Gavino V C, Dillard C J, Tappel A L
Arch Biochem Biophys. 1985 Mar;237(2):322-7. doi: 10.1016/0003-9861(85)90283-8.
The effect of in vivo lipid peroxidation on the excretion of immunoreactive prostaglandin E2 (PGE2) in the urine of rats was studied. Weanling, male Sprague-Dawley rats were fed a vitamin E-deficient diet containing 10% tocopherol-stripped corn oil (CO) or 5% cod liver oil (CLO) with or without 40 mg dl-alpha-tocopheryl acetate/kg. To induce a high, sustained level of lipid peroxidation, some rats were injected intraperitoneally with 100 mg of iron as iron dextran after 10 days of feeding. Iron overload stimulated in vivo lipid peroxidation in rats, as measured by the increase in expired ethane and pentane. Dietary vitamin E reversed this effect. Rats fed the CLO diet excreted 9.5-fold more urinary thiobarbituric acid-reactive substances (TBARS) than did rats fed the CO diet. Iron overload increased the excretion of TBARS in the urine of rats fed the CO diet, but not in urine of rats fed the CLO diet. Dietary vitamin E decreased TBARS in the urine of rats fed either the CO or the CLO diet. Iron overload decreased by 40% the urinary excretion of PGE2 by rats fed the CO diet, and dietary vitamin E did not reverse this effect. Iron overload had no statistically significant effect on urinary excretion of PGE2 by rats fed the CLO diet. A high level of lipid peroxidation occurred in iron-treated rats, as evidenced by an increase in alkane production and in TBARS in urine in this study, and by an increase in alkane production by slices of kidney from iron-treated rats in a previous study [V. C. Gavino, C. J. Dillard, and A. L. Tappel (1984) Arch. Biochem. Biophys. 233, 741-747]. Since PGE2 excretion in urine was not correlated with these effects, lipid peroxidation appears not to be a major factor in renal PGE2 flux.
研究了体内脂质过氧化对大鼠尿液中免疫反应性前列腺素E2（PGE2）排泄的影响。将断乳的雄性Sprague-Dawley大鼠喂以含10%生育酚去除玉米油（CO）或5%鱼肝油（CLO）的维生素E缺乏饮食，添加或不添加40mg dl-α-生育酚乙酸酯/kg。为诱导高水平、持续的脂质过氧化，部分大鼠在喂食10天后腹腔注射100mg右旋糖酐铁形式的铁。通过呼出乙烷和戊烷的增加来衡量，铁过载刺激了大鼠体内的脂质过氧化。膳食维生素E可逆转此效应。喂食CLO饮食的大鼠排泄的尿硫代巴比妥酸反应性物质（TBARS）比喂食CO饮食的大鼠多9.5倍。铁过载增加了喂食CO饮食大鼠尿液中TBARS的排泄，但对喂食CLO饮食大鼠的尿液无此作用。膳食维生素E降低了喂食CO或CLO饮食大鼠尿液中的TBARS。铁过载使喂食CO饮食大鼠的PGE2尿排泄量降低40%，膳食维生素E不能逆转此效应。铁过载对喂食CLO饮食大鼠的PGE2尿排泄无统计学显著影响。本研究中，铁处理大鼠出现高水平脂质过氧化，表现为烷烃生成增加和尿液中TBARS增加，且在先前研究中[V.C.Gavino、C.J.Dillard和A.L.Tappel（1984年）《生物化学与生物物理学档案》233，741 - 747]铁处理大鼠肾切片的烷烃生成也增加。由于尿液中PGE2排泄与这些效应无关，脂质过氧化似乎不是肾脏PGE2通量的主要因素。
