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新生大鼠的脂质过氧化:禁食和高氧对呼出气体中乙烷和戊烷的影响。

Lipid peroxidation in the newborn rat: influence of fasting and hyperoxia on ethane and pentane in expired air.

作者信息

Roberts R J, Rendak I, Bucher J R

出版信息

Dev Pharmacol Ther. 1983;6(3):170-8. doi: 10.1159/000457292.

Abstract

The rate of lipid peroxidation, as determined by expired air pentane and ethane measurements, was assessed in suckled or fasted newborn rats exposed to air or hyperoxia (FIO2 greater than 0.95). Pentane and ethane production in suckled newborn rats did not significantly change with exposure to hyperoxia after birth. Pentane production averaged over a 3-day exposure period was 2.8 pmol/100 g/min in hyperoxia versus 2.5 pmol/100 g/min in air. However, significant increases in ethane production occurred in fasted newborn rats over the first 18 h of life (less than 2.5 pmol/100 g/min increasing to greater than 6 pmol/100 g/min), which were not observed in suckled animals. Although hyperoxia did not cause an increase in pentane or ethane production above air-exposed controls, nutritional deprivation in newborn rats appeared to accelerate lipid peroxidation events and resulted in high mortality in newborn rats exposed to hyperoxia.

摘要

通过测量呼出气体中的戊烷和乙烷来确定脂质过氧化率,对暴露于空气或高氧环境(FIO2大于0.95)的哺乳或禁食新生大鼠进行评估。出生后暴露于高氧环境下,哺乳新生大鼠的戊烷和乙烷生成量没有显著变化。在3天的暴露期内,高氧环境下戊烷的平均生成量为2.8 pmol/100 g/分钟,而空气中为2.5 pmol/100 g/分钟。然而,禁食新生大鼠在出生后的前18小时内乙烷生成量显著增加(从低于2.5 pmol/100 g/分钟增加到高于6 pmol/100 g/分钟),而哺乳动物中未观察到这种情况。尽管高氧环境并未导致戊烷或乙烷生成量高于暴露于空气的对照组,但新生大鼠的营养剥夺似乎加速了脂质过氧化事件,并导致暴露于高氧环境的新生大鼠死亡率很高。

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