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61.
Flooding-induced membrane damage, lipid oxidation and activated oxygen generation in corn leaves 总被引:19,自引:1,他引:18
Flooding effects on membrane permeability, lipid peroxidation and activated oxygen metabolism in corn (Zea mays L.) leaves were investigated to determine if activated oxygens are involved in corn flooding-injury. Potted corn plants were flooded at the 4-leaf stage in a controlled environment. A 7-day flooding treatment resulted in a significant increase in chlorophyll breakdown, lipid peroxidation (malondialdehye content), membrane permeability, and the production of superoxide (O
2
-
) and hydrogen peroxide (H2O2) in corn leaves. The effects were much greater in older leaves than in younger ones. Spraying leaves with 8-hydroxyquinoline (an O
2
-
scavenger) and sodium benzoate (an .OH scavenger) reduced the oxidative damage and enhanced superoxide dismutase (SOD) activity. A short duration flooding treatment elevated the activities of SOD, catalase, ascorbate peroxidase (AP), and glutathione reductase (GR), while further flooding significantly reduced the enzyme activities but enhanced the concentrations of ascorbic acid and reduced form glutathione (GSH). It was noted that the decline in SOD activity was greater than that in H2O2 scavengers (AP and GR). The results suggested that O
2
-
induced lipid peroxidation and membrane damage, and that excessive accumulation of O
2
-
is due to the reduced activity of SOD under flooding stress. 相似文献
62.
Satoshi Muraki Masahiro Yamasaki Yoshito Ehara Kunio Kikuchi Kunihiro Seki 《European journal of applied physiology and occupational physiology》1996,74(5):481-483
The purpose of the present study was to examine the effect of maximal arm exercise on the skin blood circulation of the paralyzed
lower limbs in persons with spinal cord injury (PSCI). Eight male PSCI with complete lesions located between T3 and L1 performed
graded maximal arm-cranking exercise (MACE) to exhaustion. The skin blood flux at the thigh (SBFT) and that at the calf (SBFC)
were monitored using laser-Doppler flowmeter at rest and for 15 s immediately after the MACE. The subject's mean peak oxygen
uptake and peak heart rate was 1.41 ± 0.22 1·min−1 and 171.6 ± 19.2 beats·min−1, respectively. No PSCI showed any increase in either SBFT or SBFC after the MACE, when compared with the values at rest.
These results suggest that the blood circulation of the skin in the paralyzed lower limbs in PSCI is unaffected by the MACE. 相似文献
63.
64.
本文从物质和能量交换的角度,运用非平衡态热力学超熵产生理论,分析了寒害定态的稳定性,并建立了超熵产生判据.理论分析所得的结论与实验结果基本相符. 相似文献
65.
M. Viswanathan A. M. de Oliverira R. -M. Wu C. C. Chiueh J. M. Saavedra 《Cellular and molecular neurobiology》1994,14(1):99-104
Summary 1. Intracerebral injection of the oxidative metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1-methyl-4-phenylpyridine (MPP+), into the substantia nigra of adult rats resulted in a lesion at the injection site.2. Using autoradiography, we localized specific [125]CGP 42112 binding that was not recognized by angiostensin II or angiotensin II AT1 or AT2 receptorselective ligands.3. Our results suggest that [125I]CGP 42112 may be binding to activated microglia that appear at the lesion site. 相似文献
66.
M. Renuka Prasad H. S. Dhillon T. Carbary R. J. Dempsey S. W. Scheff 《Journal of neurochemistry》1994,63(2):773-776
Abstract: Regional levels of lactate and inositol 1,4,5-trisphosphate (IP3 ), a cellular second messenger of the excitatory neurotransmitter system, were measured after lateral fluid percussion (FP) brain injury in rats. At 5 min postinjury, tissue lactate concentrations were significantly elevated in the cortices and hippocampi of both the ipsilateral and contralateral hemispheres. By 20 min postinjury, lactate concentrations were elevated only in the cortices and hippocampus of the ipsilateral hemisphere. Whereas the IP3 concentrations were elevated in the hippocampi of the ipsilateral and contralateral hemisphere and in the cortex of ipsilateral hemisphere at 5 min postinjury, no elevation in these sites was found at 20 min postinjury. Histologic analysis revealed neuronal damage in the cortex and CA3 regions of hippocampus ipsilateral to the injury at 24 h postinjury. The present results suggest activation of the phosphoinositide signal transduction pathway at the onset of injury and of a possible requirement of early persistent metabolic dysfunction (>20 min) such as the lactate accumulation in the delayed neuronal damage. 相似文献
67.
Efficiency of serum copper/zinc ratio for differential diagnosis of patients with and without lung cancer 总被引:1,自引:0,他引:1
Tsunehiro Oyama Koji Matsuno Toshihiro Kawamoto Tetsuya Mitsudomi Takayuki Shirakusa Yasushi Kodama 《Biological trace element research》1994,42(2):115-127
We examined serum copper (Cu), serum zinc (Zn), and the serum copper/zinc ratio (Cu/Zn) in 162 patients. All of them were
seen to have an abnormal shadow in the chest X-ray films, that is, 109 patients with lung cancer (LC) and 53 patients with
no lung cancer (NLC). The mean Cu and Cu/Zn in LC patients were significantly higher than those in NLC patients (p<0.05). In LC patients, Cu and Cu/Zn were higher and Zn was lower in advanced tumors than early ones. There was a significantly
clear relation between Cu or Cu/Zn and the tumor (T) stages. When the relative risk (RR) of LC was estimated, it was seen
that the higher Cu and Cu/Zn became, the higher RR became. Furthermore, we showed the sensitivity of the receiver operator
characteristic of the test (ROC) curve for Cu, Cu/Zn, and carcinoembryonic antigen (CEA) to diagnose LC, as explained in a
paragraph of methods.The determinations of Cu, Zn, and Cu/Zn are simple and inexpensive. They also appear to have a great diagnostic value in determining the local invasion of LC and as a screening test in the
high-risk patients for LC. 相似文献
68.
Preexisting magnesium deficiency may alter the susceptibility of rat hearts to postischemic oxidative injury (free radicals). This was examined in rats maintained for 3 weeks on a magnesium-deficient (Mg-D) diet with or without concurrent vitamin E treatment (1.2 mg/day, SC). Magnesium-sufficient (Mg-S) rats received the same diet supplemented with 100 mmol Mg/kg feed. Following sacrifice, isolated working hearts were subjected to 30-, 40-, or 60-min global ischemia and 30-min reperfusion. Postischemic production of free radicals was monitored using electron spin resonance (ESR) spectroscopy and spin trapping with -phenyl-N-tert butylnitrone (PBN, 3 mM final); preischemic and postischemic effluent samples were collected and then extracted with toluene. PBN/alkoxyl adduct(s) (PBN/RO·; H = 1.93 G,N = 13.63 G) were the dominant signals detected in untreated Mg-S and Mg-D postischemic hearts, with comparably higher signal intensities observed for the Mg-D group following any ischemic duration. Time courses of postischemic PBN/RO· detection were biphasic for both groups (maxima: 2–4 and 8.5–12.5 min), and linear relationships between the extent of PBN/RO· production and the severity of both mechanical dysfunction and tissue injury were determined. Following each duration of ischemia, Mg-D hearts displayed greater levels of total PBN adduct production (1.7 –2.0 times higher) and lower recovery of cardiac function (42–48% less) than Mg-S hearts. Pretreating Mg-D rats with vitamin E prior to imposing 40-min ischemia/reperfusion, led to a 49% reduction in total PBN/RO· production, a 55% lower LDH release and a 2.2-fold improvement in functional recovery, compared to untreated Mg-D hearts. These data suggest that magnesium deficiency predisposes postischemic hearts to enhanced oxidative injury and functional loss, and that antioxidants may offer significant protection against pro-oxidant influence(s) of magnesium deficiency. 相似文献
69.
Difference between effects of sulfur dioxide (SO2) and ozone (O3) on groundnut plants (Arachis hypogaea L.) was studied by use of an exposure system of enzymatically-isolated mesophyll cells. SO2 inhibited photosynthesis of intact groundnut leaves but induced no visible injury on leaves. SO2 also inhibited photosynthesis of isolated mesophyll cells but did not kill the cells, suggesting that SO2 inhibits photosynthesis by attacking rather specifically the photosynthetic apparatus in chloroplasts. O3 inhibited photosynthesis of intact leaves and at the same time induced visible injury corresponding to the extent of photosynthesis
inhibition. O3 also inhibited photosynthesis of isolated mesophyll cells and killed the cells to the extent corresponding to photosynthesis
inhibition, suggesting that O3 inhibits photosynthesis not directly by attacking the photosynthetic apparatus but indirectly by killing cells. Since the
response of intact leaves to each pollutant resembled that of isolated mesophyll cells, the difference between responses of
intact leaves to both pollutants may considerably reflect that of mesophyll cells. 相似文献
70.
Felix P. Exkenstien 《Developmental neurobiology》1994,25(11):1467-1480
Fibroblast growth factors (FGFs) exhibit widespread mitogenic and neurotrophic activities. Nine members of the family are currently known, and FGF-1 and FGF-2 are present in relatively high levels in CNS. FGF-1 is expressed by a subset of neuronal populations, while FGF-2 is expressed by astrocytes. FGF-1 and FGF-2 lack signal peptides and appear to be present mainly in inracellular compartmens. This suggests that the factors may act as initiators of a repair response after injury. Support for this notion comes from observations that FGF-1 and FGF-2 levels are low during critical phases of development, but high in the adult CNS. A family of transmembrane tyrosine kinase receptors (FGFRs) mediates the effects of FGFs. Four different genes coding for FGF receptors are currently known, three of which are expressed in cell type-specific patterns in the CNS The main receptor variants present in this tissue, however, can by themselves not distinguish between FGF-1 and FGF-2. Additional selectivity may be established by interaction of the FGFs and their receptors with select heparan proteoglycans (HSPGs). Therefore, the precise physiological role of FGFs is determined by the combination of cell type-specific patterns of expression of FGFs, FGFRs and HSPGs together with the mechanisms that regulate the extracellular availability of FGFs. 1994 John Wiley & Sons, Inc. 相似文献