were administered intraperitoneally
1 time/wk for 4 wk. Compared to control hearts, Cu, Zn superoxide dismutase activity was decreased by 9% in MCu rats and by
21–40% in−Cu rats. Glutathione peroxidase activity was elevated 5–15% in−Cu rats. Doxorubicin administration increased heart Cu, Zn superoxide dismutase activity in+Cu and−Cu rats 18 h after the last of 4 injections, but not 18 h after 1 injection. There was no synergism between doxorubicin and
Cu deficiency on lipid peroxidation, plasma creatine phosphokinase, cardiac hypertrophy, electrocardiographic abnormalities,
or morphological changes. Heart glutathione S-transferase activity was decreased by Cu deficiency, and like Cu, Zn superoxide
dismutase activity, returned to normal in−Cu rats given doxorubicin. Thus, the Cu deficient rat heart may be able to compensate for doxorubicin-induced oxidant stress
by increasing the activity of Cu,Zn superoxide dismutase and glutathione S-transferase. 相似文献
134.
To determine mechanisms of structural plasticity in adult CNS neurons, we investigated the expression of immediate early genes (IEGs) in the rat retina. Gene products of different IEG families (JUN and FOS proteins) and cAMP-responsive element binding protein (CREBP) were examined by immunohistochemistry under three different paradigms. Normal rats which were not axotomized were compared with axotomized animals, where retinal ganglion cells (RGCs) were axotomized by intraorbital optic nerve cut and retrogradely labeled with fluorogold (FG). Under these circumstances, RGCs show only transient sprouting, followed by continuous retrograde RGC degeneration. In the third group, after the optic nerve lesion, adult rats additionally received a sciatic nerve graft to the transected optic nerve stump. This allows some RGCs to regenerate an axon into the grafted nerve. In both groups, the time course of RGC survival and JUN, CREB, and FOS protein expression was monitored. In normal animals, JUN-Immunoreactivity (JUN-Ir) was not detectable in the retinal ganglion cell layer. JUN-Ir was induced in about 70% of all FG-positive RGCs 5 days after axotomy. The expression of JUN-Ir started to decline 8 days after axotomy. Only a few JUN-Ir-positive RGCs were found after 2 weeks. In transplanted animals, however, the numbers of JUN-Ir-positive RGCs were significantly higher 2 and 3 weeks after transplantation compared to animals that exclusively received axotomy. Furthermore, in grafted rats about 70% of the regenerating RGCs expressed JUN-Ir 2 weeks after grafting as compared to only 38% JUN-positive RGCs among the surviving but not regenerating RGCs. In normal animals CREBP-Ir was constitutively expressed in nearly all cells of the retinal ganglion cell layer. The decline in number of CREBP-Ir-positive cells paralleled the axotmy-induced RGC death. FOS-Ir-positive cells were not found in the ganglion cell layer at any time. These results demonstrate a selective and transient JUN expression of RGCs after axotomy which is sustained during axonal regeneration. This suggests that sciatic nerve grafts are able to regulate the expression of JUN proteins in axotomized RGCs of adult rats. 1994 John Wiley & Sons, Inc. 相似文献
135.
Neil R. Brandt Anthony H. Caswell Stephanie A. Lewis Carl Donald G. Ferguson Tara Brandt Jean-Pierre Brunschwig Arthur L. Bassett 《The Journal of membrane biology》1993,131(3):219-228
Summary Dyads (transverse tubule—junctional sarcoplasmic reticulum complexes) were enriched from rat ventricle microsomes by continuous sucrose gradients. The major vesicle peak at 36% sucrose contained up to 90% of those membranes which possessed dihydropyridine (DHP) binding sites (markers for transverse tubules) and all membranes which possessed ryanodine receptors and the putative junctional foot protein (markers for junctional sarcoplasmic reticulum). In addition, the 36% sucrose peak contained half of the vesicles with muscarine receptors. Vesicles derived from the nonjunctional plasma membrane as defined by a low content of dihydropyridine binding sites per muscarine receptor and from the free sarcoplasmic reticulum as defined by the Mr 102K Ca2+ ATPase were associated with a diffuse protein band (22–30% sucrose) in the lighter region of the gradient. These organelles were recovered in low yield. Putative dyads were not broken by French press treatment at 8,000 psi and only partially disrupted at 14,000 psi. The monoclonal antibody GE4.90 against skeletal muscle triadin, a protein which links the DHP receptor to the junctional foot protein in skeletal muscle triad junctions, cross-reacted with a protein in rat dyads of the same Mr as triadin. Western blots of muscle microsomes from preparations which had been treated with 100mm iodoacetamide throughout the isolation procedure showed that cardiac triadin consisted predominantly of a band of Mr 95 kD. Higher molecular weight polymers were detectable but low in content, in contrast with the ladder of oligomeric forms in rat psoas muscle microsomes. Cardiac triadin was not dissolved from the microsomes by hypertonic salt or Triton X-100, indicating that it, as well as skeletal muscle triadin, was an integral protein of the junctional SR. The cardiac epitope was localized to the junctional SR by comparison of its distribution with that of organelle markers in both total microsome and in French press disrupted dyad preparations. Immunofluorescence localization of triadin using mAb GE4.90 revealed that intact rat ventricular muscle tissue was stained following a well-defined pattern of bands every sarcomere. This spacing of bands was consistent with the interpretation that triadin was present in the dyadic junctional regions. 相似文献
136.
Alain Gerbi Marcel Debray Jean-Michel Maixent† Claude Chanez Jean-Marie Bourre 《Journal of neurochemistry》1993,60(1):246-252
Abstract: The Na+ sensitivity of whole brain membrane Na+ ,K+ -ATPase isoenzymes was studied using the differential inhibitory effect of ouabain (α1, low affinity for ouabain; α2, high affinity; and α3, very high affinity). At 100 m M Na+ , we found that the proportion of isoforms with low, high, and very high ouabain affinity was 21, 38, and 41%, respectively. Using two ouabain concentrations (10−5 and 10−7 M ), we were able to discriminate Na+ sensitivity of Na+ , K+ -ATPase isoenzymes using nonlinear regression. The ouabain low-affinity isoform, α1, exhibited high Na+ sensitivity [ K a of 3.88 ± 0.25 m M Na+ and a Hill coefficient ( n ) of 1.98 ± 0.13]; the ouabain high-affinity isoform, α2, had two Na+ sensitivities, a high ( K a of 4.98 ± 0.2 m M Na+ and n of 1.34 ± 0.10) and a low ( K a of 28 ± 0.5 m M Na+ and an n of 1.92 ± 0.18) Na+ sensitivity activated above a thresh old (22 ± 0.3 m M Na+ ); and the ouabain very-high-affinity isoform, α3, was resolved by two processes and appears to have two Na+ sensitivities (apparent K a values of 3.5 and 20 m M Na+ ). We show that Na+ dependence in the absence of ouabain is the result of at least of five Na+ reactivities. This molecular functional characteristic of isoenzymes in membranes could explain the diversity of physiological roles attributed to isoenzymes. 相似文献
137.
Angiotensin II Type 1 Receptor mRNA Levels in the Brains of Normotensive and Spontaneously Hypertensive Rats 总被引:4,自引:0,他引:4
Abstract: The type 1 angiotensin II (All) receptor (AT1 -R) has been implicated in the physiological actions mediated by All in the brain. In view of the reported hyperactivity of the brain All system in the spontaneously hypertensive rat (SHR), we compared the expression of AT,-R mRNAs in the brains of normotensive [Wistar Kyoto (WKY)] and SHR animals. Northern blot analysis showed about three- and ∼20-fold increases in the levels of AT1 -R mRNAs from the hypothalamus and brainstem areas, respectively, of the SHR compared with the WKY rat brain. This was attributable to greater levels of both AT,1A - and AT,1B -R mRNA subtypes in these areas from the SHR. These observations suggest that increased All receptor levels in SHR brain may, in part, be a result of increased expression of the AT1 -R gene. 相似文献
138.
Ashok K. Srivastava Rafick-Pierre Sékaly Jean-Louis Chiasson 《Molecular and cellular biochemistry》1993,121(2):127-133
The effect of nicotinamide-adenine dinucleotides (NAD+ and NADP+) on Ca2+ transport in rat liver nuclei was investigated. Ca2+ uptake and release were determined with a Ca2+ electrode. Ca2+ uptake was dependent on adenosine triphosphate (ATP; 2mM). The presence of NAD+ (2mM) or NADP+ (1 and 2mM) caused a significant inhibition of Ca2+ uptake following addition of 2mM ATP. Ca2+, which accumulated in the nuclei during 6 min after ATP addition, was significantly released by the addition of NAD+ (0.5–2mM) or NADP+ (0.1–2mM). However, the effect of NADH (2mM) or NADPH (2mM) on Ca2+ uptake and release clearly weakened in comparison with the effects of NAD+ and NADP+. Meanwhile, ryanodine (10M), thapsigargin (10M) or oxalate (0.5mM) had no effect on Ca2+ uptake and release in rat liver nuclei. These reagents did not significantly alter the effects of 2mM NAD+ on Ca2+ uptake and release. Thus, NAD+ and NADP+ had a potent effect on Ca2+ transport in rat liver nuclei. The present findings suggest that the liver cytosolic NAD+ (NADP+) is a factor in the regulation of the nuclear Ca2+ concentration. (Mol Cell Biochem121: 127–133, 1993) 相似文献
139.
Enzymatic activities catalysing the inter-conversion of L-methionine and its oxy analogue 4-methylthio-2-oxobutyric acid (2,4-KMB) were detected in the liver, skeletal muscle and heart of the laboratory rat and of sheep. In both species the highest activity of methionine transamination was found in the liver and was located in the cytoplasm and mitochondria. We propose that physiological and nutritional role of the cytoplasmic methionine transamination is amination of 2,4 KMB and formation of L-methionine while in mitochondria the activity is responsible for disposal of excess methionine is oxidised through oxidative decarboxylation of 2,4 KMB. 相似文献
140.
Takaharu Ishibashi Mikio Nakazawa Shoichi Imai 《Molecular and cellular biochemistry》1993,119(1-2):109-120
Using31P-,23Na- and39K-NMR, we assessed ischemic changes in high energy phosphates and ion contents of isolated perfused rat hearts continuously and systematically. To discriminate intra- and extracellular Na+, a shift reagent (Dy(TTHA)3–) was used in23Na-NMR study. In39K-NMR study, the extracellular K+ signal was suppressed by inversion recovery pulse sequence in order to obtain intracellular K+ signal without using shift reagnets. During the early period of ischemia, increases in intracellular Na+ and inorganic phosphate (Pi) were observed in addition to the well-documented decreases in creatine phosphate and ATP and a fall of intracellular pH, suggesting an augmented operation of Na+–H+ exchange triggered by a fall of the intracellular pH resulted from breakdown of ATP. At around 15 min of ischemia, a second larger increase in intracellular Na+ and a decrease in intracellular K+ were observed in association with a second increase in Pi. This was accompnanied by an abrupt rise of the ventricular end-diastolic pressure. As there was a depletion of ATP at this time, the increase in intracellular Na+ and associated decrease in intracellular K+ may be explained by inhibition of the Na+–K+ ATPase due to the depletion of ATP. A longer observation with31P-NMR revealed a second phosphate peak (at lower magnetic field to ordinary Pi peak) which increased its intensity as ischemic time lengthened. The pH of this 2nd peak changed in parallel with the changes in pH of the bathing solution, indicating the appearance of a compartment whose hydrogen concentration is in equilibrium with that of the external compartment. Thus, the peak could be used as an index of irreversible membrane damage of the myocardium. 相似文献