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膜脂成分的变化加速了幼鼠心脏在经历2周缺氧后再进行高氧处理时的脂质过氧化。

Change in the membranous lipid composition accelerates lipid peroxidation in young rat hearts subjected to 2 weeks of hypoxia followed by hyperoxia.

作者信息

Oka Tatsujiro, Itoi Toshiyuki, Terada Naoto, Nakanishi Hiroki, Taguchi Ryo, Hamaoka Kenji

机构信息

Department of Pediatric Cardiology and Nephrology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.

出版信息

Circ J. 2008 Aug;72(8):1359-66. doi: 10.1253/circj.72.1359.

Abstract

BACKGROUND

The effects of chronic hypoxia on cardiac membrane fatty acids and on lipid peroxidation were examined, as well as the effect of l-carnitine (LCAR), which suppresses lipid peroxidation, on this process.

METHODS AND RESULTS

Four-week-old Sprague-Dawley rats were exposed to 10% oxygen for 14 days ("Hypoxia"), and then to 100% oxygen for 12 h (O2). LCAR (200 mg/kg) was administered by intraperitoneal injection daily for 2 weeks. Fatty acid composition, malondialdehyde (MDA) as a lipid peroxidation product, and antioxidants (superoxide dismutase (SOD), glutathione peroxidase and catalase) were measured. The concentration of linoleic acid was lower, and that of docosahexaenoic acid, which has more double bonds than linoleic acid, was increased in hypoxic hearts. SOD activity decreased in hypoxia, whereas MDA was unchanged, but significantly increased in "Hypoxia"+O2. LCAR reduced the increase in MDA, and had no effect on SOD activity or fatty acid composition. The administration of LCAR caused an increase in the ventricular levels of acetylcarnitine.

CONCLUSIONS

These results suggest that chronic hypoxia changes the cardiac fatty acid composition of juvenile rats to fatty acids that contain more double-bonds and reduce SOD activity, and that lipid peroxidation was augmented by exposure to oxygen.

摘要

背景

研究了慢性缺氧对心脏膜脂肪酸和脂质过氧化的影响,以及左旋肉碱(LCAR)对该过程的影响,LCAR可抑制脂质过氧化。

方法与结果

将四周龄的Sprague-Dawley大鼠暴露于10%氧气环境中14天(“缺氧”组),然后再暴露于100%氧气环境中12小时(O2组)。每天腹腔注射LCAR(200mg/kg),持续2周。检测脂肪酸组成、脂质过氧化产物丙二醛(MDA)以及抗氧化剂(超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶和过氧化氢酶)。缺氧心脏中亚油酸浓度降低,而双键比油酸更多的二十二碳六烯酸浓度升高。缺氧时SOD活性降低,MDA含量未变,但在“缺氧”+O2组中显著增加。LCAR减少了MDA的增加,对SOD活性或脂肪酸组成无影响。给予LCAR导致心室中乙酰肉碱水平升高。

结论

这些结果表明,慢性缺氧会使幼年大鼠的心脏脂肪酸组成转变为含有更多双键的脂肪酸,并降低SOD活性,且暴露于氧气会加剧脂质过氧化。

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