Hepatic oxidative stress in an animal model of sleep apnoea: effects of different duration of exposure.
Hepatic oxidative stress in an animal model of sleep apnoea: effects of different duration of exposure.
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DOI：
10.1186/1476-5926-10-1
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发表时间：
2011-07-05
期刊：
影响因子：
--
通讯作者：
Marroni NP
中科院分区：
文献类型：
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作者：
Rosa DP;Martinez D;Picada JN;Semedo JG;Marroni NP
反复的呼吸暂停事件会导致间歇性低氧(IH)，从而改变各种系统的功能，产生自由基和氧化应激。我们研究了成年小鼠在间歇性低氧状态下的肝脏氧化应激，模拟睡眠呼吸暂停。三组分别接受高血压21d(IH-21)、高血压35d(IH-35)或假高血压35d。我们用TBARS和彗星试验评估了脂质和DNA的氧化损伤；用HE染色的玻片评估了肝组织的炎症。抗氧化剂通过过氧化氢酶、超氧化物歧化酶、谷胱甘肽过氧化物酶活性和总谷胱甘肽来衡量。IH-21治疗后，肝组织氧化应激无明显变化。IH-35后，出现明显的氧化应激、脂质过氧化、DNA损伤和内源性抗氧化剂的减少。在睡眠呼吸暂停的动物模型中，间歇性低氧在35天后会由于氧化应激而导致肝脏损伤，但在21天后不会。
Repeated apnoea events cause intermittent hypoxia (IH), which alters the function of various systems and produces free radicals and oxidative stress. 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. 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. In an animal model of sleep apnoea, intermittent hypoxia causes liver damage due to oxidative stress after 35 days, but not after 21 days.