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21.
碘缺乏与机体脂质过氧化关系的探讨   总被引:2,自引:0,他引:2  
对四川省叙永县碘缺乏病区学生血清中超氧化物歧化酶(SOD)和脂质过氧化物(LPO)含量测定的结果表明,碘缺乏病区学生血清中SOD含量明显下降和LPO含量增加的现象,与对照组间有显著性差异(P<0.01)。通过对碘缺乏与机体脂质过氧化相互关系的初步探讨,认为由碘缺乏引起的机体中SOD含量减少和LPO含量增加,将可能导致甲状腺细胞膜的损伤,甲状腺功能障碍。  相似文献   
22.
目的:研究枸杞地黄汤对老年小鼠学习记忆、自由基及免疫系统的影响。方法:采用水迷宫行为实验检测枸杞地黄汤对老年小鼠学习记忆的影响,通过测定皮层、海马中MDA和SOD水平检测药物对老年小鼠自由基系统异常改变的影响,通过测定老年小鼠免疫器官指数变化检测药物对老年免疫系统异常改变的影响。结果:5、10、20g/kg的枸杞地黄汤不同程度减小老年小鼠学习记忆障碍,降低皮层、海马中MDA水平,增加SOD活性,提高胸腺、脾指数。结论:枸杞地黄汤能够改善老年小鼠学习记忆障碍.调节不正常自由基系统和免疫系统。  相似文献   
23.
王少洪  彭杰青 《广东医学》1998,19(11):815-817
研究超氧化物歧化酶复合酶在急性肾小球肾炎病程中对组织结构和功能的保护 作用。方法诱发大鼠急性肾小球肾炎,并肌注SOD复合酶抗氧化保护性治疗。  相似文献   
24.
刺玫果对老龄小鼠衰老指标SOD、MDA的影响作用   总被引:1,自引:0,他引:1  
目的 :研究刺玫果提取物 (喷雾干燥粉 )对衰老小鼠脑、肝组织中超氧化物歧化酶 (SOD)和丙二醛(MDA)含量的影响。方法 :SOD测定为黄嘌呤氧化酶法 ,MDA测定为硫代巴比妥酸法。结果 :刺玫果提取物可显著增强老龄小鼠脑和肝SOD活性 ,降低MDA含量。结论 :刺玫果提取物具有一定的抗衰老作用  相似文献   
25.
Lmmunohistochemical analyses were made of the superoxide dismutases (Mn-SOD and CuiZn-SOD) in biopsied muscles from 7 patients with mitochondrial encephalomyopathies that included mitochondrial encephalomyopathy, lactic acidosis and strokelike episodes (MELAS), and chronic progressive external ophthalmoplegia (CPEO). Mn-SOD mainly was present in the subsarcolemmal region, but it also was found in a coarsely granular, reticular, or diffuse pattern of staining within the muscle fibers. These Mn-SOD-positive fibers corresponded almost completely to the ragged-red fibers. The immunoreaction for CuiZn-SOD was weakly positive in some of the muscle fibers positive for Mn-SOD. In CPEO, Mn-SOD-positive fibers predominantly showed decreased cytochrome c oxidase (COX) activity. In MELAS, Mn-SOD-positive fibers tended to be stained deeply for COX although a few were COX-negative. These findings suggest that Mn-SOD-positive fibers can be used to make a differential diagnosis between CPEO and MELAS and that in mitochondrial encephalomyopathies Mn-SOD in the raggedred fibers may protect against oxidative stress. © John Wiley & Sons, Inc.  相似文献   
26.
活性氧自由基在生物体内参与生理,病理过程并起重大作用,在筛选和评价抗氧化药物时,越来越需要一种快速,简便,价廉而又可靠的抗氧化活性测定方法,本文发展了一种具备了上述优点新方法,SOD(超氧化物歧化酶)及其模拟物的工作已有很多,很多文献报道了其活性一;Cu(Ⅱ)。本文着重研究了另一个金属辅基,Zn^2+并且发现了Zn^2+独特的,但为人们忽视了的;抗氧化活性加强作用。  相似文献   
27.
目的:探讨了肾病综合征患者红细胞免疫功能与脂质过氧化的关系。方法:应用红细胞酵母花环法测定了31例肾病综合征患者的红细胞免疫功能和化学法测定血清丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)含量,并与35名正常健康人作比较。结果:肾病综合征患者RBC-ICR花环率和MDA水平明显升高(P〈0.01),而RBC-C3bR,SOD,GSH-PX水平则〈正常(P〈0.01),相关分析显示:RBC-C3b花环与MDA呈显著负相关(r=-0.4786,P〈0.01),RBC-ICR与MDA呈正相关(r=0.6702,P〈0.01)。结论:肾病综合征患者红细胞免疫黏附功能的降低与活性代谢紊乱密切相关。  相似文献   
28.

Aims

We explored the effect of remote ischaemic conditioning (RIC) on endothelial function and on circulating mediators.

Methods and results

In 20 healthy male volunteers (mean age 31?±?10 years), flow-mediated dilation (FMD) was measured before and after 20?min of arm ischaemia, followed by reperfusion. Remote ischaemic conditioning (RIC) was performed by applying 3 cycles of 5?min of ischaemia of the leg at the onset of index arm ischaemia. Each volunteer underwent the IR-induced vascular injury protocol with and without RIC in a crossover study design.In the control group, IR significantly reduced FMD (5.9?±?2.9% before IR vs. 2.2?±?3.7% after IR; p?<?0.001). This effect was significantly attenuated by performing RIC (FMD of 5.5?±?3.1% before IR vs. 4.0?±?3.4% % after IR; p for interaction?=?0.01). Serum levels of SOD and ADMA increased significantly whereas MCP-1 and VEGF levels decreased significantly.Only changes in SOD levels were significantly related to the degree of RIC induced protection (r²?=?0.34; p?=?0.018).

Conclusion

RIC has protective effects against endothelial IR injury. Our biomarker study suggests that anti-oxidative stress mediators, such as SOD, seem to be more involved in the pathogenesis of RIC-induced protection in humans than angiogenesis factors or chemo-attractant cytokines.  相似文献   
29.
磷脂酰胆碱500mg/kg灌胃20日可使O_3环境中的小鼠超氧化物歧化酶(SOD)活性显著增强,血浆丙二醛(MDA)含量及外周血正染红细胞(NCE)微核率明显下降。结果提示:磷脂酰胆碱具有抗氧化作用及拮抗自由基造成遗传的损伤。进一步证实了自由基在微核形成中具有重要意义。  相似文献   
30.
Extracellular superoxide dismutase (EC-SOD) controls the availability of extracellular superoxide (O 2 - ), which is important for a variety of physiological pathways, including the primary means of inactivating nitric oxide (NO). The role of EC-SOD in neurobehavioral function has been until now unexplored. In the current studies, the phenotypic expression of genotypic alterations of EC-SOD production in mice were characterized for spatial learning and memory. Dramatic impairments in spatial learning in the win-shift 8-arm radial maze were seen in both EC-SOD knockout mice and EC-SOD overexpressing mice. The EC-SOD overexpressing mice were further characterized as having significant deficits in a repeated acquisition task in the radial-arm maze, which permitted the dissociation of long and short-term learning. Long-term learning was significantly impaired by EC-SOD overexpression, whereas short-term learning was not significantly affected by EC-SOD overexpression. NO systems have been shown to be importantly involved in learning and memory. This may be important in the current studies because EC-SOD has primary control over the inactivation of NO. We found that EC-SOD overexpressing mice were resistant to the cognitive effects of L-NAME (NG-nitro-L-arginine methyl ester hydrochloride), an NO synthase inhibitor. Decreased NO catabolism in these mice may have served to counter the effects of NOS inhibition by L-NAME. The current finding that EC-SOD levels that were either higher or lower than controls impaired learning demonstrates that the proper control of brain extracellular (O 2 - ) may be more vital than merely reduction of brain extracelluar (O 2 - ) in maintaining adequate learning function.  相似文献   
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