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首页> 外文期刊>Gene Therapy and Molecular Biology >Similar effects of chronic voluntary alcohol intakeand high dose superoxide dismutase gene deliveryon oxidative and carbonyl stress in rats
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Similar effects of chronic voluntary alcohol intakeand high dose superoxide dismutase gene deliveryon oxidative and carbonyl stress in rats

机译：长期自愿摄入酒精和高剂量超氧化物歧化酶基因传递对大鼠氧化和羰基应激的类似影响

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Experimental and clinical studies demonstrate a crucial role of alcohol in the etiology of various diseases. Oxidative stress is among the major mechanisms of detrimental effects of alcohol. Our previous study showed a protective effect of low molecular weight antioxidants on the level of oxidative and carbonyl stress markers in a model of chronic compulsory alcohol intake. The aim of this study was to evaluate the effects of an enzymatic high molecular weight antioxidant (manganese superoxide dismutase - Mn-SOD) gene delivery on oxidative and carbonyl stress in a rat model of chronic voluntary alcohol intake. Male Wistar rats received either water (control, SOD) or alcohol solutions (alcohol, alcohol + SOD) instead of drinking water during a period of 28 days. The concentration of ethanol gradually increased every week (5, 10, 15, 20% v/v). Plasmid encoding mitochondrial Mn-SOD or saline was injected intramuscularly once a week. At the end of the study, the levels of advanced glycation end products (AGEs) and ascorbic free radicals in serum were decreased by both, chronic alcohol treatment and SOD gene application independently. These effects had an additive potential, as the combination of alcohol and SOD treatment resulted in the lowest levels of these markers (p<0.001). As expected, SOD gene therapy decreased the levels of serum advanced oxidation protein products (AOPP). Interestingly, chronic alcohol intake had no effect on the oxidative damage of proteins and the combination of treatments significantly increased AOPP (p<0.001). Further, alcohol and SOD independently decreased lipoperoxidation in cerebellum, as estimated by malondialdehyde measurement (p<0.05). Malondialdehydelevels in alcohol + SOD group were similar to those observed in the control group. In summary, carbonyl and oxidative stress markers were decreased by a high dose SOD gene therapy as well as by chronic voluntary alcohol intake. The combination treatment resulted in contradictory effects on the monitored parameters – additive, if considering antioxidative status and AGEs production; antagonistic, if considering malondialdehydeand AOPP levels. Further studies are needed to explain and prove these results.
机译：实验和临床研究表明，酒精在各种疾病的病因中起着至关重要的作用。氧化应激是酒精有害作用的主要机制之一。我们先前的研究表明，在慢性强制性酒精摄入模型中，低分子量抗氧化剂对氧化和羰基应激指标水平具有保护作用。这项研究的目的是评估在长期自愿摄入酒精的大鼠模型中，酶促高分子量抗氧化剂（锰超氧化物歧化酶-Mn-SOD）基因传递对氧化和羰基应激的影响。在28天的时间内，雄性Wistar大鼠接受水（对照，SOD）或酒精溶液（酒精，酒精+ SOD）代替饮用水。每周乙醇浓度逐渐增加（5、10、15、20％v / v）。每周一次肌肉内注射编码线粒体Mn-SOD或盐水的质粒。在研究结束时，慢性酒精治疗和SOD基因应用均可降低血清中晚期糖基化终产物（AGEs）和抗坏血酸自由基的水平。这些作用具有加和潜力，因为酒精和SOD处理的组合导致这些标记物的最低水平（p <0.001）。不出所料，SOD基因治疗降低了血清高级氧化蛋白产物（AOPP）的水平。有趣的是，长期饮酒对蛋白质的氧化损伤没有影响，并且联合治疗显着增加了AOPP（p <0.001）。此外，通过丙二醛测定可知，酒精和SOD独立降低了小脑的脂质过氧化作用（p <0.05）。酒精+ SOD组丙二醛水平与对照组相似。总之，通过高剂量的SOD基因治疗以及长期自愿饮酒，羰基和氧化应激指标均降低。如果考虑抗氧化状态和AGEs的产生，联合处理会对所监测的参数-添加剂产生矛盾的影响;如果考虑丙二醛和AOPP含量，则为拮抗药。需要进一步的研究来解释和证明这些结果。

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