睡眠呼吸暂停动物模型中的肝脏氧化应激:不同暴露时间的影响。

Darlan P Rosa, Denis Martinez, Jaqueline N Picada, Juliane G Semedo, Norma P Marroni
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引用次数: 26

摘要

背景:反复的呼吸暂停事件会导致间歇性缺氧(IH),从而改变各种系统的功能,产生自由基和氧化应激。方法:我们研究了成年小鼠在间歇性缺氧、模拟睡眠呼吸暂停条件下的肝脏氧化应激。三组分别接受21天的IH(IH-21)、35天的IH35或35天的假IH。我们通过TBARS评估脂质的氧化损伤,并通过彗星分析评估DNA的氧化损伤;在HE染色的玻片中评估肝组织炎症。通过过氧化氢酶、超氧化物歧化酶、谷胱甘肽过氧化物酶活性和总谷胱甘肽测定抗氧化剂。结果:IH-21后,肝脏氧化应激无明显变化。IH-35后,检测到显著的氧化应激、脂质过氧化、DNA损伤和内源性抗氧化剂的减少。结论:在睡眠呼吸暂停的动物模型中,间歇性缺氧在35天后会因氧化应激而导致肝脏损伤,但在21天后不会。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Hepatic oxidative stress in an animal model of sleep apnoea: effects of different duration of exposure.

Background: Repeated apnoea events cause intermittent hypoxia (IH), which alters the function of various systems and produces free radicals and oxidative stress.

Methods: We investigated hepatic oxidative stress in adult mice subjected to intermittent hypoxia, simulating sleep apnoea. Three groups were submitted to 21 days of IH (IH-21), 35 days of IH (IH-35), or 35 days of sham IH. We assessed the oxidative damage to lipids by TBARS and to DNA by comet assay; hepatic tissue inflammation was assessed in HE-stained slides. Antioxidants were gauged by catalase, superoxide dismutase, glutathione peroxidase activity and by total glutathione.

Results: After IH-21, no significant change was observed in hepatic oxidative stress. After IH-35, significant oxidative stress, lipid peroxidation, DNA damage and reduction of endogenous antioxidants were detected.

Conclusions: In an animal model of sleep apnoea, intermittent hypoxia causes liver damage due to oxidative stress after 35 days, but not after 21 days.

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