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An elevated level of copper zinc superoxide dismutase fails to prevent oxygen induced retinopathy in mice.

机译:升高水平的铜锌超氧化物歧化酶不能预防小鼠中氧引起的视网膜病变。

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摘要

BACKGROUND: To determine whether a higher level of copper zinc superoxide dismutase (CuZnSOD) can reduce the severity of oxygen induced retinopathy (OIR) in a mouse model. METHODS: CuZnSOD transgenic mice with a threefold increase in CuZnSOD activity and control non-transgenic mice were exposed to 90% oxygen for 12 hours a day during the first 5 days of life. After oxygen treatment, all mice were reared in room air for 10 days. Another group of transgenic and non-transgenic mice were kept in room air for 15 days and served as control groups for the oxygen effect. At day 15, all mice were killed and perfused with India ink. The retinas were flat mounted on slides and examined with a light microscope. RESULTS: There was a statistically significant increase in the incidence of OIR in mice exposed to high levels of oxygen, whether or not they were transgenic. However, there was no statistically significant difference in the severity of OIR between oxygen treated transgenic and non-transgenic mice. CONCLUSION: A threefold higher CuZnSOD activity does not protect against OIR in mice. This is an unexpected finding, since oxygen radicals are considered a major factor causing OIR, and increased CuZnSOD activity has reduced oxygen radical induced damage in several neuronal and non-neuronal systems. The possibility of a damaging role for other radicals not affected by CuZnSOD cannot be excluded.
机译:背景:为了确定更高水平的铜锌超氧化物歧化酶(CuZnSOD)是否可以降低小鼠模型中氧致视网膜病变(OIR)的严重程度。方法:在生命的前5天中,每天将CuZnSOD转基因小鼠的CuZnSOD活性提高三倍,而对照非转基因小鼠则每天暴露于90%的氧气中12小时。氧气处理后,将所有小鼠在室内空气中饲养10天。将另一组转基因和非转基因小鼠在室内空气中放置15天,并作为氧效应的对照组。在第15天,杀死所有小鼠并用印度墨水灌注。将视网膜平坦地安装在载玻片上,并用光学显微镜检查。结果:暴露于高水平氧气的小鼠中,无论是否是转基因的,OIR的发生率都有统计学意义的增加。但是,经氧气处理的转基因小鼠和非转基因小鼠之间的OIR严重程度无统计学差异。结论:高三倍的CuZnSOD活性不能保护小鼠的OIR。这是一个出乎意料的发现,因为氧自由基被认为是导致OIR的主要因素,而增加的CuZnSOD活性减少了氧自由基在几个神经元和非神经元系统中引起的损伤。不能排除不受CuZnSOD影响的其他自由基具有破坏性作用的可能性。

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